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Genes and Environment > W1 > Flashcards

W1 Flashcards

1
Q

why name and classify?

A
  1. order
  2. extrapolation of important info from closely related species eg. lab mice
  3. understand evolutionary affinities, therefore, undertsand phylogeny
  4. testing: biodioversity assessment, ecological impact, conservation impact
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2
Q

what is taxonomy and why do we need it

A

taxonomy refers to the naming of organisms and is needed so because:

  1. common names are unrelaible
  2. we can have a agreed upon name
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3
Q

describe linneaus naming system

A
  1. binomial names
  2. latin names
  3. italicised
  4. capital genus and lower case species
  5. arranged in taxonmic hierachy whereby hierarchy reflects ordered information about organism
  6. hierachy should contain all species derived from a common ancestor
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4
Q

what are type specimens and why do we need it

A

this is a requirement of new species formalisation whereby a physical sample is need for comparison. note: this underlies taxonomy

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5
Q

what are the rules in naming a species

A
  1. first published name is the legitmate name
  2. must use correct latin grammar
  3. must describe species
  4. must not use author name
  5. must provide type specimen
  6. not have same name in species
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6
Q

what are some of the issues with the taxonomic code

A
  • limited clear descriptions for microscopic eukaryotes
  • double barreled names
  • codes are seperate, so two species can have the same name
  • names can have authority
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7
Q

describe the principles of biological classification

A
  1. nomenclature/ taxonomic organisation of groups should show that closely related organisms are more similar than distantly related organisms
  2. groups should be monophyletic compared with paraphyletic and polyphyletic. (para: includes common ancestor but not all descendants, poly: does not include all common ancestors, mono: single common ancestor for all members in that group not shared with any other species)
  3. categorisation occurs on the basis of visible traits and molecular evidence
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8
Q

what is systematics

A

in general: the study of diversity

  1. reveals evolutionary relationships
  2. classification reflects those relationships
  3. creates hierarchal system that organises out understanding
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9
Q

what is cladistics

A

a type of systematics where we infer relationships on the basis of ancestral and derived traits. it allows us to identify branch points (ie. have the trait or not) In evolution.

how to do this:

  • use homologous traits which have a common origin issue: divergence whereby different functions but similar look
  • use analogous traits which results from convergent evolution, homoplasies (trait not following a common ancestor)
  • trait can be lost or reduced or not obvious
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10
Q

what is parsimony

A

this is the concept of producing an outcome with the least number of steps required
eg. looking at these traits; jaws, lungs, claws/nails, warm blooded, mammaries

BEWARE!: groups can be inverted around a node

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11
Q

describe how molecular evidence can be used to deduce evolutionary relationships

A
  • dna encodes the information for organisms to have specific traits

why is DNA good?
- has a large amount of neutral variation (no effect on fitness) allowing advantages in comparison
an example of these areas could be
A. non coding regions of the genome
B. changes in dna sequence in genes that do not impact protein sequence
C. changes that lead to different protein sequences without impacting protein function

note: human and chimpanzees are 99% same in DNA

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12
Q

what can we do with molecular data

A

construct phylogenies by comparing DNA sequencing databases for a particular protein, eg. cytochrome B (conserved gene)

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13
Q

what is a virus

A
  1. infectious agent
  2. not cellular
  3. cannot reproduce itself
  4. needs a host cell to make copies of itself
  5. comprised of a genome, capsid and sometimes a lipid membrane (from host)
  6. no ribosomes, organelles and energy metabolism
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14
Q

what are giant viruses

A
  • 3 types: Mimivirus, Megavirus, Pandoravirus
  • some are related but others appear to represent distinct viral lineages
  • some have their own parasites

Pandoravirus:

  • 1 um
  • P.salinus has 2500 genes
  • P.dulcis 1.9Mb genome
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15
Q

what are the general properties of viruses

A
  1. small, usually range in size from 20-300um
  2. obligate parasites so they are uncultivable
  3. infectious particles of nucleic acid and protein
  4. complete infectious particle is known as virion

Virion:

