block E - archaea and protozoa Flashcards
what are the two domains that prokaryotes are separated into?
bacteria and archea
what way do archea and bacteria look similar?
they look similar morphologically
how are cell walls and membranes different between archea and bacteria?
bacteria can have gram positive and negative cell walls which are made up of peptidoglycan and have both a cell membrane and cell wall whereas archaea only have a cytoplasmic membrane with no peptodoglycan cell wall
what is the semi-rigid lattice in archaea made up of?
pseudomurein, sugars and proteins or glycoproteins
what type of prokaryotes have peptidoglycan?
bacteria
what are the differences between archaeal and bacterial head groups in membranes?
archaeal membranes
- ether linkages in their head groups
- 2,3-un-glycerol
bacterial membranes
- ester linkages in their head groups
- 1,2-un-glycerol
what are the 4 ways archaeal membranes are different?
1- ether-linked lipids (not ester)
2- side-chains are branched isoprenes (not fatty acids)
3- different chiral form of glycerol
4- some archaeal possess lipid monolayers
how are archaeal and bacterial flagella different?
bacterial flagella
- helical filaments that rotate to provide motility
- they’re produced by the addition of flagellin subunits at the tip
- they’re thicker and hollow to allow flagellin subunits to pass through
archaeal flagella
- theyre superficially similar to bacterial flagella
- theyre considered non-homologus (convergent evolution)
-
what are the five main groups archaea are split into?
Euryarchaeota
Crenarchaeota
Thaumarchaeota
Korarchaeota
Nanoarchaeota
how do extreme halophiles maintain osmotic balance?
its usually achived by the accumulation or synthesis of compatible solutes
they pump large amounts of K+ into the cell from the environment so that the intracellular conc of K+ is bigger than the extracellular Na+ conc to maintain the positive water balance
what are the characteristics of halophiles?
- they’re highly acidic
- they contain fewer hydrophobic amino acids and lysine residues
- some haloarchaea are capable of light-driven synthesis of ATP
what is some of the different cell wall chemistries found in methanogens?
Pseudomurein (e.g., Methanobacterium)
Methanochondroitin (e.g., Methanosarcina)
Protein or glycoprotein (e.g., Methanocaldococcus)
S-layers (e.g., Methanospirillum)
what are the substrates for methanogens?
- obligate anaerobes, 11 substrates divided into 3 classes which can be converted into CH4 by pure cultures of methanogens
other compounds can be converted to methane, but only in cooperative reactions between methanogens and other anaerobic bacteria
how have thermoplasma developed a unique cytoplasmic membrane?
- they’ve developed it to maintain positive osmotic pressure and tolerate high temps and low pH levels
- the membrane contains lipopolysaccharide-like material (lipoglycan) consisting tetraether lipid monolayer membrane with mannose and glucose
- it contains glycoproteins but not sterols
what are the characteristics of ferroplasma?
- theyre chemolithotrophic
- acidophilic
- oxidises Fe2+ to Fe3+, generating acid
- grows in mine tailigns containing pyrite (FeS2)
what are the characteristics of picrophilus?
- theyre extreme acidophiles which grow optimally ar pH 0.7
- model microbe for extreme acid tolerance
what are the upper temp limits for life?
new species of thermophiles and hyperphiles are being discovered
lab experiments with biomolecules suggest that the limits are 140-150 degrees
what are structural features that improve thermostability?
high hydrophobic cores
increases ionic interactions on proteins surfaces
what is amino acid composition similar to?
its similar to that of non-thermostable proteins
what is an example of a more heat-stable molecule?
use of non-heme iron proteins instead of proyeins that use NAD and NADH
how has DNA stability adapted to life at high temps?
