week 5 notes 409
week 5 notes 409 Bio 409
U of L
Popular in Evolutionary Biology
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This 5 page Class Notes was uploaded by Mary-elizabeth Notetaker on Friday September 23, 2016. The Class Notes belongs to Bio 409 at University of Louisville taught by Jeffery Bara in Fall 2016. Since its upload, it has received 8 views. For similar materials see Evolutionary Biology in Biology at University of Louisville.
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Date Created: 09/23/16
Week 5 Tuesday, September 20, 2016 2:16 PM Ex) allele freqs? 150AA 70Aa 80aa ○ AA: 150/(150+70+80)=0.5 ○ Aa= 70/300=0.233 ○ Aa=80/300=0.266 ○ A= 2(150)+70=370/600=0.616 ○ a= 1-0.616=0.3840.384 HWE- null model, no evolution.. If violated, pop is evolving ○ assumptions:no selection,mutation, migration, genetic drift, & indivs choose mates at random ○ if final allele freq diff than initial, evolution is occurring and HWE is violated 5 forces of evol: mutation, mig, selection, genetic drift, nonrandom mating mutation:generates new genetic alleles/genesso NS can act..rates vary widely among species ○ point mutations- sources of new alleles spontaneous deamination, misalignment, proofreading/correctionalerrors before replication is paramount premutations are very common 20 AAs for 64 codons.. redundant synonymous-silent.. doesn’t change AA coded for nonsynonymous:change AA.. missense/nonsense/readthrough ○ duplications- new genes fates: lose fx(becomepseudogene), keep current fx, gain new fx ○ chromosomeconversions-inversions segment breaks and reanneals(reordersgenes on chrom) □ affects linkage, crossing over, all genes in inversion inherited together-->supergenes genome duplications in plants- instant speciation.. triploid have indivisble genes ○ fitness effects of mutations- most deleterious, beneficial rare lower than 1 is dec in fitness so bad mutation,above 1 is good and beneficial..0 is lethal, 1 is neutral □ neutral mutations may affect mRNA secondary stxs in mammals causes genome changes which could cause future mutations ex)VSV(rna virus)..created many mutants □ competedeach mutant against progenitor and effect it had □ relative fitness- of mutants compared to progenitor(WT) □ mutations actually observed,proportionally fewer deleterious bc some eliminated from selection proportionallymore neutral alleles beneficial mutations still rare but proportionallymore common ○ mutations rates can evolve-pops close to fitness optimum have more to lose than gain from high mutation rates pops poor fit to envir have fewer deleterious mutations so can benefit from higher rate rna virus has highest mutation rate bc no proofreading fx □ WT kills mice at higher rate- rna viruses like high mutation rate □ inc fidelity of polio polymerasedecreases its fitness ○ mutation not rapid mech of evol… if beneficial selectionwill drive them to fixation migration: maintains genetic variation by preventing extinction of alleles that are currently being selected against ..mech of gene flow ○ anything that movesalleles from one pop to another(inc human activities) ○ dispersal of juvenile animals ○ transport pollen/seeds …acts as homogenizing evol process- most imp process in preventing pops from diverging ○ …acts as homogenizing evol process- most imp process in preventing pops from diverging will homogenize allele freq unless its balanced by another mech of evol ex) red bladder campion: continually emerging..1st to colonize new islands □ collected samples on islands and looked at genotypic diversity □ predictions: new islands more variability in genotypes intermediatepops morehomologousfrom gene flow btwn islands old pops no longer exchanging genes should inc in variability □ FST- measure of genetic diversity variation among pops □ predictions supported ex) one island model- large source of migrants to island from mainland □ assume island has AA indivs, mainland aa migrating indivs from mainland cause change in allele freqs fewer heteros than expected over time… would homogenizeto look like mainland ○ gene flow events maintain variability in pops even w genetic drift ○ gene flow from mainland helps inc variability, dec gene flow contributes to pop decline ○ ex) water snake color pattern from single allele if gene flow btwn mainland island high, expect freq on island to match mainland banded alleles favored on mainland, unbanded favored on island □ unbanded fitness= 1, banded is 0.7-0.8 □ migrants less fit but keep migrating onto island so maintains variance □ slows rate of divergence/adaptationof island pop.. if gene flow stopped all snakes on island would be unbanded genetic drift- diff reprod success by chance ○ ns deterministic,but genetic drift random ○ in pop of finite size, sampling error in drawing gametes can lead to evolution ○ ex) A & a have freq .6 & .4… randomly sample most "likely" outcomeis