  • nucleic acid genome
  • 6400 nucleotides in TMV
  • capsid
  • sometimes a lipid envelope and enzymes
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16
Q

describe viral genomes

A
  1. type of nucleic acids: ssRNA, dsRNA, ssDNA, dsDNA
  2. DNA/RNA acts as the genome or template encoding 4 proteins
  3. proteins produced: capsid, replication, intracellular movement
  4. sometimes highly mutable

special case: retrovirus

  • have reverse transcriptase enzyme whereby RNA is reverse transcribed into DNA. DNA then inserts into host genome. eg. HIV
    note: the ⅓ of the human DNA looks like transposable elements similar to the retrovirus
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17
Q

describe viral protein capsid

A
  1. constructed from protein subunits
  2. self assembling into:
    - helical array eg. TMV
    - icosahedral eg. papilloma
    - complex eg. bacteriophage
    - other eg. brick like, worm like, bullet shaped, bacilliform
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18
Q

describe the process of viral replication

A
  1. virus take up by injection or endocytosis
  2. genome released
  3. parasites of translation
  4. RNA acts as a template for mRNA for protein synthesis or in case of a retrovirus, reverse transcriptase makes DNA
  5. DNA viruses replicate genome in host nucleus and direct capsid synthesis via mRNA
  6. newly formed various can destroy host cells (leading to small pox and chicken pox)
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19
Q

Describe phage growth

A

Firstly: phages are viruses of bacteria

they grow in the pattern of some clear areas, some plaques and some cloudiness which is the bacterial growth areas

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20
Q

describe viral classification

A
  • common names often based on host and symptoms
  • naming is based on 1. morphology
    2. type of nucleic acid
    3. single or multi particle virion ie. packages how many virions
    4. host-virus vector relationship

note: same type of hierarchal system used fro classification
note: Baltimore system is used for viral naming

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21
Q

list some examples of viral diseases

A

smallpox, yellow fever, influenza and AIDS

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22
Q

how can viruses be combated?

A

through vaccination, however dealing with viruses is difficult as viruses use host’s cellular machinery for replication

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23
Q

what is zoonosis and in what disease is it very dangerous in

A

zoonosis is when a pathogen can jump from animals ie. birds to humans and it is seen most commonly in influences. this is bad because new strains of influenza can form

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24
Q

what are the two key molecules in influenza

A
  • H and N particles
  • Haemaglutinin enables the virus to enter the cell
  • neuraminidase enables the virus to leave the cell

remembering: think about the alphabet, H is before N, like how H is entry and N is exit

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25
Q

describe how emergence of new flew strains in influenza can occur

A
  • there are multiple viral strains in infleunza become there are multiple different versions of H and N in virus strains
  • each flu carries one gene for H and one gene for N
  • the genes are on seperate pieces of RNA (note: there are 8 genes in a flu virus)

How new strains form and why this is bad?

  • two different strains of flu infecting one host cell can exchange version of H and N to make new combinations
  • the immune system cannot recognise new combinations
26
Q

describe treatments of the flu

A
  1. relenza or tamiflu

2. both of these are neuraminidase inhibitors that prevent the flu virus from exiting used host cells

27
Q

describe one method of viral disease outbreak management

A

investigating the epidemiology of the disease bu tracking the outbreaks and spread of the disease eg. SARS

28
Q

what infectious agents are smaller than viruses

A

viroids which are 1/1000 of a virion

prions

29
Q

what are the key traits of a viroid?

A
  1. single circular strand of naked RNA (associated with ~30 plant diseases)
  2. particles are 1/1000 of a virion. there are 246-380 nucleotides of ssRNA which is not enough to encode a protein
  3. parasites of transcription
  4. RNA is catalytic
30
Q

what are the key traits of prions?

