Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Sem 1: Parasite and pathogen ecology > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What is the strict definition of co-evolution?

A

The joint evolution of two (or more) ecologically interacting species, each of which evolves in response to selection imposed by the other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the loose definition of co-evolution?

A

The evolution of one species caused by its interaction with another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the general definiton of co-evolution?

A

Each party exerts selective pressure on the other, thereby affecting each others evolution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the relationship between hosts and pathogens?

A

Pathogens want to consume host tissue/energy to covert it into more pathogens
Hosts limit damage by slowing or killing the pathogen
This places a strong selection pressure on both hosts and pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 3 co-evolutionary concepts for parasites and hosts?

A

1 - Specific host and pathogen co-evolve
2- Several species involved and their efffects are not independant (host many evolve to more than one pathogen)
3- Host species evolves a major new defence against pathogens, escape 1 pathogen and another evolves later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How can host species escape a pathogen?

A

Evolves a new defence against pathogens
Escapes pathogens and can proliferate and diversify
Later new pathogens adapt to host clade and therefore also diversify

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is used to analyse co-evolution?

A

Phylogenetic analysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some issues with assessing co-evolution?

A

Most congruent phylogeny - some mismatches
Host switching
Extinction of Lineages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is relationship between pigeons, wing and body lice?

A

Body lice competitively superior to wing lice
More host switching in wing lice
Both transmit vertically - parent to child
Wing lice also has phoretic horizontal transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are examples of specific parasite co-evolutions adaptation?

A

Parasitic trematode larvae (Leucochloridium) - migrats to the eye stalk of its intermidiate host (land snail)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are examples of specific host co-evolutions defences?

A

Wild parsnips (Pastinaca Sativa) produce chemical defence furanocoumarins against insects (webworms)
Vertebrates - Major Histocompatability Complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the costs of furanocoumarin production in wild parsnips?

A

High energetic cost to produce furanocoumarins
Can be up to 10% energy costs
Parsnips with high furanocoumarins produce less seeds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 3 outcomes of a pathogen and host relationship?

A

Unending arms race
Extinction of one of the species
Stable genetic equilibrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 2 complex models of co-evolution?

A

Attack and defence
Cost and benefits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the mechanisms of pathoegn-mediated selection?

A

Frequency dependance
Heterozygote advantage
Fluctuating selection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is virulence?

A

The relarive ability of a pathogen to cause a disease
The host’s loss of fitness due to the pathogen
Virulence depends on host-pathogen co-evolution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is coincidental evolution?

A

Accidental virulence with selection of other traits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is an example of conincidental evolution?

A

Tetnus (Claustridium tetane)
Chemical secretions - selected for life in soil
Neurotoxin in humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is short-sighted evolution?

A

Generations of evolution within a host before transmission
Trsits for within host firtness evolve
Even if detrimental to transmission to new host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is an example of short-sighted evolution?

A

Poliovirus in humans - normally in gut lining
May evolve to exploit nervous system
But will never be transmitted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the trade off hypothesis?

A

Selection favours pathogens that strike the optimal balance between the cost and benefits of harming their hosts - to optimise transmission rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What factors affect trade off and therefore virulence?

A

Multiple infections - competition between different strains of pathogens within host
Speed/effectiveness of the host’s immune system
Pathogen transmission
- Form of transmission - horizontal vs vertical
- Means of transmission - vector vs direct contact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

As shown in bacteriophages in E.Coli, what is the method for horizontal transmission?

A

Virus induces cell to produce and secrete new phages- but this slows E.Coli cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

As shown in bacteriophages in E.Coli, what is the method for vertical transmission?

A

E.Coli divides - virus copies in both daughter cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How can you block different forms of transmission of bacteriophages?

A

1 - Anti virals to block horizontal
2 - To block vertical transmission move phages to new uninfected E.Coli cultures every generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What was the experiments done by Messenger in 1999?

A

Created 2 sets of selection lines of virus (13 in each)
1 set can only vertical transmission virus lines and the other horizontal transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What were the predictions for the Messenger experiments based off of trade off hypothesis?