- High intracellular solute levels stabilize DNA
- Reverse DNA gyrase
- Introduces positive supercoils into DNA
- Stabilizes DNA
- Found only in hyperthermophiles
- High intracellular levels of polyamines (e.g., putrescine, spermidine) stabilize DNA and RNA
- DNA-binding proteins (histones) compact DNA into nucleosome-like structures
how has lipid stability adapted to life at high temps?
they possess dibiphytanyl tetraether type lipids; form a lipid monolayer membrane structure
how has small subunits (SSU) rRNA stability adapted to high temps?
theyve got a higher GC content
why are hyperthermophilic archaea important in microbial evolution?
they may be the closest descendants of ancient microbes
hyperthermophilic archaea and bacteria are found on the deepest, shortest branches of the phylogenetic tree
the oxidation of H2 is common to many hyperthermophiles and may have been the 1st energy-yielding metabolism
what are the 5 main ways the body protects against viral infection?
- skin
- mucus
- cilliated epithelium
- gastric acid
- bile
what are the antigen-non-specific antiviral responses in the immune system?
- interferon, cytokines (TNF, IL-1)
- NK cells and macrophages
- fever
what are the antigen-specific immune responses in the immune system?
- t-cell response
- antibody
why can a fever be an effective defence used by the immune system against RNA viruses?
because they don’t replicate well above 37 degrees so that’s why you don’t get high temperatures
if you get flu-like symptoms, what would be the immune mediators causing that and what would they be trying to protect your body against (what microbes)?
immune mediators- interferons and lymphokines
examples - respiratory viruses and arboviruses
if the immunopathogenesis is delayed-type hypersensitivity and inflammation, what would be examples of viruses that cause this and what immune mediators would be activated as a result?
example - enveloped viruses
immune mediators- t-cells, macrophages, polymorphonuclear leukocytes
if the immunopathogenesis is immune complex disease what would be examples of viruses that cause this and what immune mediators would be activated as a result?
example- hep B and rubella
immune mediators - antibodies and compement
if the immunopathogenesis is haemorrhagic disease what would be examples of viruses that cause this and what immune mediators would be activated as a result?
example- dengue fever and measles
immune mediators- t cells, antibodies and complement
if the immunopathogenesis is immunosuppression, what would be examples of viruses that cause this and what immune mediators would be activated as a result?
examples- HIV, measles, rubella virus
immune mediators- none
if the immunopathogenesis is post-infection cytosis what would be examples of viruses that cause this and what immune mediators would be activated as a result?
examples- enveloped viruses (e.g. post measles encephalitis)
immune mediators- t-cells
what are the properties of alpha-interferon?
producer cells- leukocytes
physical properties- acid-stable, non-glycosylated protein
exammples- dsRNA virus infcetion
what are the properties of beta-interferons?
producer cells- fibroblasts
physical properties - acid-stable, glycoprotein
examples- virus infection, bacterial components (TNF,IL-1)
what are the properties of y-interferons?
producer cells - t-cells and nk cells
physical properties - acid-liable glycoprotein
examples- antigens, mitogens, cytokines (IL-2)
what are the induction interferons?
- dsRNA (virus intermediates)
- viral inhibition of cellular protein synthesis
- enveloped virus interaction with rare blood leukocyte
what is the mechanism of action for interferons?
- release from initial infected cell
- interferons bind to specific receptor on another cell
- interferon induces the ‘antiviral state’ - synthesis of protein kinase, 2’-5’olgioenylate synthease, ribonuclease L
- stops protein synthesis that blocks viral replication
what are the 4 basic steps in viral disease?
- acquisition
- initiation of infection
- incubation period
- infection of target tissue
what goes on in the acquisition step of viral disease?
begin life cycle at the primary site of replixation e.g. cell binding to receptor in the airway then get into the body and travel though the blood stream and infect at the initial site of replication than move onto secondary replication
what happens in the incubation period of the viral disease infection?
during this period, the flu like symptoms are established, as the body has detected that there’s an infection, the major symptoms aren’t present yet
what are the different ways viruses can access target tissue?