A
  1. variant protein fibrils that affect the NS
  2. unknown pathogenesis (disease development)
  3. found to be the cause of many diseases eg. BSE, MAD cow disease, sheep scrapie, CJD and kuru (humans)
  4. disease causing gene is highly conserved in humans
  5. PrPc and PrPsc are chemically identical but structurally different
31
Q

describe prion mechanism of action

A
  1. PrPc Is the normal brain prion protein
  2. in infected animals much PrPc is converted to PrPsc
  3. PrPsc when mixed with PrP will cause the PrP to convert to PrPsc ( chain reaction)
  4. if we eat PrPsc, it spontaneously converts to PrP and PrPsc
  5. PrPsc forms insoluble plaques in brain disease
  6. PrPsc can be extracted from sick animals make other animals sick with it-hence it is a infectious agent
32
Q

how does kuru and prions relate

A

Kuru is linked to ritual practice of eating Brians of deceased relatives. since some of those relatives had PrPsc in their brains, it was transmitted

33
Q

how does Mad cow disease link to prions

A

castles were fed ground up bodies of sheep and of other cows, some had PrPsc causing conversion of PrP to PrPsc, causing BSC (bovine spongiform encephalopathy) disease

when humans ate brains of cows with PrPsc, it is called induced CJD

34
Q

what features of viruses make them able to overcome a hosts immune system

A
  • each flu carries one gene for H and one gene for N
  • the genes are on seperate pieces of RNA
    two different strains of flu infecting one host cell can exchange version of H and N to make new combinations
  • the immune system cannot recognise new combinations
35
Q

compare protein causing diseases with toxins from bacteria or fungi

A

whilst bacteria and fungi toxins target specific parts of cells, prions target the CNS and many other brain regions

whilst bacteria and fungi affect cell function, prions have plaque formation

bacteria causes diseases via DNA viruses replicating in the genome of the host nucleus and subsequently releasing newly formed virions which can destroy host cells

prions cause disease by mixing the diseased protein PrPsc with the normal protein PrP leading to the normal proteins becoming diseased. this leads to insoluble plaque formations in the brain

the diphtheria toxin is released from prophage beta cells that have an active A subunit that can block protein synthesis by targeting a uniquely modified histidine, diphthamide in EP-2 leading to cell death

36
Q

compare and contrast viruses, viroids and prions

A

where: viruses can have affect anywhere in the body. viroids do not have a specified location of action. prions are variant protein fibrils infecting the NS
what: viruses are uncultivable obligate parasites. viroids are single circular strands of naked RNA that a re parasites of transcription. prions are brain prion proteins.

size/structure: viruses are around 20-300nm and its structure is based around a virion which is its infectious particle with a capsid, nucleic acid genome and sometimes a lipid envelope and enzymes. viroids and prions are smaller than viruses

replication: viruses replicate by RNA acting as a template or via reverse transcription in retroviruses. viroid RNA is catalytic. prions replicate by mixing with normal PrP where PrP can then be converted to PrPsc

37
Q

what is consistent with the three domains of life

A 
•  Conduct glycolysis
•  Replicate DNA semi-
conservatively
•  DNA encodes proteins
•  Use transcription and translation
•  Cells surrounded by membranes
38
Q

what are the main prokaryotic features

A
  1. lack a membrane bound nucleus, organelles and cytoskeleton
  2. different cell walls where there is peptidoglycan in bacteria
  3. different rRNA sequences- therefore, different ribosomes and therefore different antibacterial targets
  4. may be heterotrophic or autotrophic

note: heterotrophic means requires pre formed organic molecules for growth
autotrophic means can live exclusively on inorganic matter and an energy source

39
Q

describe ancient prokaryotes in terms of feeding, environmental conditions and when the main prokaryote (most important one) came about and what it did

A
  • earliest was probably a chemoautotroph (get E from Chem reactions)
  • photosynthetic species were anoxygenic
  • environment was hot, saline, high UV since no ozone
  • cyanic bacteria which is oxygenic bacteria appeared about 3.5 billion years ago. it contains chlorophyll meaning it is photosynthetic. this created the o2 atmosphere
40
Q

how have prokaryotes become the agents of global climate change

A
  1. transformed inorganic environment by introducing, atmospheric oxygen, organic carbon, nitrification where nitrogen fixers convert n2 to ammonia, with nitrifies converting ammonia to nitrate, sulfur metabolism
  2. most prokaryotes are saprophytes or symbionts, only a few are pathogenic
41
Q

describe the domain archaea, with reference to an example

A
  1. originally grouped with bacteria
  2. sometimes considered extremophiles
  3. methanogens

eg. Halobacterium halobium
- discovered in 1880 as salted fish
- extremophile whereby membranes rupture below 1.5M NaCl
- can use opsin proteins for energy capture when nutrient levels are low

