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Molecular Biology BSc First Year > MBB11002 -Microbiology 1 > Flashcards

MBB11002 -Microbiology 1 Flashcards

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1
Q

What are microfossils?

A

microorganisms trapped in rocks which resemble modern species
-found in stromatolites/sediments
-photographic (rather than experimental) evidence

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2
Q

What are stromatolites?

A

sediments made from alternating layers of limestone and microbial mats (entrapped bacterial communities)

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3
Q

What are the 4 main theories to explain the origin of life?

A

-chemical origin (pre-biotic soup forming simple molecules abiotically)
-RNA world (RNA as the first macromolecule)
-apparition of cellular life (prebiotic chem leading to cellular life)
-panspermia (life on Earth originating from space) -Fred Hoyle and Chandra Wickramasinghe

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4
Q

What was Miller’s experiment for the chemical origin of life?

A

-most amino acids and nucleotides can be formed from simple molecules (H2, CH4, NH3) in conditions mimicking Earth primitive conditions
-in UV and presence of H2S, HCN can produce amino acid, lipid and nucleotide precursors

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5
Q

What are the limitations for Miller’s experiment for the chemical origin of life?

A

-no evidence of aas in sediments
-H2 required -based upon (controversial) hypothesis of a reducing atmosphere

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6
Q

Why might RNA have been the first macromolecule encoding complex information (the RNA world origin of life theory)?

A

-has 4 building blocks (rather than 20 for proteins)
-less energy to form and degrade compared to DNA
-early biochem pathways can form uracil
-ssDNA is used as genome by viruses
-can have catalytic activity (ribozymes)

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7
Q

What is the activity of ribozymes?

A

-cleavage/ligation of RNA (splicing)
-replication
-formation of peptide bonds

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8
Q

What is the theory of apparition of cellular life?

A

compartmentalisation occurs to give rise to last universal common ancestor
-compartmentalisation created by phospholipids
-aas and nucleotides trapped

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9
Q

Why is compartmentalisation needed?

A

-protection from environment
-selective barrier
-rate enhanced (conc of molecules for metabolism)

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10
Q

What are the two hypothesises for the apparition of cellular life?

A

-surface origin
-subsurface origin

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11
Q

What is the surface origin hypothesis for the apparition of cellular life?

A

-primitive cells formed spontaneously on surface of Earth from a prebiotic soup
-metabolic processes were optimised by natural selection

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12
Q

What is the subsurface origin hypothesis for the apparition of cellular life?

A

-life appeared in stable conditions on ocean floor in hypothermal mounds (geothermal heated water from a crack in floor and cool ocean water)
-H2 and H2S as source of e- to form organic molecules
-redox/pH gradients used as prebiotic proton motor force

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13
Q

What are microbes?

A

small, unicellular organisms
-wide range!
-10nm-1mm

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14
Q

What is genetic plasticity?

A

phenotypic variation due to genetic factors
-drives microbial diversity

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15
Q

Why are microorganisms more diverse?

A

-bacteria are haploid, meaning a mutation will def be passed on
-rapid divisions (binary fission) rather than reproduction
-horizontal gene transfer can occur (transformation, conjugation, transduction)

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16
Q

What ways can horizontal gene transfer occur in microbes?

A

-transformation (DNA is taken up from surrounding cells)
-conjugation (genetic material can be exchanged)
-transduction (bacterial cells can be infected by phages targeting them)

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17
Q

What is taxonomy?

A

the discipline dealing with classifications of organisms into taxonomic subdivisions

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18
Q

What is the taxonomic hierarchy?

A

domain
kingdom
phylum
class
order
family
genus
species

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19
Q

How is taxonomy defined?

A

-phenotypic analysis (morphology, differential sraining, phage typing, fatty acid profiles, mass spec, metabolism comparisons)
-genetic analysis (DNA hybridisation, FISH, rRNA sequencing, multi locus sequencing, whole genome sequencing)

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20
Q

How is taxonomy studied using phenotypical analysis?

A

-morphology and differential staining
-phage typing (resistance, etc studied in agar plates)
-fatty acid profiles (membrane compositions -both gram +ve and -ve bact)
-mass spec (using isolate of whole bact as sample)
-metabolism comparisons (spread on diff medias, metabolic galeries, etc)

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21
Q

How is taxonomy studied using genetic analysis?

A

-rRNA sequencing (most widely used with taxonomy!! -rRNA is v.specific to species)
-DNA hybridisation (compare 2 purified genomes)
-FISH
-multi locus sequencing (sequencing and comparing house keeping genes)
-whole genome sequencing

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22
Q

What is phylogeny?

A

study of evolutionary history of organisms

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23
Q

How is phylogeny defined?

A

-genetic info compared using molecular clocks (DNA/protein seqs)
-seqs compared
-% divergence calculated
-phylogenetic trees created

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24
Q

What are molecular clocks?

A

technique where the mutation rate of biomolecules is used to deduce the time in prehistory when two or more life forms diverged

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25
Q

How were organisms divided into the three domains bacteria, archae and eukarya?

A

by the phenotypic tree of life (comparing rRNA gene seqs)

by Carl Woese

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26
Q

What are the three domains?

A

-Bacteria
-Archae
-Eukarya

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27
Q

What are the major differences between eukaryotic and prokaryotic cells?

A

-size (eukaryotic ~1µm, prokaryotic ~0.5µm)
-presence/absence of nucleus
-compartmentalisation

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28
Q

What are the components of eukaryotic cells?

A

-nucleus
-endoplasmic reticulum
-golgi complex
-lysosomes
-peroxisomes
-mitochondria
-chloroplasts
-flagella/cilia

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29
Q

What is the structure of the nucleus in eukaryotic cells?

A

-contains chromatin (histones + DNA)
-euchromatin and heterochromatin

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30
Q

What is the function of the nucleus?

A

mRNA, tRNA and rRNA synthesis

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31
Q

What is the structure of the endoplasmic reticulum?

A

-extension of nuclear membrane
-rough has ribosomes, smooth doesn’t

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32
Q

What is the function of the rough endoplasmic reticulum?

A

-protein synthesis
-protein quality control

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33
Q

What is the function of the smooth endoplasmic reticulum?

A

-lipid synthesis
-metabolic activities (eg. toxin breakdown)

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34
Q

What is the structure of the golgi complex?

A

-network of membranes (cisternae)
-polarised -has cis and trans face (cis -entry, trans -exit)

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35
Q

What is the function of the golgi complex?

A

-carbohydrate synthesis (eg. cell walls, extracellular matrix)
-protein modification (for specific targeting)
-secretes proteins/incorporates proteins into membranes

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36
Q

What is the function of lysosomes?

A

-metabolic processes -hydrolysing macromolecules (contain digestive enzymes for this!)

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37
Q

What is the function of peroxisomes?

A

-incorporate lipids and proteins from the cytoskeleton
-lipid metabolism (oxidise alcohols and fatty acids)

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38
Q

What is the function of mitochondria?

A

-respiration, oxidative phosphorylation, Krebs cycle

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39
Q

What is the structure of chloroplasts?

A

-stacks of thylakoids, forming grana
-stroma (~matrix)
-own circular DNA

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40
Q

What is the function of chloroplasts?

A

-Calvin cycle (converts light to organic compounds)

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41
Q

What is the structure of flagella/cilia?

A

-bundle of 9 pairs of microtubules surrounding a central pair (axoneme)
-nexin molecules connect microtubules to adjacent microtubules
-dynein molecules (drive motion by ATP hydrolysis)

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42
Q

What are the components of prokaryotic cells?

A

-nucleoid
-cytoplasm
-envelope
-appendages (pilus, fimbriae, flagella)

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43
Q

What is the structure of a nucleoid?

A

-usually a single circular chromosome (<10Mbp)
-dsDNA complexed w/histone-like proteins
-also plasmids

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44
Q

What is the structure of cytoplasm in prokaryotes?

A

-contains proteins, tRNA, mRNA, ribosomes
-contains protein-bound inclusion bodies (carboxysomes, storage granules, gas residues)
-generally thought to have no organelles but some do (magnetosomes, photosynthetic membranes, internal membranes)

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45
Q

What is the structure of the envelope in prokaryotes?

A

inside…
cytoplasmic membrane
peptidoglycan
polymers cov bound to peptidoglycan
outer membrane
…outside

-varies depending on species

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46
Q

What appendages can prokaryotes have?

A

-pilus
-fimbriae
-flagella

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47
Q

What is a pilus?

A

prokaryotic appendage dedicated to conjugation (plasmid exchange)
-1 per cell

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48
Q

What is a fimbriae?

A

prokaryotic appendage involved in adherence to host cell surfaces
-antigenic structures
-made of 1 protein

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49
Q

What is a flagella?
(prokayotes)

A

appendage involved in motility
-moves via rotation
-have diff configurations -can have 1 or lots, diff ones exist, etc
-anchored in cytoplasmic membrane (varies in gram +ve/-ve)
-usually 1 protein in proks (diff to euks!)

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50
Q

What is the theory of the endosymbiotic origin of eukaryotes?

A

stable incorporation of endosymbiotic bacteria in formation of mitochondria and chloroplasts
-nucleus appears before mitochondria and chloroplasts by endosymbiosis

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51
Q

What properties of eukaryotes are in favour of the endosymbiotic origin of eukaryotes?

A

-mitochondria and chloroplasts have inner and outer membranes
-mitochondria and chloroplasts have specific ribosomes (called mitoribosomes and chlororibosomes) which are diff to eukaryotic ribosomes
-mitochondria and chloroplasts multiply by binary fission (like proks)

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52
Q

What are the issues with the endosymbiotic origin of eukaryotes?

A

-eukaryotes and prokaryotes have similar lipid compositions

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53
Q

What unicellular eukaryotes are there?

A

-fungi (obvs can be multicellular too!)
-unicellular algae (plant-like protists)
-protozoa (animal-like protists)
-slime moulds (protists)

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54
Q

What are the types of fungi?

A

-molds (filamentous fungi)
-yeast (unicellular fungi)
-basidiomycetes (mushrooms)

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55
Q

Why are fungi important?

A

-ecological role -act as decomposers in the carbon cycle
-economical benefits -biotech, plant pathogens, etc
-human health -fungal infections

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56
Q

What are the common properties of fungi?

A

-most form hyphae (multicellular filaments)
-most are pleomorphic (exist in various forms)
-have carbohydrate cells walls -often chitin, mannans and/or glucans
-have 2 phases in life cycle involving asexual and sexual reproduction (haploid and diploid forms) -can undergo transitions

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57
Q

What is the structure of moulds?

A

-have filament structures known as hyphae (which grow mycelium)

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58
Q

Whereabouts in moulds does growth and the absorption of nutrients occur?

A

tip of hyphae

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59
Q

What occurs in the lifecycle of moulds?

A

alternation between haploid and diploid phases
-fusion
-spores prod

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60
Q

How do basidiomycetes live in symbiosis with trees or algae?

A

-fungus supplies nutrients and minerals
-trees provides prods of photosynthesis

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61
Q

What occurs in the lifecycle of basidomycetes?

A

-primary mycelium (gametes) fuse to prod secondary mycelium
-secondary mycelium produces basidium
-basidium produces basidospores

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62
Q

Why are yeast important?

A

-ecologically -used in brewery and bakery
-human health -infections, some S.cerevisiae strains used as probiotics
-used as model organism

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63
Q

What is S.cerevisiae used as a model organism for?