- through an enterance portal
- ability to cross mucous epithelial cells
- stavility of virus in the body (temperature, acid and bile, host defences)
- ability to establish viremia
- tissue trophism (specificity of viral attachment proteins, tissue specific expression of receptors)
- cellular permissiveness for virus replication
what are cytolytic infections?
theyre the classic type of viral infection, naked infections cause the cell to lyse and then burst out of the cell
what are persistant infections?
they are chronic infections, its how enveloped cells infect, they all bud away from the cell, eventually the cell will go on and diw after its produced loads of viruses
what are latent infections?
they infect the cell and then sit there, not doing anything, they can then be reactivated when the immune system is less active
what is the cytopathologic activity of the virus?
the virus is lytic and depends on efficiency of viral replication, immortilizeing the infection
it causes changes in the cells macromolecular synthesis and accumulation of cytotoxic viral proteins
non-specific histological changes such as vascuolisation
what are the differnt mechanisms of viral cytophathogenisis?
- inhibition of protein synthesis
- inhibition and degradation of DNA
- alteration of membrane structure
- disruption of cytoskeleton
- syncytia formation
- permeability
- inclusion bodies
- toxicity of virion components
what are the different types of inclusion bodies?
- negri bodies
- owls eye
- cowdy type A
- intranuclear basophilic
- intranucelar acidophilic
- perinuclear cytoplasmic acidophilic
what does syncytia formation mean?
in giant multicellular cells, they reproduce but stay connected to that cell, its indicative of infection
what characteristics contribute to the severity of the disease?
- cytopathic ability of virus
- virus inoculum size
- length of time before infection resolution
- general health of the host
- genetics of virus and host
- age
- immune status
- immunopathology
what does it mean by immune status?
-competence of the immune system
- prior immunity to the virus
what does virus inoculum size mean?
- it means viral load, the less viral particles, the faster your immune system can get on top of the infection
give one example of the incubation period of a common viral infection?
chickenpox- 13-17 days
what are inapparant viruses?
the infected tissuw is undamages
infection is controlled before the virus reaches target tissue, target tissue is expendable and damaged tissue is rapidly repaired
extent of damage is below funtional threshold
what are disease and viral factors that promote transmission?
- stability of viriton in environment (drying, detergent and heating)
- transfer of virus into transmissible aerosols or secretions
- asymptomatic transmission
- ineffectiveness of immune response to control reoccurrence
what are the mechanisms of viral transmission? [from most fragile virus transmitted to least fragile]
- aerosols
- food + water
- fomites
- sexual contact or direct contact with secretions
- birth
- blood transfusion
- zoonoses (animals)
- genetic
what are risk factors for catching viruses?
- age
- health/ nutrition/ genetics
- immune status
- occupation: contact with agent or vector
- travel history
- lifestyle
- sexual activity
- children
how are geography and season risk factors of catching viruses?
it means that there is a population of serongative, sisceptible people
- precence of co-factors in the enviroment (wet season= more dengue fever)
- habitat and season for arthopod vectors
- winter
- summer
what are the modes of control to stop viral transmission?
- quarantine
- elimination of vector
- antiviral agents
- immunization (natural infection and vaccination)
- changes in lifestyle (improve hygiene)
what are the stages of organelle formation over co-evolutionary time?
- free-living and extracellular
- facultitive intracellular
- obligate intracellular
- obligate intracellular mutualist
- organelle
how many human cells and bacterial cells are there in a human body?
1x10^13 human cells
1x10^14 bacterial cells
how many human and bacterial genes are there in a human body?
~23,000 genes from the human genome and >1,000,000 human microbiome genes
how many types of human cells are there in the human body?
~200 different cell types
how many species of bacteria are there in and on the human body?