42
Q

describe the unique membranes in archaea

A
  1. phospholipids are from ether linkages in archaea versus ester linkages in bacteria
  2. diagnostic of the presence of archaea in environ. samples
43
Q

describe domain bacteria and the differences between archaea and bacteria

A
  • some are pathogens and some are model organisms
  • differences between archaea and bacteria:
    1. cell wall composition is that bacterial mostly have peptidoglycan
    2. membrane lipids are ester linked rather than ether linked
    3. sensitivity to toxins and antibiotics
44
Q

describe bacterial reproduction

A
  1. asexual so no meiosis
  2. some species produce spores
  3. genetic exchange does occur in bacterial reproduction and it can occur four ways: A. conjugation where bacteria attach and either some or all(with PLASMID) bacterial genome are shared
    B. transformation where the bacteria dies and releases its DNA for adjacent cells to take it up and incorporate into their own genome
    C. transduction with bacteriophage where an initial virus has some bacterial DNA packaged into its head. the same virus can then transmit the bacterial DNA into another bacteria when infecting the other bacteria

what is so good about genetic exchange?

  • the transfer of genes across genera
  • antibiotic resistance (but not good for humans)
45
Q

contrast the two bacterial cell walls

A

gram positive: thick peptidoglycan and one membrane

gram negative: thin peptidoglycan, has lipopolysaccharide, has inner and outer membrane regions

46
Q

What are mycoplasmas, with reference to size, genome, cell wall and what problems it causes

A
  • smallest known cells of 200nm
  • smallest genomes with 600,000 bases
  • lack cell walls so no peptidoglycan and therefore no antibiotic resistance
  • parasites and commensals
  • cause of panumonia in humans
47
Q

what is the importance of the interaction between host and microbe and a an outcome from a disease

A

according to the disease framework, it suggests that the hosts response to. microbes governed the outcome of the interaction

with outcomes being,

  1. commensalism
  2. colonisation, latency, disease, death

note: death can either occur by the pathogen itself or an overpowering response to the disease by the immune system

48
Q

describe actinomycetes in terms of genomes, staining and main benefit

A
  • same as actinobacteria
  • have a high GC content in genomes
  • many, but not all eg. mycobacterium stain Gram positive

Streptomyces pharmaceuticals: comes from Streptomyces griseus to form streptomycin
- first effective drug against TB
- more than ⅔ of antimicrobial agents used today derive from Streptomyces species eg.
• Amphotericin B, chloramphenicol, erythromycin, neomycin, nystatin, tetracycline.

49
Q

what are the three mechanisms of host damage

A
  1. toxin synthesis eg. diphtheria comes from bacteria with Prophage beta to produce an AB subunit toxin
  2. mycolic acid producing inhibiting phagosome and lysosome fusion in TB
  3. grows in macrophages in cooler parts of the body ie. nerve and skin to schawnn cells
50
Q

describe Diphtheria in terms of symptoms, treatment and how it is bad

A
  • highly contagious respiratory disease
  • 1901 Nobel to Behring for antitoxin
  • prevented by vaccination and antibacterials for treatment
  • infection leads to inflammation and formation of a pseudomembrane on the pharynx
    + membrane comprises dead host cells and bacterium
    +exotoxin is disseminated in the blood stream where to can cause damage to the heart, kidneys, NS
    + toxin inhibits protein synthesis
    +symptoms are upper respiratory tract to paralysis to death
51
Q

describe the diphtheria toxin

A
  • Corynebacterium diphtheriae
  • bacteria containing the prophage beta can produce the diphtheria toxin which is 3rd in potency
  • it is an examples of an AB subunit toxin

AB subunit toxins:

  1. B domain attaches to heparin binding epidermal growth factor receptors on host cells
  2. The cleaved subunit is active and attaches ADP-ribose to elongation factor 2 (EF-2).
  3. – A single molecule of A subunit can inhibit all the EF-2 in a cell, thereby blocking protein synthesis and leading to cell death.
  4. – Specifically targets the unique modified histidine, diphthamide, in EF-2.
52
Q

how does the bacteria containing the diphtheria toxin protect itself against this toxin?

