Experimental genome evolution

Question 1

early models of evolution

Answer 1

biometricians (measure stuff), mendelians (stuff has discrete traits)

Question 2

infetissimal model

Answer 2

reconcillation of mendelian vs continuous traits- if you have enough alleles controlling stuff you get a normal distribution

Question 3

fisher’s geometrical model of adaptation

Answer 3

smaller mutations are more likely to be beneficial- less risk of ‘overshooting’ optimal phenotype

Question 4

methods for studying genomics of adaptations

Answer 4

genome comparisons (dN/dS)
ecological genomics- using examples of ecological adaptation and tracing back to genetics
experimental evolution

Question 5

fisher-muller model

Answer 5

sexual reproduction allows beneficial alleles to combine, and deleterious alleles to not add up - recombination, rather than competition

Question 6

long term experimental evolution study- number of generations

Answer 6

over 70,000 since 1988

Question 7

non-coding vs coding - dynamics of evolution

Answer 7

mutations tail off less in non-coding regions, adaptation seems to happen then stop for non-coding

Question 8

mutation bias

Answer 8

idea of ‘mutational hotspots’- points where lots of mutation happens, points where much less happens

Question 9

population sequencing- why is it useful?

Answer 9

allows much better tracking of allele frequency over time- see something which looks like fisher-muller

Question 10

what is hitch-hiking

Answer 10

neutral mutation moving through generations alongside a beneficial mutation

Question 11

ruby in the rubbish

Answer 11

beneficial mutations in low fitness background- recombination helps these mutations separate themselves out from worse alleles

Question 12

importance of enzymes

Answer 12

‘template’ for innovation- dynamic etc

Question 13

example of regulatory re-writing

Answer 13

in flagella evolution- can change which genes regulate it, when the original regulator is experimentally mutated

Question 14

fastest vs slowest mjutations to spread

Answer 14

gene regulatory responses spread very fast, point mutations are much slower (easy to ‘miss’)

Question 15

importance of gene duplication

Answer 15

removes the cost of messing with genes, as there is a backup present

Question 16

sub-functionalisation

Answer 16

multi-functional gene gets split up after a duplication into narrower functional roles

Question 17

HGT costs

Answer 17

biosynthetic burden
toxic interactions with existing genes
exposure to competetors or phage for it to happen at all, inherent issue