A

-lipid biology
-protein folding, quality control and degradation
-vesicular trafficking and fusion
-lysosomal and peroxisomal function
-apoptosis
-cell cycle
-mitochondrial and oxidative stress

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64
Q

What occurs in the lifecycle of yeast?

A

-cell division by budding and binary fission
-some form hyphae under specific conditions (dimorphic!)

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65
Q

What are the types of algae?

A

-primary endosymbiotic algae
-secondary endosymbiotic algae (diatoms)
-predatory algae (dinoflagellates)

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66
Q

What are primary endosymbiotic algae?

A

“true algae”
-green or red
-autotrophs

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67
Q

What are diatoms?

A

secondary endosymbiotic algae
-can be centric (have radial symmetry) or pennate (have non-radial symmetry)

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68
Q

What are dinoflagellates?

A

predatory algae
-very diff to endosymbiotic algae

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69
Q

What are mixotrophs?

A

organisms which can use a mix of energy sources
-dinoflagellates (predatory algae) -result from primary endosymbiotic algae being engulfed by a protist

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70
Q

What is the difference between primary and secondary endosymbiotic algae?

A

-primary have one membrane, whilst secondary have 2 membranes
-chloroplasts in primary endosymbiotic algae have a double membrane, while chloroplasts in secondary endosymbiotic algae have a triple membrane

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71
Q

Why are algae ecologically important?

A

-components of phytoplankton (produce lots of O2!)
-key food item in ocean web and aquaculture

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72
Q

What are the key properties of algae?

A

-photosynthetic organisms
-have chloroplasts

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73
Q

What are the properties of diatoms like?

A

-large biomass
-more complex chloroplasts than plants
-mobile (produces mucus to slide on -no appendages)
-have cell walls called frustule (made of silica)

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74
Q

What are the two types of diatoms?

A

-centric diatoms (radial symmetry)
-perinate diatoms (bilateral symmetry)

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75
Q

What are diatoms cell walls like?

A

frustules
-in two halves
-made of silicon dioxide crosslinked to form silica
-very rigid -makes life cycle more complicated

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76
Q

What happens in the life cycle of diatoms?

A

-each daughter cell inherits half of frustule, making it smaller than parents
-cells get smaller and smaller each generation, until they can’t divide anymore so undergo meiosis to form gametes
-gametes fuse, forming frustule same size as parents’

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77
Q

What are the cell walls of secondary endosymbiotic algae like?

A

frustules made of CaCO3 growing in multiple scales

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78
Q

What happens in the life cycle of primary endosymbiotic algae?

A

-colonial lifecycle
-asexual and sexual reproduction

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79
Q

What are the types of protozoa?

A

-ciliates (predatory protists)
-apicomplexans (parasites)
-dinoflagellates (predatory algae)
-metamonds
-trypanosomes

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80
Q

Which types of protozoa are alveolates?

A

-ciliates (predatory protists)
-apicomplexans (parasites)
-dinoflagellates (predatory algae)

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81
Q

What are the properties of alveolates?

A

-have alveoli (bags of fluid surrounded by lipid membrane)
-mobile (have cilia, can glide)
-mostly aquatic

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82
Q

What is the ecological importance of alveolates?

A

ciliates: food web (zooplankton)
apicomplexans: human health
dinoflagellates: involved in carbon cycle

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83
Q

What happens in the life cycle of ciliates?

A

-binary fission (asexual reprod.)
-conjugation (sexual reprod.)

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84
Q

What are the properties of paramecium (model ciliate)?

A

-alveoli under cytoplasmic membrane
-cilia and trichocyst
-oral groove (for food entry)
-contractile vacuole (for H2O reg)
-digestive vacuole
-3 nuclei (macronucleus, 2 micronucleus)

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85
Q

What’s the difference between macronuclei and micronuclei?

A

macronuclei
-transcriptionally active
-lots of copies of diff genomes
micronuclei
-transcriptionally inactive
-genetic recombination

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86
Q

What are the properties of apicomplexans?

A

-have flagella, cilia or pseudopods
-contain apical complex (aid entry into host)
-have apicoplast (degenerate chloroplast -no chlorophyll, no photosynthesis -involved in fatty acid metabolism)

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87
Q

What happens in the life cycle of apicomplexans?

A

-use a vector to infect host
-inside host, undergo morphological changes and multiplies, releasing merozoates, which differentiate into gametocytes
-in vector, gametes fuse, forming zygote which invades vector, producing sporozoites

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88
Q

What are the properties of dinoflagellates?

A

-mixotrophs (undergo photosynthesis and feed on bacteria, algae, etc)
-have 2 flagella
-have chloroplasts with complex membranes
-cell walls made of overlapping cellulose plates (theca)
-have extrusome (ejectable, membrane bound organelle which can discharge contents)

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89
Q

What happens in the life cycle of dinoflagellates?

A

-vegetative reproduction via binary fisson and sexual reproduction
-can exist in dormant forms (cysts)

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90
Q

What are the properties of slime moulds and amoebas?

A

-found in damp environments
-have complex life cycles involving the same developmental stage

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91
Q

How are amoebas mobile?

A

using pseudopod mobility
-actin polymerisation/disassembly

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92
Q

How do amoebas use pseudopod motility?

A

actin polymerisation/disassembly

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93
Q

What are amoebas?

A

parasitic unicellular eukaryotes

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94
Q

What happens in the lifecycle of cellular slime moulds?

A

-binary fission
-when stressed, release cAMP, which drives aggregation to form a “slug” (social motility!)
-release of spores (cysts) initiates new cycles

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95
Q

What happens when cellular slime moulds are stressed (eg. under starvation of nutrients)?

A

-release cAMP
-aggregation occurs, forming a slug (lots of cells together)
-slug differentiates into fruiting body (made of sporangium and stalk)
-fruiting body can form cysts
-cysts/spores released, initiating new cycle

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96
Q

What happens in the life cycle of a plasmodial slime mould?

A

-binary fission
-individual cells can aggregate to form a plasmodium (single cell with lots of nuclei)
-plasmodium differentiaes into fruiting body
-fruiting body can form cysts
-cysts/spores released, initiating new cycle

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97
Q

What are the general properties of viruses?

A

-needs host mechanism machinery to replicate (obligatory parasite)
-small
-made of nucleic acid genome surrounded by protein coat (capsid) and facultative lipid envelope
-can infect all living organisms

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98
Q

What is the general structure of viruses?

A

-nucleic acid genome
-capsid (protein coat made of capsomers, can contain polysaccharides)
-lipid envelope (lipid bilayer w/proteins from host)

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99
Q

What is the composition of a viral genome?

A

ss/ds DNA/RNA

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100
Q

What is the size of a viral genome?

A

2-20kb (small)
-minimal info needed (can get from host)
-only specific genes
-generally ds>ss and DNA>RNA

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101
Q

How is a viral genome generally organised?

A

as one molecule
-can be fragmented

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102
Q

What is the composition of a viral capsid?

A

1+ proteins called capsomers

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103
Q

What is the structure of a viral capsid?

A

-highly ordered
-self-assembly prods

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104
Q

What are the two types of viral capsids?

A

-icosahedral symmetry (spherical)
-helical symmetry (rod-shaped)

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105
Q

What is the structure of a nucleocapsid?

A

nucleic acid surrounded by capsomers

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106
Q

What is the composition of a viral envelope?

A

-lipid bilayer
-glycoproteins/proteins from host or viral encoded

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107
Q

What is the role of a viral envelope?

A

allows entry into host cell via fusion/endocytosis

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108
Q

What is the structure of a bacteriophage?

A

-mixture of icosahedral and filamentous structures
-head
-collar
-tail (ejects genetic info into host once strong connections are established)
-endplate
-tail fibres (recognise cell surface)

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109
Q

What are the issues with some nomenclatures for viral classification?

A

lots of diff systems going on
-names after disease
-named after place disease was first reported
-named after host/signs of disease
-named after shape of virus
-named after discoverer
-named after mechanism of transmission

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110
Q

How are viruses classified using the Baltimore classification?

A

into 7 classes
-separated by whether they are DNA or RNA viruses and how the genome is replicated and transcribed

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111
Q

What does the Baltimore classification take into account?

A

-the nature and type of genome (DNA/RNA, ss/ds)
-how genome is replicated
-how genome is transcribed

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112
Q

Which classes are DNA viruses?

A

1, 2 and 7

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113
Q

Which classes are RNA viruses?

A

3, 4, 5 and 6

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114
Q

Name an example of a class 1 virus

A

Papillomavirus
-dsDNA

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115
Q

Name an example of a class 2 virus

A

Adeno-associated virus
-ssDNA

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116
Q

Name an example of a class 3 virus

A

Reovirus
-dsDNA

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117
Q

Name an example of a class 4 virus

A

Foot-and-mouth disease virus
-ssRNA

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118
Q

Name an example of a class 5 virus

A

Influenza
-ssRNA

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119
Q

Name an example of a class 6 virus

A

HIV
-reverse RNA

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120
Q

Name an example of a class 7 virus

A

Hepatitis B
-reverse DNA

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121
Q

What are the major steps in the life cycle of a virus?

A

-attachment to host
-genome injection (entry)
-production of viral nucleic acids and proteins
-maturation (viral particles assembling)
-release of virus (exit)

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122
Q

What happens in the lifecycle of a bacteriophage?

A

lytic cycle
-attachment (using tail fibres) and genome injection
-cellularisation of phage DNA
-synthesis of phage DNA and proteins, assembled into virions
-cell lysis, releasing phage virions
lysogenic cycle (dormant)
-attachment and genome injection
-recombination of phage DNA into bacterial genome generates prophage
-cell divisions
-if prophage exists, goes into lytic cycle

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123
Q

What happens in the lifecycle of a DNA virus?

A

-attachment and entry
-viral DNA uncoated (capsids removed) and transferred to nucleus
-synthesis of viral DNA and proteins
-maturation (virions assemble)

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124
Q

What happens in the lifecycle of a RNA virus?

A

-attachment and entry
-depends on virus -mRNA transcription and translation

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125
Q

What happens in the lifecycle of a Retrovirus?

A

-entry via fusion
-viral DNA and enzymes reeased
-viral DNA copied to dsDNA by reverse transcriptase
-dsDNA transported into nucleus and integrated into host genome
-new genomes and RNA produced
-mature retrovirus buds out of host

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126
Q

How are viral particles packaged?

A

fragmented genomes: genome fragments in complex with proteins paired before encapsulation
dsDNA viruses: encapsulation coupled with replicative genome maturing
ssRNA viruses and Retroviruses: capsomers cooperatively assemble, promoted by electrostatic interactions between capsid proteins and RNA genome

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127
Q

How are viral fragmented genomes packaged?

A

genome fragments in complex with proteins paired before encapsulation

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128
Q

How are dsDNA viral particles packaged?

A

encapsulation coupled with replicative genome maturing

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129
Q

How are ssRNA viral and Retroviral particles packaged?

A

electrostatic interactions between capsid proteins and RNA genome promote the cooperative assembly of capsomers

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130
Q

What different morphologies of bacteria are there?

A

-cocci (round)
-rod-shaped
-curved
-spiral
-exotic

-morphologies can change during cell cycle

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131
Q

What are the advantages of bacteria having a large surface area to volume ratio?

A

-nutrient exchange and growth rates
-high intracellular nutrient conc
-rapid evolution (high selection rate of mutations)

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132
Q

What is bacterial colour due to?