A

1 - Correlation between phage reproduction rate and virulence - virus lines that reproduce the most - slow host growth most
2 - Mainly vertical transmission lines - evolves lower phage reproduction rates and lower virulence (allow their host to reproduce more)
3 - Mainly horizontal transmission lines - favour viral strains that reproduce quicker - more virulent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What was the result of the Messenger experiments?

A

The predictions where found to be correct horizontal transmission has high virulence and vertical transmission had low virulence with a positive correlation between virulence and phage reproduction rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does transmission form impact virulence?

A

Vector born pathogens - carried away from severly debilitated host
Pathogens transmitted by direct contact - cannot afford to be too virulent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What happened to the Myxoma virus in the European rabbit (Oryctologus cuniculus) populations in Australia?

A

Introduced to Australia (1950)
Spread by fleas, mosquitos and man
Causes localised skin tumours
Kills 99.8% rabbits but soon dropped off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Why did the rabbit death percentage drop off?

A

Myxoma epidemics exerted strong selective pressure for resistance
Rabbits populations that had been exposed to more epidemics had lower mortality
Genetic variation conferring resistance to myxoma before indroduction of virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What happened to the virulence of the myxoma virus?

A

Virus strains that didn’t kill hosts were more readily disperse to new hosts - stabilises at an intermediate level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the endosymbiotic theory?

A

A rickettsia species of bacteria has so co-evolved that it only lives in cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the Major Histocompatibility complex?

A

Set of genes coding for cell surface glycoprotein molecules in all vertebrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the major histocompatibility complex called in human?

A

Human leukocyte anitgen (HLA) complex

36
Q

How was the HLA first identified?

A

Organ transplants

37
Q

What is the function of major histocompatibility complex?

A

Distinguishing self from non-self

38
Q

What does the major histocompatibility complex code for?

A

Molecules that bind and present antigens on the cell surface

39
Q

What are antigens?

A

Non-self peptides

40
Q

How does the major histocompatibility complex help in immune response?

A

Major role in determining acquires immune response

41
Q

How many classes of major histocompatibility complex are there?

A

3

42
Q

What is the function of class 1 major histocompatibility complex?

A

Present antigenic peptides to Cytotoxic cells
Endogenously derived peptides
Used against intracellular pathogens

43
Q

What are class 2 major histocompatibility complexes?

A

Present antigenic peptides to T helper cells
Process exogenous antigens
Extracellular pathogens e.g Gut parasites

44
Q

What are class 3 major histocompatibility complexes?

A

Secrete proteins that have an immune function
Involved in inflammation

45
Q

What are major histocompatibility complex genes?

A

Complicated set of replictaed genes (multiple gene duplications

46
Q

Are major histocompatibility complex genes linked?

A

Yes, they are linked together in a haplotype (set of alleles across loci)

47
Q

How are major histocompatibility complex inherited?

A

Inherited as a haplotype - little recombination

48
Q

How are the 2 sets of major histocompatibility complex genes expressed?

A

Believed to be co-dominant

49
Q

What are possibilities for different individuals?

A

Heterozygous or homozygous

50
Q

What does MHC genes means for host variation?

A

Results in lots of MHC molecules with slightly different structure on each cell

51
Q

What is Peptide Binding Region (PBR)?

A

PBR are key area of MHC loci

52
Q

How does PBR change per molecule?

A

Different amino acids at the PBR - result in different binding properties

53
Q

Are PBR limit to only complementary binding?

A

Potentially promiscuous binding

54
Q

What are examples of MHC allele pathogen associations in Humans?

A

Malaria
HIV progression

55
Q

What are examples of MHC allele pathogen associations in other animals?

A

Sheep and nemotodes
Chickens and merek disease
Chickens and avian flu
Passerines and avian malaria

56
Q

How many alleles are there of the HLA-B gene?

A

499 alleles

57
Q

How does natural selection promote variation in the MHC?

A

Maintains genetic polymorphism across individuals within a population

58
Q

How can you detect evidence for historical balancing selection?