> 1000 species
what do human git microorganisms produce?
enzymes
amino acids
vitamins
what are beleived to be responsible for maturation of the gastrointestinal tract and the immune system?
human gut microorgansism
where are the microorganisms in the body that can play a role in obesity?
human gut microorganisms
what can a faecal matter transplant help with?
some disease states
what is vibrio fischeri?
its a symbiont of squid and fish
what form of nitrogen is usable for plants and what do microorgansms do to it?
it has to be fixed from the relatively intert N2 to biologically accesible NH3
its called the haber process in chemistry
what does industrial process of ammonia cost of global energy?
it costs 1-2% of global energy production and produces 1% of manmade greenhouse gases
what are the critical steps in root nodule formation?
step 1- recognition and attachment of baccterium to root hairs
step 2 - excretion of nod factors by the bacterium
step 3- bacterial invasion of the root hair
step 4- travel to the main root via the infection thread
step 5 - formation of the bacteriod state within plant cells
step 6- continued plant and bacterial division, forming the mature root nodule
what genes direct the steps in nodulation?
bacterial nod genes
what is NodD?
its a positive regulator that is induced by plant flavonoids
what does NodABC do?
its an operon which encodes proteins that produce olgiosaccharides called Nod factors
what are nod factors?
they:
- induce root hair curling
- trigger plant cell division
- signal legumes to develop root nodules
what is legume-bacteria symbiosis characterised by?
it characterised by several metabolic reactions and nutrient exchange
where can microbial symbionts be aquired form?
-enviromental resivoirs (horizontal trabsfer)
- parebt (vertical or heritable transmission)
- heritable symbionts of insects are obligaet (lack of free livign replicative state)
what are primary symbionts needed for?
host replication
what types of genes do primary symbionts need?
they only need genes for host fitness
what types of genes do primary symbionts lose?
- catabolic genes
- pathogens normally lose anabolic genes
what types of benifits could secondary symbionts provide?
- nutritional
- protection from enviroment
- protection from pathogens
how can secondary symbionts live?
extracellularly or by invading different cells
what are secondary symbionts not required for?
reproduction
how do primary symbionts exibit extreme gene reduction?
- the genome of insect symbiont ~160 to 800kbp
- genome of related free-living bacteria ~2 to 8 Mbp
what can the manipulation of insect symbionts prevent?
the spread of diseases such as dengue fever
what are lichen?
theyre leafy/ encrusting microbial symbionts
where are lichen often found?
theyre often found growu=ing on bare rocks, tree trunks, house roofs or the surfaces of bare soils
what is the mutualistic relationship between a fungus and an alga?
alga is photosynthetic and produces organic matter
the fungus provides a structure within which the phototrophic partner can grow and be protected from erosion
what is the name of fresh water microbial mutualisms?
consortia
what do consortia consist of?
green sulphur bacteria (called epibionts, they’re obligate anaerobic phototrophs ) and a flagellated rod shaped bacterium
what two organelles have been suggested that they’re descendants of ancient prokaryotic cells (primary endosymbiosis)?
chloroplasts and mitochondria
what is the supporting evidence for the endosymbiont theory?
- mitochondria and chloroplasts have their own chromosomal DNA
- mitochondria and chloroplasts have their own ribosomes
- antibiotics that affect prokaryotic ribosome function work against mitochondria and chloroplasts
- eukaryotic genomes often contain bacterial genes
- DNA sequencing reveals that mitochondrial and chloroplast DNA is phylogenetically related to bacteria
what does mtDNA have all the hallmarks of? also what is mtDNA?
mitochondrial DNA has all the hallmarks of prokaryotic DNA
what does it mean by ‘mitochondria are semi-autonomous’?
theyre not synthesised from scratch (de novo), but grow and divide like bacteria
they can make some of their own proteins using their own ribosomes from their own DNA
what is secondary endosymbiosis?
its the process of engulfing a green or red algal cell, retaining its chloroplast and becoming phototrophic
they’re apparently common and still ongoing
what are the phylogenetic lineages of eukarya?
18S rRNA genes for phylogeny of eukaryotes is far less strong for eukaryotes than 16SrRNA genes are for prokaryotes
these phylogenys have been created using other genes and molecular phylogeny is still being refined