A

the production of pigments

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133
Q

What is bacterial smell due to?

A

the production of secondary metabolites
-side prods from metabolism (mechanisms in growth and division)

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134
Q

In what ways are bacterial phenotypes diverse?

A

-morphologically (diff shapes: cocci, rod, curved, spiral)
-size
-colour
-smell

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135
Q

How is the gram stain carried out?

A

-stain with crystal violet
-fix with iodine (mordant)
-wash with alcohol
-counter stain with safranin

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136
Q

What is the gram stain used for?

A

bacteria diagnostics
-can be used with complicated (rather than isolated) populations

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137
Q

What bacteria is stained purple by the gram stain?

A

gram positive

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138
Q

What are the properties of gram positive bacteria?

A

-no outer membrane
-thick cell wall

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139
Q

What bacteria is stained pink by the gram stain?

A

gram negative

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140
Q

Why is gram positive bacteria stained purple in the gram stain?

A

-crystal violet penetrates into peptidoglycan and gets trapped when the mordant is added

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141
Q

Why is gram negative bacteria stained pink in the gram stain?

A

-crystal violet sits on top of envelope and gets washed away
-safranin stains the outer membrane pink

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142
Q

What are the properties of gram negative bacteria?

A

-outer membrane
-thin cell wall

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143
Q

What is the structure of a S-layer in bacteria?

A

-made of proteinaceous crystalline arrays (self-assembled proteins)
-non-covalently bound to cell surface (in gram +ve, directly bound to peptidoglycan, in gram -ve, anchored to lipid membrane)

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144
Q

How are S-layers bound to the cell surface differently in gram positive and negative bacteria?

A

gram +ve: are directly bound to peptidoglycan/anything on peptidoglycan
gram -ve: anchored to lipid membrane

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145
Q

What is the structure of capsules in bacteria?

A

-made of polysaccharides or amino acids
-covalently bound to cell wall/outer membrane (anchored)

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146
Q

What do capsules do?

A

-gives resistance to host’s phagocytes/bacteriophages
-keeps environment hydrated (because polysaccharides are hydrophilic)

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147
Q

What is the structure of exopolysaccharides in bacteria?

A

-complex repeating units containing 2-20 sugars (variable!)
-non-covalently bound to cell surface
-homo or hetero -polysaccharides
-encase biofilms (thin layer of community of microorganisms protecting cells from environment)

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148
Q

How are exopolysaccharides important in biotechnology?

A

xanthan gum in toothpaste, ice cream, salad dressing, etc

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149
Q

What is the structure of the outer membrane in bacteria?

A

-asymmetric lipid bilayer (diff to inner membrane, w/symmetric bilayer)
-contains phospholipids, proteins (porins), lipoproteins, lipopolysaccharide (LPS)

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150
Q

What is LPS?

A

lipopolysaccharide
-contains lipid anchor, core polysaccharide, O-specifc polysaccharide)
-found in bacterial outer membranes

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151
Q

What was the structure of peptidoglycan (murein) in bacteria originally thought to be like vs what we know now?

A

originally…
-rigid exoskeleton (protective role)
now…
-flexible, elastic, dynamic

-composed of alternating N-acetylglucosamine (G) and N-acetylmuramic acid (M) substituted by short polypeptides (L and D amino acids)

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152
Q

How has better understanding of the structure of peptidoglycan in bacteria come about?

A

atomic force microscopy
-gives info on shape, height, elasticity, etc based upon deflection

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153
Q

What are the roles of peptidoglycan in bacteria?

A

-cell shape
-exoskeleton (resistance to osmotic stress)
-scaffold for displaying polymers and proteins (covalently and non-covalently anchors them)

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154
Q

What is the highly conserved structure of peptidoglycan?

A

alternating N-acetylglucosamine (G) and N-acetylmuramic acid (M)
-from M, pentapeptides (L and D amino acids) -sometimes w/a lateral chain

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155
Q

How is the alternating sequence of N-acetylglucosamine and N-acetylmuramic acid in peptidoglycan assembled?

A

by D,D-transpeptidases
-bifunctional enzymes (aa transfer, bind to penicillin)

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156
Q

What is the structure of the cytoplasmic membrane like in bacteria?

A

-phospholipids
-hopanoids (like steroids)
-proteins

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157
Q

What are chromosomes like in bacteria?

A

-always dsDNA
-usually singular circular chromosome
-varies in size (0.5-14Mbp)
-organised as nucleoid (supercoiling, histone-like proteins)

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158
Q

What are plasmids like in bacteria?

A

-always dsDNA
-usually circular
-varies in copy number (1-100s)
-varies in size (2-600kbp)
-can be transferable (self or non-self) via horizontal transfer
-can carry resistance genes

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159
Q

How is bacterial gene organised in regards to expression (What is its gene structure like)?

A

-genes made of continuous coding sequence known as open reading frame
-no introns
-organised in operons
-genes relatively small (compared to eukaryotes)

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160
Q

What happens in transcription initiation in bacteria?

A

-RNAP scans DNA, forming a loose complex
-sigma factor binds to 2 specific sequences upstream from the start codon, forming a closed complex
-RNAP is recruited, increasing its affinity for DNA
-DNA unwinds, forming an open complex and sigma factor is released

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161
Q

What happens in transcription termination in bacteria?

A

-palindromic GC-rich region (upstream of AT-rich region) is needed for termination
-once GC-rich region is transcribed, a hairpin structure forms
-this makes RNAP dissociate (helped by there being less H-bonds in AT-rich region)
or
-Rho proteins bind to 72 res GC-rich
-RNA downstream wraps around itself, when it reaches RNAP Rho proteins unwind the RNA-DNA duplex, releasing RNAP

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162
Q

What are the differences between bacterial and eukaryotic transcription?

A

-transcription site (bact-cytoplasm, euks-nucleus)
-1 RNAP in proks, 3 in euks
-euk termination involves mRNA cleavage using AAUAAA seq
-euks modify mRNA (capping, polyadenylation, splicing)

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163
Q

What are the differences between bacterial and eukaryotic translation?

A

-proks have 70S ribosomes, euks have 80S ribosomes (80S ribosomes can bind mRNA in tRNA absence)
-in pros translation is coupled to transcription
-translation is specifically inhibited by cyclohexamine in euks but not proks

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164
Q

What are the requirements for bacterial growth?

A

-temperature
-pH
-osmotic pressure
-nutrients
-oxygen

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165
Q

What are cardinal temperatures?

A

the specific temperature range a bacteria can survive
-minimum, optimum and maximum temperatures
-diff cardinal temps for diff organisms

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166
Q

What is happening in bacteria at the minimum temperature for growth?

A

-membrane gelling
-transport processes so slow that growth can’t occur

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167
Q

What is happening in bacteria at the optimum temperature for growth?

A

-enzymic rxns occurring at max possible rate

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168
Q

What is happening in bacteria at the maximum temperature for growth?

A

-protein denaturation
-cytoplasmic membrane collapse
-thermal lysis

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169
Q

What are the cardinal temps for psychrophiles?

A

0-20°C

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170
Q

What are the cardinal temps for mesophiles?

A

10-45°C

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171
Q

What are the cardinal temps for thermophiles?

A

40-80°C

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172
Q

What are the cardinal temps for extreme thermophiles?

A

60-120°C

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173
Q

What are the adaptions of psychrophiles to cold temperatures?

A

-increased membrane fluidity (high content of unsaturated and methyl-branched fatty acids and shorter acyl-chains -to limit membrane cohesion and homogenity)
-production of anti-freeze proteins
-production of cryoprotectants (trehalose, exopolysaccharides)
-production of cold-adapted enzymes (higher proportion of helices, less weak bonds and interdomain interactions)

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174
Q

Why do psychrophiles have increased membrane fluidity?

A

-limits membrane cohesion and homogenity

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175
Q

What do anti-freeze proteins do?

A

bind to small ice crystals which inhibits their growth/formation (as the proteins cover their water accessible surfaces)

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176
Q

What are the properties of cold-adapted enzymes (produced by psychrophiles)?

A

-have a higher proportion of helices
-have less weak bonds and interdomain interactions
-increased flexibility

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177
Q

What are the adaptions of thermophiles to high temperatures?

A

-genome protection (stabilisation by DNA binding proteins, high GC%, supercoils)
-modification of membrane composition (ester-linked phospholipids, single lipid layer)
-production of thermostable proteins
-existence of thermostable chaperones

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178
Q

How are the genomes of thermophiles protected to be adapted to high temperatures?

A

-DNA-binding proteins stabilise the DNA
-supercoils (introduced by reverse DNA gyrases) make it harder for strands to be untwisted and denatured (higher temps required to do so)
-high G-C% makes DNA more resistant to denaturation

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179
Q

How is the membrane composition modified in thermophiles?

A

-phospholipids are linked by ether bonds rather than phosphodiester bonds
-single lipid later (glycerol tetraethers)

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180
Q

What are the properties of thermostable proteins (produced by thermophiles)?

A

-higher proportion of ionic interactions and hydrophobic interactions

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181
Q

What are the different types of micro-organisms adapted to specific pHs?

A

-acidophiles (pH 0-6)
-neutrophiles (pH 6-8)
-alkaliphiles (pH 8-14)

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182
Q

What are the metabolic adaptions of acidophiles?

A

-respiratory chains pump H+
-H+/Na+ antiporters used to maintain internal pH below external pH
-membrane impermeability/stability
-reverse membrane potential
-H+ motor force drives flagellar motor, ATP synthesis and substrate symport
-H+/K+ antiporters excrete H+

SUMMARY: MOSTLY USE H+ TO POWER PROCESSES TO MAINTAIN HIGHER [H+] OUTSIDE CELL

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183
Q

What are the metabolic adaptions of alkaliphiles?

A

-respiratory chains pump Na+
-H+/Na+ antiporters used to maintain internal pH above external pH (take in H+)
-Na+ driven ATPases export Na+
-Na+ motor force drives flagellar motor, ATP synthesis and substrate symport
-Na+ secreted by decarboxylases

SUMMARY: MOSTLY USE NA+ TO POWER PROCESSES TO MAINTAIN HIGHER [H+] INSIDE CELL
∴ live in salty places

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184
Q

What are the different types of micro-organisms adapted to different osmotic pressures?

A

-non-halophiles (not salty conditions)
-halotolerants
-halophiles (salty conditions)
-extreme halophiles

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185
Q

How are micro-organisms adapted to respond to osmotic stress?

A

-regulate water movement (by passive diffusion and aquaporins)
-produce compatible solutes
-release solutes by mechano-sensitive channels

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186
Q

How are halophiles adapted in terms of their salt requirement?

A

-stabilisation of S layer glycoprotein by Na+
-accumulate K+ as compatible solute

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187
Q

What nutrients do microorganisms require?

A

-nitrogen
-sulphur
-phosphorus
-some vitamins
-cofactors -K+, Ca2+, Mg2+
-trace factors -Fe, Cu, Zn

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188
Q

What do phototrophs use as their source of electrons carbon?

A

light
organic compounds

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189
Q

What do chemotrophs use as their source of electrons and carbon?

A

inorganic compounds

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190
Q

What are reactive oxygen species?

A

toxic forms of oxygen
-superoxide (O2 -)
-hydrogen peroxide (H2O2)
-hydroxy radical (OH*)

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191
Q

Which enzymes can detoxify reactive oxygen species?