A

Ratio of non-synonymous (amino acid altering) to synonymous (silent) substitutions in the DNA
dN:dS

59
Q

What happens if the dN:dS ratio is greater than 1?

A

Postive selection

60
Q

What happens if the dN:dS ratio is less than 1?

A

Negative selection

61
Q

What happens if the dN:dS ratio is equal to 1?

A

Neutral

62
Q

What is trans-species persistance of MHC alleles?

A

Related of MHC genes across species

63
Q

What is an example of trans-species persistance?

A

At MHC loci, chimp alleles can be more closely related to human alleles than to other chimp alleles

64
Q

What do the dN:dS ratios and trans-species persistance mean?

A

That the balancing selection has been operated for some time

65
Q

What are the 3 main models for how balancing selection maintains variation?

A

Heterozygote advantage
Rare allele advantage
Fluctuating selection

66
Q

What is the heterozygote advantage?

A

Heterozygote gentotypes have an advantage over homozygote ones

67
Q

How does being heterozygous provide an advantage?

A

2 different alleles at a locus allow for:
Detect more pathogen strains
Better detection of any single pathogen strain

68
Q

Why is heterozygous dominant?

A

More likely to contain the ‘best’ allele

69
Q

Why are heterzygous overdominant?

A

Combination of alleles in Hz is better than both alleles alone

70
Q

What evidence is there for heterozygous domiance?

A

Hz more resistant
Over-representation of Hz gentotypes in a population ( deviation from Hardy-Weinberg expectations in adult popualtion and deviation from medelian proportions in offspring)

71
Q

What is the rare allele advantage?

A

Relative fitness of an allele declines when the frequency of that allele is high

72
Q

What is the advantage of having a new/rare MHC alleles?

A

Better able to detect pathogen variants that have evolves to evade common MHC alleles

73
Q

How many generations does it take for allele frequency to decrease from 1% to 0.1%?

A

1000 generations

74
Q

What is the theoritcal support for rare allele advantage?

A

Mechanistic models

75
Q

Is there empirical eveidence for rare allele advantage?

A

Very hard to show as changes occur evolutionary time

76
Q

How is rare allele advantage inferred?

A

Spatial variation in relationship between resistance to a specific pathogen and MHC alleles
Changes in allele frequencies over time in a population
Correlation between frequency of MHC allele and resistance

77
Q

What is fluctuating selection?

A

Spatio-fluctuations in pathogens infecting host and thus selection
This selects for different MHC alleles at different places at different times
Host gene flow and temporal fluctuations - maintains MHC variation in metapopulation

78
Q

What is the evidence fluctating selection for MHC?

A

Greater among subpopulations variations at MHC than at neutral markers
Shows different selection acting in different places at different times

79
Q

Which of the theories are most likely?

A

All three causing a positive reinforce

80
Q

What are side benefits of MHC variation?

A

May help determine quantitive traits like size or secondary sexual characteristics
Linked to individual fitness behaviour in natural populations

81
Q

What is the romantic model?

A

Females prefer males with compatible MHC genes to their own which is determined by direct clues like smell

82
Q

What is the Hotshot model?

A

Individual survival is partially determined by the MHC genes they carry, this is boosted by diversity and specific alleles

83
Q

How is MHC-dependant mate choice seen in humans?

A

T-shirt tests
Hutterite couples
Dissimilar European american couples

84
Q

How is MHC variation impacting Seychelles warbler?

A

Positive association between MHC diversity and juvenile survival
Mean life span:
less than 4 alleles = 1 year
More than 4 alleles = 2.5 years

85
Q

What pre-copulatory factors drive MHC-dependant fertilisation patterns?

A

MHC based mate choice
MHC dependant male-male competition

86
Q

What post-copulatory factors drive MHC-dependant fertilisation patterns?

A

MHC related selective fertilisation
MHC dependant selective abortion
MHC dependant mortality of eggs/embryos

87
Q

Why is conservation important for MHC?

A

Individuals with greater MHC variations mean can combat wder range of pathogens
Populations with greater MHC variations can identify an process larger number of antigens therefore combat larger number of pathogens

Sem 1: Parasite and pathogen ecology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions