Extra Flashcards

1
Q

What did eshel argue about sex?

A

Prevents rapid evolution

breaks apart favorable gene combinations more than it creates them.

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2
Q

PBS model of anisogamy evolution

A

PBS - Parker Baker Smith model
2 selection pressures on gamete production - no. gametes and fitness of zygote.
Protosperm are caused by a mutation and parasitised the investment of eggs - cheating strategy.
PBS requires zygote fitness must increase disproportionately with volume. and as adult size increases selection for anisogamy increases.

Anisogamy evolved due to sperm limitation - greater egg size gives sperm a greater target, and in sea urchin species, egg size negatively correlates with mean sperm concentration.

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3
Q

What is a gonochore and what does sex allocation theory explain about hermaphrodites?

A

Gonochore - fixed sex throughout life
Simultaneous hermaphrodites - sex allocation theory predicts optimal allocation an individual should make to m and f function.
- Sequential hermaphrodites - when and why they should change sex.

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4
Q

eg of hermaphrodite fish

A

Lythrypnus fish - Mature gametes of both sexes in gonad but functions as one sex. anatomically simultaneous hermaphrodites but functionally sequential.

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5
Q

Why may animals choose to change sex?

A
  1. Decision to become a primary male might be a response to local social conditions - bluehead wrasse.
  2. when RV of one sex is greater than the other - Size advantage theory.
  3. as a response to rapid demographic changes - unknown if in response to change in average size of other fish or directly demographic. eg following disappearance of largest male in harem. no change if the combined RV of all females is lower than the dominant one.
    4 bidirectional - eg coral gobies when they find a mate can change sex so the bigger one is female.
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6
Q

which sex changes dominate in polygynous and monogamous systems?

A

polygynous - female to male

monogamous - male to female.

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7
Q

an experiment which contradicted holland and rice drosophila sexual conflict experiment.

A

Promislow, Smith and Pearce
sexual selection lines lives longer than monogamous lines. sexual selection leads to overall increased adult viability due to female choice of good genes.

differed in amount of time flies could interact for - Holland and Rice - 5 days, Promislow 3 hours.

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8
Q

2 precopulatory costs of sexual selection to females.

A
  1. risk of injury in coercive mating attempts,

2. male exploitation of female sensory preferences may result in females mating suboptimally.

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9
Q

Mechanisms of mate choice coevolution

A
  1. fisherian sexy sons
  2. Zahavi handicap principle
  3. Direct phenotypic effects - ornament may reflect ability to provide material advantages eg good territory, protection.
  4. Sensory bias - Originally evolved for other reasons but expoits female bias.
  5. Genetic compatibility mechanisms - eg MHC - non additive effects from choosing a mate with alleles which complement the genome of the chooser.
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10
Q

Methods of ‘bottom up’ genetic testing.

A

Identify, sequence and characterise function of a gene locus with several alleles which influence expression of an attractive trait.
DNA microarrays used to detect expression level polymorphism.

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11
Q

What is important in a model system

A

study in natural environment - to see NS and sexual selection.
conspicous sexual dimporphism strongly correlated to sexual selection.
Microevolutionary tests allowed by short gen time, small body size and known genetics.

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12
Q

what is a prerequisite for sperm competition?

A

multiple mating by females.

Cryptic female choice is post copulation.

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13
Q

what is the good sperm hypothesis?

A

M with high fertilisation success have underlying genetic quality, so if successful in sperm competition will sire offspring with high viability.

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14
Q

describe Immunocompetecnce handicap hypothesis

A

Trade off btw 2nd sexual ornaments and success in sperm competition, with future investment in immune function

indicator mechanism- males who can afford fancy displays must have a high immune function and offspring resistant to disease.
evidence in crickets.

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15
Q

How does Gettys model of optimal investment work?

A

Absolute costs increase with signal size, marginal costs decrease with increasing signaller quality.
Multiplicative model (Grafens was additive)
Fitness = fecundity x viability
- a good and bad peacock add an eyespot to feather - increased fecundity. however the good peacock has a higher viability so results in higher fitness.
Worse signallers have lower quality conversion of fitness to signal which selects against exaggeration/cheating.

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16
Q

Describe MC mating preference in Soay sheep in St kilda

A

no deficiency of MHC homozygotes .
Tested using 5 microsatellite markers on 887-1209 new born lambs and used the liklihood approach to analyse ewe mating patterns.
No evidence of MHC dissassortative mating preference
Inbreeding mechanisms often are selected out during domestication.
Maybe only when risk of inbreeding depression will use MHC in mating choice.

17
Q

MHC mating preference in Amerindian tribes - Hedrick and Black

A

South American Indians show MHC homozygote deficiency, but no evidence due to mating preferences.
Examined MHC sharing in 194 couples using serotypes, although criticized as ignored EPPs which females usually look for good genes rather than financial security in marriage. Also ignored socially enforced cousin marriages which are prevalent among tribes.

18
Q

Study which shows correlation of MHC and spur length in male pheasants.

A

Schantz et al
direct support of hamilton and Zuk good genes hypothesis.
METHOD: trapped and measured male peasants in winters 1983-1992. Study area no hunting and no captive birds released for 30 years.
Biometric measurements and if unmarked then ringed. Plucked innermost and 6th primary feather of wing for aging and measurements.
Attached radiotransmitter and released.
survival rate 0 if found dead, and 1 if retrapped next year. If lost, excluded from analyses.
Genomic DNA extracted from blood, RFLP patterns analysed from MHC 1 and 2.
ANCOVE showed tarsus length significant covariate with MHC type.
Deficiency of MHC homozygotes compared to predicted from hardy weinberg.

19
Q

Wolbachia extra deets

A

Werren - using PCR found wolbachia infected 17%species in panama
Hoy - only long PCR can detect it, so may be more than what werren thought. found in 76% arachnids and insects.
if it really is this common, may be a powerful evolutionary force and could drive speciation.
Not transmitted as efficiently at higher temps so species in warmer climates may not be affected.
Wolbachia may end up being mutualistic, as genome is slimming and some nematodes need wolbachia to survive - treated with antibiotics which kill wolbachia.

20
Q

How could genes involved in sexual conflict be identified?

A

Identify genes involved in sexual conflict
see divergence between sexual conflict genes and non gonad genes
eg. unidentified ovary proteins in drosophila show elevated levels of divergence between drosophila species compared to non gonad genes.

21
Q

Do bumble bees mate multiply?

A

females benefit from multiple mating but behaviour and genetic studies show they only mate once in their lifetime due to mating plugs and seminal substances.

22
Q

what have crosses of drosophila shown about rates of coevolution due to sexual antagonism?

A

Differential rates of evolution.

Males crossed between allopatric strains induced oviposition in mates more than males crossed within strains.
Shows females weaker resistance to mating with makes from different strain.

23
Q

Drosophila accessory gland proteins.

A

accessory gland proteins are 80 or so in ejaculate, evolve very fast. high levels of interspecific divergence.
Gene sequences were identified using males genetically engineered to lack them. Showed necessary for sperm transfer and costly to females.
compare performance of WTand knockout mutant.

Can also study over expression. OE of acp62F caused sig reduction in adult lifespan