A

-catalase/peroxidase (convert hydrogen peroxide to water)
-superoxide dismutase and catalase/superoxide reductase and catalase (convert superoxide to hydrogen peroxide to water)

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192
Q

What are the different types of microorganisms adapted to different oxygen availabilities?

A

-obligate aerobes (only use oxygen for respiration)
-facultative aerobes (can use oxygen for respiration)
-microaerophiles (require an exact amount of oxygen for respiration)
-aerotolerant anaerobes (don’t use oxygen for respiration but can survive in the presence of oxygen)
-obligate anaerobes (don’t use oxygen for respiration and can’t grow in the presence of oxygen)

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193
Q

What are obligate anaerobes?

A

organisms which can only use oxygen for respiration
-have catalase and superoxide dismutase enzymes
eg. Pseudomonas aeruginosa

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194
Q

What are facultative aerobes?

A

organisms that can use oxygen for respiration
-have catalase and superoxide dismutase enzymes
eg. Escherichia coli

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195
Q

What are microerophiles?

A

microorganisms that require oxygen in exact amounts for respiration
eg. Campylobacter jejuni

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196
Q

What are aerotolerant anaerobes?

A

organisms that do not use oxygen for respiration but can still grow in the presence of oxygen
-have superoxide dismutase enzymes (but not catalase)
eg. Streptococcus mutans

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197
Q

What are obligate anaerobes?

A

organisms that do not use oxygen for respiration and can not grow in the presence of oxygen
eg. Clostridium difficile

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198
Q

How can bacterial growth be measured?

A

direct measurements
-microscopic counts (spreading suspense on cell counter and counting)
-viable counting (spreading serial dilutions on agar plates and counting colonies)
-flow cytrometry (pumping suspension through capillary and measuring how much light scatters)

indirect measurements
-optical density
-dry weight
-metabolic activity

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199
Q

How can bacterial growth be measured directly?

A

-microscopic counts (spreading suspense on cell counter and counting) -don’t know if cells are dead or alive
-viable counting (spreading serial dilutions on agar plates and counting colonies) -doesn’t directly tell us the number of cells
-flow cytrometry (pumping suspension through capillary and measuring how much light scatters) -gives idea of cell density, can distinguish between dead and alive cells

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200
Q

How can bacterial growth be measured indirectly?

A

-optical density
-dry weight
-metabolic activity

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201
Q

What are the limitations of using optical density to indirectly measure bacterial growth?

A

-requires high cell densities
-doesn’t distinguish between dead and living cells
-OD values differ depending on organisms
-doesn’t work on mounds or filamentous bacteria

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202
Q

What are the phases of a typical bacterial growth curve?

A

-lag phase
-log phase
-stationary phase
-death phase

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203
Q

What happens in the lag phase of a typical bacterial growth curve?

A

constant no. cells
-metabolism starts
-no divisions

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204
Q

What happens in the log phase of a typical bacterial growth curve?

A

no. cells increases exponentially
-divisions

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205
Q

What happens in the stationary phase of a typical bacterial growth curve?

A

no. deaths = no. new cells
-nutrients exhausted
-inhibition

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206
Q

What happens in the death phase of a typical bacterial growth curve?

A

no. cells decrease

-depends on bacteria -not all undergo lysis

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207
Q

How can bacterial growth be physically controlled?

A

-using heat (moist heat, dry heat or pasteurisation)
-using irradiation (ionizing or non-ionizing)
-using filtration (nucleopore, membrane or depth filters)

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208
Q

How can bacterial growth be physically controlled using heat?

A

-moist heat (boiling heat/autoclave)
-dry heat (direct flaming, incineration or exposure to high temp for long time)
-pasteurisation (mild heat, HTST or UHT)

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209
Q

How can bacterial growth be physically controlled using irradiation?

A

-ionizing radiation (electron beams, gamma rays, x-rays) -used in food industry, for lab equipment and medical use (destroys DNA by creating breaks in double strand and using reactive oxidative species so more sterile)
-non-ionizing radiation (UV) -used for surface decontamination (less sterile)

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210
Q

How can bacterial growth be physically controlled using filtration?

A

-sterilises gases or liquids that can be damaged by heat
-porosity of filter chosen for specific applications:
nucleopore filters (membranes w/defined holes) -v. precise control of sizes
membrane filters -quick and easy, can use for things you don’t want to heat, less specific than nucleopore filters
depth filters -recycle air, less specific than nucleopore filters

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211
Q

What are the types of chemical antimicrobial agents?

A

-bacteriostatic
-bactericidal
-bacteriolytic

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212
Q

What are bacteriostatic agents?

A

compounds which inhibits bacterial growth
-bacteria stay alive but stop growing
-viable cell count stays constant after
-rare

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213
Q

What are bactericidal agents?

A

compounds which kill bacteria
-viable cell count decreases after
-most common antibmicrobial agents

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214
Q

What are bacteriolytic agents?

A

compounds which kill bacteria (are bactericidal) by causing cell lysis
-number of cells and viable cell count decreases after

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215
Q

What are the differences between different classes of chemical antimicrobial agents?

A

-sterilants -applied on objects, kill microorganisms but not spores
-disinfectants -applied on objects, completely kill all forms of microorganism including spores
-antiseptics and germicides -applied on living tissue, inhibit growth of/kill microorganism

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216
Q

How can antimicrobial activity be measured experimentally?

A

-disc diffusion plates (discs containing antibiotics placed on surface of agar plates spread with microorganism)
-E-test (strip containing varying concentration of antibiotic placed on surface of agar plates spread with microorganism)
-minimum inhibitory concentration (MIC) assays
-minimum bactericidal concentration (MBC) assays

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217
Q

What is a minimum inhibitory concentration (MIC)?

A

lowest concentration of antibiotic that inhibits the viable growth of a microorganism after overnight incubation

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218
Q

What is a minimum bactericidal concentration (MBC)?

A

lowest concentration of antibiotic that kills 99.9% or microorganism after overnight incubation

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219
Q

What chemicals are used for antimicrobial control?

A

-phenolic compounds (aromatic derivatives)
-alcohols
-aldehydes
-quaternary ammonium compounds (quarts)
-halogen releasing agents (chlorine-releasing or iodine-releasing)

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220
Q

Why are phenolic compounds used as chemicals for antimicrobial control?

A

-local anaesthetics at low concs, antibacterial at high concs
-denature proteins and disrupt membranes
eg. phenols in TCP, chlorohexidine in mouthwashes, triclosan in soap and toothpaste

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221
Q

Why are alcohols used as chemicals for antimicrobial control?

A

-denature proteins, dissolve lipids and disrupt membranes
eg. hand sanitiser

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222
Q

Why are aldehydes used as chemicals for antimicrobial control?

A

-are alkylating agents -modify proteins and DNA, causing cell death
eg. preserving tissues, microscopy

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223
Q

Why are quaternary ammonium compounds (quarts) used as chemicals for antimicrobial control?

A

-disrupt phospholipids in cytoplasmic membranes

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224
Q

Why are quaternary ammonium compounds (quarts) used as chemicals for antimicrobial control?

A

-disrupt phospholipids in cytoplasmic membranes

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225
Q

Why are halogen releasing agents used as chemicals for antimicrobial control?

A

-chlorine-releasing agents chlorinate bases in DNA and aid oxidation of proteins
eg. household bleach
-iodine-releasing agents target DNA and proteins
eg. iodine, iodophores

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226
Q

What are the two major therapeutic strategies?

A

-antibiotics
-vaccinations

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227
Q

Who discovered penicillin?

A

Alexander Fleming

228
Q

What do the major classes of antibiotics target?

A

-cell wall synthesis
-DNA gyrase
-RNA elongation
-DNA-directed RNA polymerase
-protein synthesis (50S, 30S or tRNA inhibition)
-lipid biosynthesis
-cytoplasmic membranes
-fatty acid metabolism

229
Q

What are the modes of action of antibiotic resistance?

A

-drug inactivation
-target modification
-efflux/impermeability
-bypass

230
Q

What causes antibiotic resistance?

A

misuse in human therapeutics
-farming (excessive use of antibiotics)
-agriculture
-aquaculture
-pets

231
Q

What are the properties of an ideal antibiotic?

A

-target is selectively toxic (kills microorganism, not hosts)
-target must inhibit essential processes or virulence
-stable
-effective
-cost

232
Q

What is pharmacokinetics?

A

study of how body interacts with antibiotics

233
Q

What is pharmacodynamics?

A

study of how antibiotics work and what they do to the body

234
Q

What is the mode of action of β-lactams (type of antibiotic eg. penicillin)?

A

inhibition of peptidoglycan polymerisation, mediated by D,D-transpeptidases (aka penicillin binding proteins)

235
Q

Why do D,D-transpeptidases (aka penicillin binding proteins) act on β-lactams?

A

-β-lactams are structural analogues of D-Ala-D-Ala C-terminal residues in peptide stems
-D,D-transpeptidases (aka PBPs) use them as substrates and irreversibly inactivate them

236
Q

What are the modes of action of resistance to β-lactams?

A

-drug inactivation by β-lactamase
-target modification by overexpression or low affinity penicillin binding proteins
-efflux systems (gram -ve bacteria)
-bypass with alternative pathways

237
Q

What happens in the mechanism of resistance to β-lactams via inactivation by β-lactamase?

A

-catalytic Ser undergoes nucleophilic attack (towards C=O)
- β-lactam ring opens, forming covalent complex penicillin-β-lactamase
-hydrolysis of penicillin, splitting OH-Ser-β-lactamase off from rest of compound

-opening of β-lactam ring makes drug inactive

238
Q

What happens in the mechanism of resistance to β-lactams via mutation of target enzymes?

A

-conformation altered so that penicillin binding proteins have lower affinity for β-lactams
-overexpression of penicillin binding proteins targeted by β-lactams lowers efficiency of drug

239
Q

What happens in the mechanism of resistance to β-lactams via secretion of antibiotics?

A

-overproduction of system leads to resistance

240
Q

What are Archaea?

A

prokaryotes representing 1 domain in the tree of life

241
Q

What are the 2 major phyla of Archaea?

A

-euryarcheota
-crenarchaeote

242
Q

What are extremophiles?

A

organisms whose growth is dependent on extreme conditions, which are generally inhospitable to most forms of life

243
Q

Why is it still under debate whether there are 2 or 3 domains?

A

-euryarchaea could have evolved from Asgards (branch of Archaea)
-Asgards contain genes with equivalents in eukaryotes but no equivalents in bacteria
-diversity of microorganisms is underestimated

244
Q

Are S layers present in Archaea?

A

yes
-v common

245
Q

What are Archaea cell walls made from?

A

pseudomeurin
(occasionaly found in bact, never in euks)

246
Q

What is the structure of pseudomeurin?

A

-heteropolymer
-N-Acetylglucosamine and N-Acetyltalosaminurmonic

247
Q

What are Archaea cell walls resistant to?

A

-lysozymes
-most antibiotics which target bacterial peptidoglycan synthesis

248
Q

Why can pseudomeurin not be studied in the same ways peptidoglycan can be?

A

-diff compositions
-at the moment, no commercial enzymes can hydrolyse pseudomeurin
-pseudomeurin isn’t affected by β-lactases

249
Q

What unusual structures exist in Archae?

A

-Archaellum (sim. to flagella)
-Cannulae (tubes connecting cells)
-Hooks

250
Q

What are Archaellum?