A
  • one would think that surely the toxin would attacks its own EF-2 homologue

the toxin functions by binding to a specific modified form of His

  • however, only one protein has this amino acid residue and that is EF-2
  • since the bacteria does not have EF-2, neither can it make it, the toxin cannot attack the bacteria
53
Q

what are the twelve diseases that changed the world

A
  • Irish potato blight
  • cholera
  • smallpox
  • bubonic plague
  • syphillis
  • TB
  • malaria
  • yellow fever
  • influenza
  • AIDS
54
Q

describe TB

A

Some Mycobacterium species are free-living saprophytes; best known are the animal pathogens.
• M. bovis causes tuberculosis in cattle, and can be
transmitted to humans. (an example of a domesticated type of disease)

Mycobacterium tuberculosis causes one of the most common and problematic infectious diseases in history.
• 1/7 of all deaths in Europe when Robert Koch identified M. tuberculosis as the causative agent.
• 1/3 world is still currently infected, causing an estimated 2 million deaths annually.

55
Q

what are Mycobacterium tuberculosis virulence properties

A
  1. no toxins
  2. slow growing with a division time of once per day
  3. disease is slow to progress and may take 4-12 weeks for symptoms to show
  4. thus, it may enter a latent state
  5. does produce mycolic acids that provide a hydrophobic surface to bacterium and protection against antimicrobials, host defences and ph changes
  6. functions by inhibiting the fusion between the P+L
  7. antibacterial treatments last nine months
  8. one can detect the presence of Mycobacterium by using acid fast staining

6/7 are bad because since TB is now inside phagosome, it is protected inside the host. secondly, the long treatment time means compliance can decrease and a person is likely to develop antibacterial resistance

56
Q

Leprosy

A
  • Mycobacterium leprae
  • Hansen’s disease
  • human specific disease with the exception of armadillos and a few primate species
  • unculturable
  • • Mostly found in tropical countries, with 11 million cases a year world wide.

• Transmission of (and susceptibility to) the disease is not
well understood. It is said to be:
• Prolonged exposure, skin abrasions, nasal secretions.
• Estimated that <5% of the population is susceptible.
• Incubation period of 3 - 7 years (but may be longer.)

57
Q

describe Mycobacterium leprae growth and disease progression

A
  1. grows in macrophages of the cooler parts of the body as well as nerve and skin cells, targeting of Schwann cell infections results in loss of sensation
  2. Mild, non-progressive form from hypersensitivity to antigens on the M. leprae surface.
  3. Leptomatous form combination of bacteria, macrophages and skin cells.
58
Q

what causes Hansen’s disease symptoms

A
  1. based on damage response framework, it is HYPOTHESIZED THAT
    - the symptoms are not from bacteria releasing toxins and causing damage,
    - rather it is the host recognising and mounting an immune response
    - the stronger immune response causes damage
59
Q

describe mycobacterium leprae genome evolution

A

• 3.3Mb genome, half being
pseudogenes.
versus, M.tuberculosisis 4.0Mb, 4000 genes (only 6 pseudogenes)

Very little variation between strains , which is odd because one more expect the more pseudogenes, the more variation. a possible explanation for this is a single origin as a human pathogen which lead to subsequent spread around the world

60
Q

describe Mycobacterium diseases in history

A

• Evidence of tuberculosis in human
remains dated to 9,000 years ago.
• ‘Consumption’ had little stigma associated with it.
• In contrast, lepers were isolated from society.
• Of the two diseases, leprosy is the less contagious, less damaging, and easier to cure than tuberculosis.

61
Q

outline the process by which influenza reproduces and is then spread from the body

A
  1. influenza virino uses H to bind to specific receptors on silica acid
  2. vision is endocytose and brought in by the host itself
  3. viral RNA particles are released (from its 8 segmented genome)
  4. the viral genome is used as a template by the host translational machinery
  5. more copies of viral RNA are made
  6. self assembly occurs whereby there is packaging into viral RNA elements
  7. spread continue

Genes and Environment (12 decks)

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