A

structures present in Archaea made from lots of proteins, which move via rotation
-like flagella

251
Q

What are Cannulae?

A

tubes present between cells in Archaea, which establish physical contact between cells
-connected to S layer

252
Q

What is the structure of the cytoplasmic membrane like in Archaea?

A

-phospholipids contain isoprenes, rather than fatty acids
∴ ether links not ester links

253
Q

How is the genome organised in Archaea?

A

-circular chromosome (and plasmids)
-histones present
-have multiple replication origins

254
Q

Which DNA polymerases are encoded in Archaea?

A

polymerase B (also present in Eukarya) and polymerase D (exclusive to Archaea)

255
Q

How many RNA polymerases do Archaea have?

A

one
-very similar structure to Eukarya’s RNAP

256
Q

Are introns present in Archaea?

A

yes

257
Q

How are genes organised in Archaea?

A

in operons

258
Q

Which ribosomes are present in Archaea?

A

70S

259
Q

What is translation like in Archaea?

A

-coupled to transcription
-involves several translation factors
-uses 70S ribosomes

260
Q

In what ways are Archaea very diverse?

A

-in terms of habitats -hot springs, Antartica, volcanic environments, etc
-in terms of metabolism -phototrophs and chemotrophs, can use organic or inorganic carbon sources and can use organic or inorganic reducing equivalent sources

261
Q

What are the three major types of Archaea?

A

-(hyper)thermophiles
-halophiles
-methanogens

262
Q

Describe (hyper)thermophile Archaea

A

-high growth temps
-often acidophiles
-most require sulphur for growth
eg. Acidianus infernus
-found in hot springs
-used in biotech
-grows anaerobically or aerobically
eg. Thermococcus barcosi
-found in hydrothermal vents
-requires S
-grows anaerobically

263
Q

Describe halophile Archaea

A

-mostly Euryarchaeota
-found in evaporated ponds, salt lakes, the Dead sea
-require up to 5M NaCl for growth
eg. Halobacterium
-found in the Great Salt Lake (4M NaCl)
-uses light as energy source to secrete H+

264
Q

Describe methanogen Archaea

A

-Euryarchaeota
-found in anaerobic environments (gut, marine sediments, etc)
-use acetate, fumarate, CO2, etc as e- transporters
eg. Methanopyrus kandleri
-found in deep-ocean hydrothermal vents
eg. Methanobrevibacter smithii
-found in human gut
-removes bacterial end products of fermentation

265
Q

How are metabolic types names?

A

-chemo (molecules as energy source) or photo (light as energy source)
-organo (organic molecules as e- source) or litho (inorganic molecules as e- source)
-heterotroph (organic compounds as C source) or autotroph (inorganic compounds as C source)

266
Q

What organisms are chemoheterotrophs?

A

-animals
-fungi

267
Q

What organisms are chemoautotrophs?

A

-extremophiles

268
Q

What organisms are photoheterotrophs?

A

-purple and green non-sulphur bacteria

269
Q

What organisms are photoautotrophs?

A

-plants
-algae
-cyanobacteria

270
Q

ΔG =
(Gibbs free energy)

A

-nFΔE

where
n = no. e-s transferred
F = Faraday’s constant
ΔE = redox potential change

271
Q

What value of proton motor force (Δp) must the redox potential change (ΔE) exceed to be coupled to electron transfer and H+ translocation?

A

180mV

272
Q

What are the key energetic currencies used by chemoorganotrophs?

A

ATP
NADH and H+, FADH2

273
Q

What are the major metabolic types within chemoorganotrophy?

A

-aerobic respiration
-anaerobic respiration
-fermentation

274
Q

How are chemoorganotrophs metabolically diverse?

A

-use range of organic compounds as e- sources (carbs, lipids, peptides, aromatic comps)
-can produce acetyl-coA and pyruvate
-use ATP or NADH or FADH2 as energy currencies
-can use aerobic or anaerobic respiration or fermentation

275
Q

What are the differences between anaerobic respiration and fermentation?

A

anaerobic resp:
-resp chain and ox phos
-e- transport via cytochromes, quinones and iron-sulphur proteins
-can use many inorganic compounds

fermentation:
-no resp chain
-substrate-level phos to prod ATP (no ATP synthases)
-low yields

276
Q

What are the types of chemolithotrophy?

A

-hydrogenotrophy (incl sulphate reduction and methanogenesis)
-iron oxidation
-nitrogen oxidation (incl nitrification and anammox)
-sulfide oxidation
-sulphur oxidation

277
Q

What does chemo mean in terms of metabolic types?

A

use molecules as energy source

278
Q

What does photo mean in terms of metabolic types?

A

use light as energy source

279
Q

What does heterotroph mean in terms of metabolic types?

A

use organic compounds as carbon source

280
Q

What does autotroph mean in terms of metabolic types?

A

use inorganic compounds as carbon source

281
Q

What does organo mean in terms of metabolic types?

A

use organic compounds as electron source

282
Q

What does litho mean in terms of metabolic types?

A

use inorganic compounds as electron source

283
Q

What can chemolithotrophs use as electron donors?

A

-hydrogen
-iron
-ammonia
-nitrates

284
Q

What do hydrogenotrophs use as electron donors?

A

H2

285
Q

What do hydrogenotrophs use as electron acceptors?

A

O2
SO4 2-
CO2 (methanogenesis)
chlorinated compounds (dehalorespiration)

286
Q

What do chemolithotrophs which use iron oxidation use as electron donors?

A

Fe

287
Q

What do chemolithotrophs which use nitrogen oxidation use as electron donors?

A

ammonia (NH3)
nitrates (NO2 -)

288
Q

What is anammox?

A

anaerobic ammonia oxidation
NH4 + + NO2 - -> N2 + 2H2O
-Planctomycetes

289
Q

What is nitrification?

A

aerobic ammonia oxidation
NH4 + + NH2OH -> NO2 - -> NO3 -
-Nitrosomas and Nitrosobacter

290
Q

What do chemolithotrophs which use sulphur oxidation use as electron donors?

A

sulphur derivatives
-elemental sulphur (S)
-hydrogen sulphide (H2S)
-thiosulfate (S2O3 2-)
-ferrous sulphate (F2S2)

291
Q

What is biomining?

A

-using acid-producing microbes to dissolve metals from rocks as an alternative to commercial mining
-less hazardous waste
eg. using Acidothiobacillus ferroxidans

292
Q

What are the types of phototrophy?

A

-oxygenic
-anoxygenic

293
Q

What is oxygenic photosynthesis?

A

-carried out by plants and cyanobacteria
-uses photosystems PSI and PSII

294
Q

What is anoxygenic photosynthesis?

A

-carried out by bacteriorhodopsin, green sulphur bacteria and purple bacteria
-uses photosystems BR, PSI and PSII

295
Q

What is bacteriorhodopsin?

A

primitive photosynthetic system
-very abundant light-driven H+ pump in archeal membrane
-contains pigment retinal (undergoes conformational change when excited by light)
-produces ATP using movement of H+

296
Q

What happens when bacteriorhodopsin undergo anoxygenic photosynthesis?

A

-retinol is excited by light, causing it to undergo a conformational change (from trans to cis)
-conformational change triggers transfer of H+ to Asp85
-deprotonated retinol pushes against helix, opening channel on cytoplasmic side, inducing retinol to be deprotonated from Asp96
-Asp96 is reprotonated
-Asp85 transfers H+ outside through H-bonding, resetting retinol to trans state

297
Q

How does oxygenic photosynthesis vary between plants and cyanobacteria?

A

-occurs in chloroplasts in plants
-cyanobacteria don’t have chloroplasts -their photosynthetic apparatus varies greatly but most are made from thylakoids

298
Q

What happens in anoxygenic photosynthesis in green sulphur bacteria (eg. Chlorobium)?

A

-light captured by antenna complexes in chlorosomes and photon energy is transferred to PSI rxn centre
-PSI donates e- to ETC
-e- transport pumps H+ outside cell and reduces NADP via ferredoxin
-ATP generated by H+ gradient
PSI receives e- from inorganic sulphur derivatives

299
Q

What happens in anoxygenic photosynthesis in purple bacteria?

A

-light captured by antenna complexes in chromatophores and photon energy is transferred to PSII rxn centre
-PSII donates e- to cyclic ETC
-e- transport pumps H+ outside cell
ATP generated by H+ gradient (cyclic phosphorylation)
-inorganic compounds used as e- donors to produce NADPH (reverse e- flow)

N/B: NADH can’t be produced -there aren’t any transporter with an electronegative enough reducing potential

300
Q

What happens in oxygenic photosynthesis in cyanobacteria?

A

-2 distinct PSs are excited by light, which provides energy to take e- from H2O to produce H+
-e- transport pumps H+ outside cell and reduces NADP
-ATP generated by H+ gradient
-CO2 is fixed by NADPH and ATP, making glucose

301
Q

What is the name of the organelle which captures light in green sulphur bacteria during anoxygenic photosynthesis?

A

chlorosomes

302
Q

What is the name of the organelle which captures light in purplebacteria during anoxygenic photosynthesis?

A

chromatophores

303
Q

What is symbiosis?

A

intimate relationship between different organisms

304
Q

What are the three types of symbiosis?

A

-mutualism
-commensalism
-parasitism/predation/competition

305
Q

What is mutualism?

A

symbiosis where both organisms benefit from the interaction
eg. microbe using host’s nutrients to grow and produces vitamins host can use

306
Q

What is commensalism?

A

symbiosis where microbe benefits from the interaction, without impacting the host
eg. bacteria living on skin/in gut

307
Q

What is parasitism/predation/competition?

A

symbiosis where the microbe benefits from the interaction at the expense of the host
eg. obligate parasites

308
Q

What are the limitations of categorising the three types of symbiosis?

A

-symbiosis isn’t set in stone -can change as conditions change
-hard to tell if microbe can ever really not effect the host in any way

309
Q

What is endosymbiosis?

A

symbiosis where the parasites lives inside the host

310
Q

What is ectosymbiosis?

A

symbiosis where the parasites lives on the surface of the host

311
Q

What are bacteriocytes?

A

specialised structures in insects which contain bacteria, involved in endosymbiosis
-can aggregate to form organs called bacteriomes

312
Q

What are bacteriomes?

A

specialised organ in insects which hosts endosymbiotic bacteria

313
Q

Why do plants require nodulation?

A

-plants can’t use atmospheric N2
-some legumes (beans, peas) can fix N2 via a symbiotic interaction with bacteria in soil (Rhizobia) -form structures known as nodules

314
Q

What is Rhizobia?

A

-gram -ve bacteria (an alphaproteobacteria)
-part of rhizosphere (root microbiome -area of soil surrounding roots)
-have complex genome

315
Q

What is nodulation?

A

the formation of nodules (structures in roots containing symbiotic bacteria) in legumes

316
Q

What happens in the process of nodulation?

A

-bacteria attracted by root via secretion of root exudates, causing bacteria to migrate towards root and establish contact
-nodulation genes are activated and Nod factors are produced and secreted
-Nod factors trigger differentiation growth of root, causing root to curl, entrapping bacteria on surface
-bacteria move from outside to inside of root, forming infection thread
-bacteria bud off from infection thread and invade cortical cells
-bacteria differentiate into bacteroids, which is controlled by plant producing NCR-peptides, forming determinate or indeterminate nodules

317
Q

What distinguishes obligate symbionts, parasites and organelles?

A

-organelles are essential and conserved across wide range of organisms
-parasites are harmful to organism they have infected
-symbionts are beneficial to organism that live in association with that organism

318
Q

What has metagenomics allowed?

A

-bacteria to be studied (genomes sequenced) in their environment
-allows bacteria that can’t survive in lab conditions to be studied

319
Q

Name some examples of unusual symbiotic bacteria

A

In Mycoplasma genitalium…
-Candidatus Sulcia muelleri
-Candidatus Zinderia insecticola
-Candidatus Carsonella rudii
-Candidatus Hodgkinia cicadicola
-Candidatus Tremblaya princeps

320
Q

Why do symbionts often have a small/incomplete genome?

A

-genome size is a result of gene loss
-don’t have an independent origin

321
Q

Name an example of complex symbiosis

A

nested symbiosis in Mealybugs
-Mealybugs have organelles called bacteriocytes containing the bacteria Tremblaya and Tremblaya contain bacteria Moranella
-amino acid biosynthesis is underpinned by a mosaic biosynthetic pathway
-insect’s genes contribute to bacteria’s peptidoglycan synthesis

322
Q

What is a pathogen?

A

any agent that causes disease

323
Q

What is the difference between a pathogen and a parasite?

A

-parasites are visible to the human eye, whilst pathogens are not

324
Q

What is pathogenesis?

A

when an organism uses another organism’s resources in a way which is not beneficial to the host

325
Q

What types of organisms can be pathogens?

A

-bacteria
-viruses
-fungi
-protozoa
-prions

-NOT Archaea

326
Q

What are prions?

A

infectious proteins
-considered pathogens

327
Q

What makes a pathogen successful?

A

-able to gain access to host
-can locate a nutritionally compatible niche
-can avoid host’s innate and adaptive immune responses
-able to access host’s resources and replicate
-can exit and spread to new host (transmission)

328
Q

What is an innate immune response?

A

-rapid
-non-specific

329
Q

What is an adaptive immune response?

A

-highly-specific
-slow

330
Q

What types of transmission are there?

A

-air-borne
-water
-food
-mechanical/vector

331
Q

What is the difference between mechanical transmission and transmission using a vector?

A

mechanical: pathogen doesn’t interact with the other’s biology -just uses it as a mean of transportation
vector: pathogen interacts with other’s biology -to survive in it

332
Q

How can the success of a pathogen be measured?

A

-if it’s still here, must be successful
quantitatively… -virulence (mortality, morbidity, infectious dose)

333
Q

What is virulence?

A

the measurement of the severity of a disease

334
Q

What is mortality?

A

the number of deaths from a disease

335
Q

What is morbidity?

A

the number of cases of a disease in a population

336
Q

What is infectious dose?

A

the number of individual cells/particles required for an infection

337
Q

How can virulence be measured?

A

-mortality
-morbidity
-infectious dose

338
Q

What are virulence factors?

A

factors which enable pathogen to colonise host
-intention is for survival, not for causing disease, however disease is often caused in the process
eg. toxins, capsules

339
Q

What virulence factors are there?

A

-adhesins
-capsules/S-layers
-digestive enzymes
-toxins
-stealth mode/reductive evolution

340
Q

How do adhesins act a virulence factors?

A

find niche and colonise host

341
Q

How do capsules/S-layers act a virulence factors?

A

immune evasion/survival in host

342
Q

How do digestive enzymes act a virulence factors?

A

find niche, colonise, find host’s resources

343
Q

How do toxins act a virulence factors?

A

reprogram host’s biology to benefit the pathogen

344
Q

How does stealth mode act as virulence factors?

A

immune evasion (via absence of outer-surface structures)

345
Q

What sources are there for reliable information on pathogens?

A

-WHO
-UK Health and Security Agency (humans) and DEFRA (animals/plants)
-CDC (humans) and USDA (animals/plants)

346
Q

What is Germ Theory?

A

microorganisms (pathogens) cause disease

347
Q

What are Koch’s postulates?

A

-microbe is found in all cases of disease and absent in healthy individuals
-microbe can be isolated from diseased host and be grown in pure culture
-when a pure culture is introduced into a healthy, susceptible host, the same disease occurs
-same strain or microbe can then be obtained from the newly diseased host

348
Q

How did Koch establish a scientific method to link microbes and diseases?

A

came up with Koch’s postulates, a set of criteria a microorganism must fulfil to prove a specific pathogen causes a specific disease
-by studying Bacillus anthracis (gram +ve bact causing anthrax)

349
Q

What do treatments need to be able to do?

A

block pathogen’s steps to infection, such as…
-entry to host
-avoidance of host’s immune responses
-access to host’s reserves and replicate
-exit and spread to new host

350
Q

What treatments prevent a pathogen’s entry to host?

A

sanitation and antiseptics

351
Q

What treatments prevent a pathogen from avoiding its host’s immune responses?

A

vaccination

352
Q

What treatments prevent a pathogen from accessing its host’s resources?

A

antimicrobials

353
Q

What advancements have aided the combat of disease?

A

-better diet
-clean drinking water
-improved sanitation
-less overcrowding
-better living conditions

354
Q

What are vaccines?

A

chemical agents which prime the adaptive immune system to repel a pathogen
-tricks immune system into going through primary immune response 1

355
Q

How was smallpox treated as the first form of vaccination?

A

-puss from smallpox directly put into patient’s open vein
-got smallpox but not so badly

356
Q

Why are antibiotics the last therapeutic option?

A

-conditions for killing pathogens could also harm patient

357
Q

What is the magic bullet idea?

A

pathogenic infections need to be controlled without harming the patient

358
Q

What are antibiotics?

A

chemicals produced by bacteria or fungi which inhibit or kill other microorganisms
eg. penicillin

359
Q

How are antibiotics organised?

A

into classes and families

360
Q

How was Penicillin discovered?

A

-Fleming’s Staphylococcus plate was contaminated by Penicillin
-Staphylococcus didn’t grow around the penicillin -mold was producing compound killing bacteria

-Florey and Chain modified penicillin into a usable drug

361
Q

What is a sympton?

A

a change in body function that is felt by the patient as a result of a disease
eg. feeling tired

362
Q

What is a sign?

A

a change in body that can be objectively measured or observed as a result of a disease
eg. high temperature

363
Q

What is a syndrome?

A

a specific group of signs and symptoms that accompany a disease
eg. pneumonia

364
Q

In which scenarios do Koch’s postulates not work?

A

-when a pathogen causes multiple diseases
-when a disease can be caused by multiple pathogens

365
Q

What are the benefits of having a microbiota?

A

-helps digestion
-helps metabolism
-aids immune function
-benefits mood and behaviour

366
Q

What types of relationship can there be between a human and microbe?

A

-commensalism (organism benefits and doesn’t affect the other)
-mutualism (both organisms benefit)
-parasitism/pathogenesis (organism benefits at other’s expense)

367
Q

What is a diseased state?

A

product of relationship change/conflict between host and pathogen

368
Q

What disease does Clostridium difficle cause?

A

Clostridium difficle infection

369
Q

What are the symptoms of Clostridium difficle infection?

A

-diarrhoea
-colonisation and inflammation of colon (large intestine)

370
Q

What is the virulence of Clostridium difficle?

A

mortality ≈ 9%

371
Q

What are opportunistic pathogens?

A

microorganisms which are not normally pathogenic but can cause an infection or disease on a “compromised” host

372
Q

What is a hospital aquired infection?

A

an infection acquired as a result of a hospital stay not linked to the reason for the patient’s hospitalisation
-patient is their own source of infection
eg. C.difficile

373
Q

How has urbanisation affected pathogens?

A

higher population densities drive many potential routes of transmission

374
Q

What disease does Vibrio cholerae cause?

A

Cholera

375
Q

What are the symptoms of Cholera?

A

large amounts of watery diarrhoea (aka rice water stool)

376
Q

How is Cholera transmitted?

A

via the faecal-oral route

377
Q

What is the virulence of Vibrio cholerae like?

A

death through severe dehydration
if treated rapidly mortality can be as low as 1%

378
Q

How is Cholera treated?

A

oral rehydration

379
Q

What are the virulence factors of Vibrio cholerae?

A

cholera toxin

380
Q

What is epidemiology?

A

study of when and where diseases occur to control the spread of disease

381
Q

What are the principles of epidemiology?

A

-identify first person to have the disease (person zero)
-identify anyone who has been in contact with that person
-identify reservoir for pathogen
-block/contain its reservoir

382
Q

What are the difficulties with the principles of epidemiology?

A

-disease needs to be recognised first, by which point the disease will have already infected many individuals

383
Q

What is an epidemic disease?

A

when a disease is acquired by many hosts in a given area in a short time

384
Q

What is an endemic disease?

A

when a disease is constantly present in a population

385
Q

What is a pandemic disease?

A

when a disease is acquired by many hosts worldwide in a short time

386
Q

What disease does Salmonella typhi cause?

A

typhoid fever

387
Q

What are the symptoms of typhoid fever?

A

rose spots (rash)

388
Q

How is Salmonella typhi transmitted?

A

-human carriers (colonised gall bladder)
-faecal-oral route

389
Q

What is the virulence of Salmonella typhi?

A

without treatment mortality ≈ 30%
with treatment mortality ≈ 1%

390
Q

What disease does Polio virus cause?

A

Polio (poliomyelitis)

391
Q

What are the symptons of polio?

A

-irreversible paralysis
-muscle weakness
-atrophy
-deformities
-twisted feet/legs

normally very mild symptoms

392
Q

How is polio transmitted?

A

-faecal-oral route
-contaminated water source

393
Q

How is polio treated?

A

vaccine (attenuated virus)
-but in rare cases vaccine does make healthy carriers :(

394
Q

What disease does Yersinia pestis cause?

A

Bubonic plague
Pneumonic plague

395
Q

What are the symptoms of bubonic/pneumonic plague?

A

-buboes (swollen lymph glands)
-pneumonia

396
Q

How is bubonic/pneumonic plague transmitted?

A

-rodents, prairie dogs and fleas
-human respiratory aerosol

397
Q

What is the virulence of Yersinia pestis like?

A

if untreated
bubonic mortality ≈ 50%
pneumonic mortality ≈ 90-100%

treatable under 24hrs

398
Q

What is a zoonotic disease?

A

an infectious disease which is transferred between humans and other organisms

399
Q

What disease does Phytophthora infestans cause?

A

potato blight
late blight

400
Q

What is the virulence of Phytophthora infestans like?

A

nearly 100% with crops

401
Q

How is potato/late blight treated?

A

fungicides
copper sulphate

402
Q

What is an issue with potato blight in the UK?

A

-pathogens have similar geographic distributions to hosts and co-evolve with them
-few varieties of potatoes came to UK (genetic bottleneck)
-monoculture potatoes will all die when diseased and leave soil full of spores

403
Q

What disease does Influenza virus cause?

A

Influenza
flu

404
Q

What is the virulence of Influenza like?

A

very varied mortality (0.01-50%) due to different strains

405
Q

What disease does Zika cause?

A

Zika virus disease

406
Q

What is the virulence of Zika like?

A

very low (most no symptoms)
associated with birth defects (microcephaly, Guillon-Barré syndrome)

407
Q

How is Zika transmitted?

A

sexually
-men 6mnths, women 8wks

408
Q

What are the issues with epidemiological surveillance?

A

-time consuming
-can be inaccurate
-correlation based data (not cause and effect)

409
Q

What is epidemiological surveillance?

A

collection, analysis and dissemination of public health data

410
Q

What disease does Ebola virus cause?

A

Ebola virus disease
Ebola haemorrhagic fever

411
Q

What are the symptoms of Ebola?

A

-bleeding
(-headache and muscle ache
-fever
-sore throat)

412
Q

What is the virulence of Ebola like?

A

very high
mortality = 40-90%
death from shock, nerve damage and seizures

413
Q

What is the reservoir for Ebola?

A

unknown
maybe zoonotic (bats)

414
Q

How is Ebola treated?

A

currently no treatment
-antibody therapies and vaccinations under development

415
Q

What would be the issues with modern medicine without antbiotics?

A

-minor infections become life threatening
-surgery becomes too dangerous
-increased risks in child birth
-chemotherapy
-infectious diseases

416
Q

Why is antimicrobial resistance so complicated?

A

-antibiotics all have diff targets
-pathogens all have diff virulences and survival strategies
-resistance mechanisms are varied and not yet well understoogd

417
Q

What is immunology?

A

study of the immune system

418
Q

What is the immune system?

A

molecules/cells across the body which defend the body against disease (by reacting against infectious pathogens)

419
Q

Why is immunology medically important?

A

-can be used to manipulate the immune system medically -vaccines
-needed to understand malfunctions in the immune system eg. immunodeficiencies, allergies

420
Q

What malfunctions in the immune system are there?

A

-immunodeficiency (immune system has decreased ability to fight disease)
-allergies (immune system inappropriately reacts to a substance)
-autoimmune disease (immune system reacts against own tissues)
-graft rejection (immune system rejects and destroys transplanted tissue/organ)

421
Q

What are immunological techniques?

A

techniques which use components of the immune system eg. antibodies
-used in research, diagnostics (eg. pregnancy tests) and therapeutics

422
Q

What are the properties of the innate immune system?

A

-broad specificity
-no memory (doesn’t improve with repeat infection)
-rapid response (hours)

423
Q

Which leucocytes are involved in the innate immune system?

A

Lots!
-phagocytes
-natural killer cells

424
Q

Which soluble factors are involved in the innate immune system?

A

Lots!
-lysozymes
-complement
-integerons

425
Q

What are the properties of the adaptive immune system?

A

-highly specific
-has memory (improves with repeat infection)
-slower response than innate (days)

426
Q

Which leukocytes are involved in the adaptive immune system?

A

B and T lymphocytes

427
Q

Which soluble factors are involved in the adaptive immune system?

A

antibodies

428
Q

What are the two lineages leukocytes give rise to?

A

-myeloid cells
-lymphoid cells

429
Q

What are leukocytes derived from?

A

pluripotent stem cells in bone marrow

430
Q

What external barriers to infection does the body have?

A

-keratinized skin (diff for bact to digest/penetrate)
-secretions (sebums, fatty acids, lactic acid, lysozymes)
-mucous
-low pH (stomach)
-commensals (organisms present on surface of skin)

431
Q

What is the role of phagocytes?

A

to take up and digest pathogens/dying cells

432
Q

What are the main types of phagocytes?

A

-neutrophils
-mononuclear phagocytes (monocytes and macrophages)

433
Q

What are neutrophils like?

A

-nucleus has multiple forms
-has granules (release enzymes, etc)
-short lived
-fast moving
-main lymphocyte in blood

434
Q

What are the two types of mononuclear phagocytes?

A

monocyte -in blood
macrophages -in tissues

435
Q

What are mononuclear phagocytes like?

A

-long lived
-carry out phagocytosis and help initiate adaptive responses
-some of the first cells to respond to infections in tissues

436
Q

What do natural killer cells do?

A

-non-specifically kill virally infected cells
-(might) kill cancer cells
-self and non-self (or infected and non-infected self) recognition

437
Q

How do phagocytes recognise pathogens?

A

have pathogen-recognition receptors (PRRs) which recognise microbe-associated molecular patterns (MAMPs)

438
Q

How do natural killer cells recognise pathogens?

A

recognise self proteins (MHC) so if they are not present, they will kill the cells

439
Q

What soluble factors does the immune system have?

A

-complement (proteins involved in bact cell lysis)
-defensins (+ve charged protein that disrupt bact membrs)
-interferons (made by virally-infected cells to protect other cells by activating macrophaes and natural killer cells)
-cytokines (small proteins involved in cell-cell communication)
-inflammatory mediators (eg. histamine)

440
Q

What is inflammation?

A

localised immune response to infection/damage causing heat, redness, swelling and pain
-inflammatory mediators (eg. histamine) are released when there is infectiondamage

441
Q

What causes heat and redness in inflammation?

A

dilation of blood vessels

442
Q

What causes swelling in inflammation?

A

increased permeability of capillaries
-cells linking capillaries become leaky and release fluid into tissue

443
Q

What causes pain in inflammation?

A

stimulation of nerve endings

444
Q

Why does a fever (temp response) come about during infection?

A

macrophages release cytokines which…
-act on hypothalamus, raising temp
-stimulate phagocytosis
-decrease iron levels in blood

445
Q

Where do B lymphocytes mature?

A

-in bone marrow (antibody receptor)
-then in primary lymphoid tissue (antigen independent differentiation)
-develop further when encounters antigens

446
Q

Where do T lymphocytes mature?

A

-in thymus (T cell receptor)
-then in primary lymphoid tissue (antigen independent differentiation)
-develop further when encounters antigens

447
Q

What are antibodies?

A

anti-foreign bodies produced in response to antigens (antibody generating material)

448
Q

What is the clonal selection hypothesis?

A

-B cell with correct receptor binds to antigens on surface by chance + undergoes clonal selection
-B cell divides, giving lots of clones
-cells differentiate into plasma cells (prod antibodies) and memory cells (long-lived, after infection)

449
Q

How is lymphoid tissue organised?

A

-primary lymphoid tissue (thymus and bone marrow) -where lymphocytes reach matureity and aquire specific receptors
-secondary lymphoid tissue (lymph nodes, vessels, etc) -where mature lymphocytes are stimulared by antigen

450
Q

What is primary lymphoid tissue?

A

where lymphocytes reach maturity and acquire specific receptors
-thymus and bone marrow

451
Q

What is secondary lymphoid tissue?

A

lymphoid tissue where mature lymphocytes are stimulated by antigen
-lymph nodes, vessels, spleen, etc

452
Q

What is the structure of an antibody like?

A

-Y-shaped
-has 2 Fab (fragment antigen binding) regions and a Fc (fragment crystallisable) region
-has 2 heavy chains and 2 light chains (IgG)
-compact globular domains (2 in each light chain, 4 in each heavy chain)

453
Q

What do the Fab regions of an antibody do?

A

bind specifically to antigens
-are very variable in aa seq

454
Q

What does the Fc region of an antibody do?

A

bind to complement, Fc receptors on phagocytes/NK cells, etc
-constant aa seq

455
Q

What did the reduction of intra-chain disulphides experiment show about antibody structure?

A

presence of light and heavy chains (and ratios)

light chains: 25kDa
heavy chains: 50kDa
IgG: 150kDa ∴ L2H2

456
Q

What did the protein cleavage experiment show about antibody structure?

A

cleaved into 2:1 ratio
∴ 2 Fab arms and 1 Fc region

457
Q

What did crystallography show about antibody structure?

A

hinge region is highly flexible

458
Q

What experimental evidence is there for antibody structure?

A

-intra-chain disulphide reduction shows presence of light and heavy chains
-protein cleavage shows 2:1 ratio of Fab:Fc regions
-crystallography shows flexibility of hinge region

459
Q

What are the 5 classes of immunoglobulins?

A

-IgG (γ)
-IgM (μ)
-IgA (α)
-IgD (δ)
-IgE (ε)

460
Q

How are immunoglobulins classified?

A

-by heavy chain amino acid sequence (IgG, IgM, IgA, IgD, IgE)
-by type of light chain (kappa or lambda)

461
Q

What is IgG involved in?

A

secondary memory responses

462
Q

What is IgM involved in?

A

primary responses

463
Q

What is IgA involved in?

A

protection of mucosal surfaces

464
Q

What is IgD involved in?

A

unknown function

465
Q

What is IgE involved in?

A

allergic responses
protection from parasites

466
Q

Where is IgG found?

A

in serum
(N/B: crosses placenta from mother to foetus)

467
Q

Where is IgA found?

A

in serum and secretions (tears, saliva, breast milk, etc)

468
Q

Which immunoglobulins exist as monomers?

A

IgG
IgD
IgE
IgA (can also exist as dimer)

469
Q

Which immunoglobulins exist as dimers?

A

IgA (can also exist as monomer)

470
Q

Which immunoglobulins exist as pentamers?

A

IgM

471
Q

What is the constant region of an antibody?

A

region which is the same for antibodies of a given H and L chain class

472
Q

What is the variable region of an antibody?

A

region which differs between antibodies with different specificities found at N-terminal of heavy and light chains
-recombination and mutations of variable region exons in genome during B cell differentiation can give different antibody specificities

473
Q

How do antibodies protect against infection?

A

using specific binding
-neutralise (toxins)
-immobilise mobile microbes
-prevent binding to (and ∴ infection of) host cells
-form complexes
using effector functions
-activate complement
-bind Fc receptors

474
Q

Which classes of antibodies neutralise toxins?

A

IgG
IgA

475
Q

Which classes of antibodies immobilise mobile microorganisms?

A

IgM

476
Q

Which classes of antibodies activate complement?

A

IgG
IgM

477
Q

Which classes of antibodies bind to Fc receptors on phagocytes?

A

IgG
IgA

478
Q

Which classes of antibodies bind to Fc receptors on mast cells?

A

IgE

479
Q

Which classes of antibodies bind to Fc receptors on natural killer cells?

A

IgG

480
Q

What is complement?

A

series of around 20 proteins in the blood/serum which are normally inert but are activated as part of the immune defence against bacteria (and viruses) and induce inflammation
-activated by an enzyme cascade

481
Q

Which protein component of the classic complement pathway is most abundant?

A

C3

482
Q

Which protein component of the classic complement pathway is first in the pathway?

A

C1

483
Q

What activity do most components of the classical complement pathway have?

A

protease activity
-generates fragments with biological activity

484
Q

What does the classical complement pathway require?

A

1 antigen
2 antibodies

485
Q

What happens at the start of the classical complement pathway?

A

-C1 is activated by interacting with 2 Fc regions
-once C1, C4 and C2 are activated, C3 convertase is generated
-C5 convertase is made by C3b joining to C3 convertase

486
Q

How is C1 activated?

A

by interacting with two Fc regions

487
Q

What are the three major biological activities of complement?

A

-activation (C5a, C3a)
-opsonisation (C3b)
-cell lysis (C5-9)

488
Q

What does complement act as in order to undergo activation?

A

-as chemoattractants (induces cell movement along conc gradient)
-as anaphylatoxins (cause allergic response -mast cells release histamine, inflammation)

489
Q

Which components of complement are involved in activation?

A

C5a
C3a

490
Q

Which components of complement are involved in opsonisation?

A

C3b

491
Q

Which components of complement are involved in cell lysis?

A

C5-9

492
Q

What happens in opsonisation?

A

increased binding and phagocytosis

493
Q

How does complement cause cell lysis?

A

-whole cascade is activated
-membrane attack complex (hollow cylinder) forms
-complex forms pores in bacterial membranes

494
Q

Why can complement only cause cell lysis in gram negative bacteria?

A

Gram positive bacteria have a thick peptidoglycan coat so are resistant to the membrane attack complex forming pores in its membranes

495
Q

What do Fc receptors on phagocytes do?

A

enhance recognition of microbes

496
Q

What do Fc receptors on natural killer cells do?

A

mediate antibody dependent cell-mediated cytotoxicity (ADCC) by secreting perforin, which acts as a channel to discharge enzymes into target cell to induce apoptosis

497
Q

What do Fc receptors on mast cells do?

A

-mediate allergic response
-defence against large parasites
-sensitises mast cell and degranulation (release of inflammatory mediators)

498
Q

What are antisera?

A

blood serum containing antibodies against specific antigens injected as treatment
-generates a memory response
-conventionally use polyclonal antisera

499
Q

What is an epitope?

A

the shape an antibody binds to

500
Q

What are the issues with antisera containing a mixture of antibodies to different epitopes?

A

-difficult to standardise (antiserums vary in composition)
-may lack specificity

501
Q

How is antisera produced?

A

-sample of blood is taken from animal and allowed to clot (forming serum)
-serum is checked to see if antibodies are present

502
Q

What are monoclonal antibodies?

A

antibodies derived from a single B lymphocyte which have one single specificity (to one epitope)

503
Q

How are monoclonal antibodies produced?

A

-fusion of B cell (from animal immunised to antigen) and tumour cell (which divides indefinitely) to produce a hybrid cell
-hybrid cell divides indefinitely and produces specific antigen

504
Q

How are antibodies used in research, diagnostics and therapy?

A

-to identify and label molecules in complex mixtures
-to identify pathogens
-to characterise cell surface proteins and identify cell types
-in therapy as “humanised” antibodies

505
Q

What are the two types of T cells?

A

-T helper cells
-T cytotoxic cells

506
Q

What protein do T helper cells have on their cell surface?

A

CD4 +ve

507
Q

What protein do T cytotoxic cells have on their cell surface?

A

CD8 +ve

508
Q

What are the functions of T helper cells?

A

-help B cells to make antibodies
-activate macrophages and natural killer cells
-aid the development of T cytotoxic cells

509
Q

What are the functions of T cytotoxic cells?

A

-recognise and kill infected host cells

510
Q

What is the structure of a T cell receptor like?

A

-α and β chains each with a variable domain and a constant domain
-disulphide bridge
-anchored in cell membrane

511
Q

When can B cells recognise an antigen?

A

when it is soluble, free and native

512
Q

When can T cells recognise an antigen?

A

when it is cell-associated and processed (broken down into smaller peptides)

513
Q

How do infected host cells display foreign proteins on their surface (for T cells to detect them)?

A

using major histocompatibility protein complex (MHC)

514
Q

What is the role of major histocompatibility protein complex (MHC)?

A

-initiates T cell responses
-involved in graft rejection

515
Q

What is the major histocompatibility protein complex (MHC) encoded by?

A

major histocompatibility gene complex on chromosome 6

516
Q

What are the two major histocompatibility proteins (MHC)?

A

MHCI and MHCII

517
Q

Where is MHCI expressed?

A

in all nucleated cells

518
Q

Where is MHCII expressed?

A

in macrophages, dendritic cells (in skin, lymphatic systems), B cells

519
Q

What does MHCI do?

A

displays antigen to cytotoxic T cells (with CD8 +ve receptor)

520
Q

What does MHCII do?

A

displays antigen to T helper cells (with CD4 +ve receptor)

521
Q

How does MHCI help cytotoxic T cells to recognise an antigen?

A

-viral proteins are broken down in cytosol by proteosome
-peptides are transported to ER
-at ER, MHCI binds to peptides
-MHCI moves to cell surface and displays foreign peptides on the cell surface
-T cytotoxic cells detect foreign peptides displayed by MHCI and are activated
-once activated, they kill the infected cell by inducing apoptosis

522
Q

How does MHCII help T helper cells to recognise an antigen?

A

-macrophage/dendritic cell/B cell internalises and breaks down foreign material
-peptides bind to MHCII in endosomes
-endosomes transport MHCII to cell surface, where MHCII displays the peptides
-once activated, T helper cells help B cells to make antibodies, produce cytokines, activate other leukocytes

523
Q

What happens to T cells in the thymus?

A

-they acquire T cell receptors and are educated
-selection occurs, where only the cells which recognise self-MHC but not self peptides survive (majority do not pass test and must undergo apoptosis)

524
Q

What are cytokines?

A

small (5-20kDa) secreted proteins involved in cell communication in the immune response
-produced and act locally (unlike hormones, otherwise sim)
-bind to specific receptors (cytokine receptors) on target cell surfaces
-produced by T helper cells and macrophages

525
Q

What are the biological effects of cytokines on the target cell?

A

-changes in cell behaviour
-changes in gene expression

526
Q

What are the main groups of cytokines?

A

-interleukins
-interferons
-chemokines
-tumour necrosis factor
-colony stimulating factors

527
Q

What are interferons involved in?

A

-viral infections (IFNα, IFNβ)
-cell activation (IFNγ)

528
Q

What are chemokines involved in?

A

-cell movement/chemotaxis (IL-8 aka CXCL8)

529
Q

What are tumour necrosis factors involved in?

A

-pro-inflammatory
-can kill some cells

530
Q

What are colony stimulating factors involved in?

A

-leukocyte production (M-CSF)

531
Q

What did Edward Jenner do in terms of vaccination?

A

-showed infection with cowpox was protective against small pox (now know bc antigens are very similar)

532
Q

What are the different types of vaccines?

A

-attenuated strains of pathogen
-killed pathogen
-subunit of pathogen (toxoid, virus spike protein, etc)
-engineered virus
-RNA

533
Q

What type of virus is HIV?

A

a retrovirus (ssRNA, undergoes reverse transcription)
a tumour virus (associated with cancers)
a lentivirus (causes infection slowly)

534
Q

What is a retrovirus?

A

a virus which reverses the normal flow of genetic information (uses reverse transcription)
-have ssRNA

535
Q

What is the genetic information of HIV like?

A

ssRNA

536
Q

What is a lentivirus?

A

a retrovirus with a long incubation period
eg. HIV

537
Q

What is the structure of the HIV virion like?

A

-nucleocapsid containing ssRNA genome and enzymes (reverse transcriptase, integrase, protease)
-lipid bilayer (obtained from host)
-gp120 embedded in lipid bilayer (binds to host)

538
Q

What happens in the lifecycle of a retrovirus?

A

-virus binds to host cell receptor
-viral envelope fuses with host cell, so that nucleocapsid enters cytoplasm of host
-reverse transcription occurs to produce dsDNA (from viral RNA)
-viral DNA is transported into the host nucleus and integrated into the host genome (producing a provirus)
-provirus is transcribed to produce viral genomic RNA and mRNA, which are transported into the cytoplasm
-viral mRNA is used to translate viral proteins
-new nucleocapsids form and virus buds from the cell, acquiring a lipid envelope from host

539
Q

What are the types of retroviral infection?

A

-latent (dormant in host)
-permissive (doesn’t kill host but produces new viruses)
-lytic (host overwhelmed and undergoes lysis)

540
Q

What type of cells are susceptible to HIV infection?

A

CD4 +ve cells
-mainly T helper cells
-some monocytes, macrophages and dendritic cells

541
Q

What happens in HIV infection?

A

-T helper cells initially destroy virus however T helper cells are susceptible to infection so number of infected cells increase
-T cell stimulation activates transcription of the HIV provirus
-causes T cell lysis
-number of T cells infected increases with each round of viral replication

542
Q

What happens in the HIV infection of dendritic cells?

A

-dendritic cells present antigen to T cells in lymphoid tissue
-infection is permissive -dendritic cells act as a reservoir of virus

543
Q

What happens in the HIV infection of monocytes?

A

-monocytes can cross the blood/brain barrier so carry infection into the brain
-CNS involvement

544
Q

Why is CD4 expression not sufficient for HIV infection?

A

co-receptor for virus needed
CCR5 (chemokine receptor)
-required for virus to fuse with host cell

545
Q

What is CCR5 required for in HIV infection?

A

fusion of virus to host cell

546
Q

What does the depletion of T helper cells lead to?

A

AIDS (acquired immune deficiency syndrome)

547
Q

What causes the depletion of T helper cells (in HIV infection; leading to AIDS)?

A

-direct lysis of T helper cells by virus -syncytium formation
-T helper cells killed by cytotoxic T cells/other immune mechanisms
-apoptosis of T helper cells

548
Q

What is the blood count of CD4 +ve cells less than to lead to AIDS?

A

200cells/mm3

549
Q

Where are the infected T helper cells during HIV infection?

A

lymphoid tissue

550
Q

What symptoms are associated with AIDS?

A

-opportunistic infections (pathogens which usually have little affect are more threatening, due to compromised immune system)
-reactivation of latent viruses (eg. Herpes)
-rare cancers
-CNS involvement can lead to blindness, paralysis, dementia, etc

551
Q

What is the origin of HIV-1?

A

Central Africa

552
Q

What is the likely source of HIV-1?

A

related virus affecting chimpanzees
-cross-species transmission 1910-1930ish

553
Q

What is the origin of HIV-2?

A

West Africa
(probs predates HIV-1)
-less virulent, less easily transmitted ∴ not really left West Africa

554
Q

What is the likely source of HIV-2?

A

related virus affecting sooty mangabeys

555
Q

How is HIV transmitted?

A

-unprotected sex
-blood/blood products (drug use, sharing needles)
-breast-feeding
-mother to foetus

556
Q

What are the problems with vaccines for HIV?

A

-virus has high mutation rate
-humoral immunity may not be protective, so vaccine needs to be able to induce cytotoxic T cells

557
Q

How can HIV be treated?

A

-drug therapy
(combination therapy! -mixture of drugs)

future…
-stem cell therapy (bone marrow cells w/o CCR5)
-kick and kill (reactivating latent virus and immunotherapy)
-passive immunisation (human monoclonal antibodies or engineered T cells)
-potentially CRISPR-Cas9 gene editing

558
Q

What are the problems with drug therapy for treating HIV?

A

-virus has high mutation rate
-toxicity of drugs (could effect our cells as well as the virus’ cells)
-viral latency (remaining dormant in host)
-high cost (issue in poorer countries)

559
Q

What is combination therapy?

A

mixture of drugs directed at different viral targets
-used for treating HIV

560
Q

What drugs are included in combination therapy for HIV?

A

-azidothymidine (AZT -a nucleoside analogue)
-other reverse transcriptase inhibitors
-HIV protease inhibitors
-fusion inhibitors
-capsid inhibitors

561
Q

What is a symbiosome?

A

membrane-bound vesicles (in host cell) that contains endosymbiont (eg. rhizobium cells)

562
Q

What is a thermosome?

A

Archaeal group 2 chaperonin protein which increases tolerance to heat

563
Q

What are osmolites?

A

low molecular weight compounds which influence fluidity
-accumulated by halophiles

564
Q

Is a more negative or more positive reduction potential a better electron donor?

A

more negative

565
Q

What is a mesosome?

A

a folded invagination in bacterial membrane
-aids DNA rep and protein synth

566
Q

What is seroconversion?

A

the point where antibodies become present in the blood
-antibodies are specific to protein (eg. antibodies for HIV core protein and HIV envelope protein)

Molecular Biology BSc First Year (10 decks)

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