same freq, but only 18% chance of that. so overall prob is that freq will be higher or lower based on sampling error ○ extent to which drift influences pop is det by pop size ○ effect of sampling error dec as pop size inc ○ founder effect- when pop found by small # indivs, likely chance alone will cause allele freq in new pop to be diff than source pop ex) colonize new plant on mars- avoid founder effect, make sure have diverse pop to start pop ○ consequences of drift: flux in allele freq from gen to gen, causes each pop to be on own random trajectory more pronounced in small pops can cause substantial change in allele freq even in large pops if given enough time □ ex) beetles- diff coat color set up 12 indiv pops (50 w 50 or 5 w 5) larger pop much less variable than smaller one b allele is favored more, b allele change is about the same in small and large pop process from intx of mutation, selection,and drift: □ deleterious alleles emergeand are eliminated by NS(fitness<1) □ neutral alleles emerge and are fixed or lost due to drift (fitness=1) □ advantageous alleles appear and are usually swept to fixation by selection(fitness>1),but coul due lost due to genetic drift selection acts on phenotypes, not genotypes ○ rate of evol by drift mutation results in creation of new alleles substitution- fixation of new allele on pop(not dependent on pop size) □ when drift is only force at work, sub rate=mutationrate regardless of pop size eventually allele either fixed to freq=1 or lost freq=0 in pop eventually allele either fixed to freq=1 or lost freq=0 in pop v per locus per generation neutral mutationrate □ neutral mutation subset that can occur determined by drift alone □ ex) diploid pop w N indivs 2N alleles at locus of interest v is rate of neutral mutations every gen there will be 2Nv alleles due to mutation chance of allele fixing soley from drift=everyother allele in pop so 1/2N # new alleles destined to drift to fixation each gen is 2Nv x 1/2N=v(mutationrate) rate new mut arise prob new allele being fixed ◊ prob of fixation of allele is equal to freq in pop ◊ rate at which neutral alleles fix from drift = rate of arising ◊ alleles drift towards fixation ot loss hetero decreases □ effectivepop size- number that contribute to next gen conservationbio w endangered species characteristics of ideal pop: ◊ equal number male female ◊ random mating ◊ number breeding indivs= sub & fixation of neutral alleles □ larger pop has slower fixation rate…. rate directly related to pop size □ rate of which neutral mut fixed in pop=mut rate sub rate indep of pop size prob any given allele will drift to fixation is influenced by pop ◊ larger pops take longer prob any allele makes it is high(=1), but specific allele making it is low slower rate any 1 allele will becomefixed measure rate of heterozygosity(H ig hetero rate for this gen) – H =g+1 (g-[0.5/2N]) ◊ smaller pop, lower neutral mutation fixation rate but higher prob of any single allele making it prob drifting to fixation=initial freq study of molecular evol from mid 1960s- discoveriesconflict w evol theory at time(NS primary mech of ev) 2 main concepts: rates of mol change were high and constant □ beneficial mut rare, so high # fixed mut is problem □ NS expected to be episodic and correlated w envir change, so clocklike fashion of fixed mutations was confusing …mol change is conservative& constant Neutral theory- neutral muts that rise to fixation by drift outnumber beneficial muts fixed by NS □ drift is mech for mostmolecular evol □ assumptions: pop size not a factor (bc sub rate=mut rate) sequence evol by NS is so rare that it is insignificant □ conservativenature- less locus affects phenotype, more commonvariation and sub pseudogenes evolve faster than coding regions pop size not a factor (bc sub rate=mut rate) sequence evol by NS is so rare that it is insignificant □ conservativenature- less locus affects phenotype, more commonvariation and sub pseudogenes evolve faster than coding regions ◊ when muts fix in pseudogenes it is from drift & data suggests they accumulate more muts than other loci in nuclear genomes synonymoussites(mutsthat don’t change AA coded for) evolve faster than nonsyn sites ◊ syn usually have muted effect(higher rate & more constant) ◊ nonsyn much more likely to have more of a fitness effect bc NS acts on them …tells us most mutations are deleterious & are eliminated by purifying selection the more fx important a loci is, the larger the fraction of possible mutationsthat will be deleterious(lesswill be neutral) ◊ ex) hemoglobin- cant really get good mutations,much more negative muts ◊ only see neutral variation where purifying selection not weeding it out □ graph: mol divergence x- time y- diff in sequences (at nucleotides or loci) constancy of rate of mol change- each line reps steady constant accumulationof changes over time clocklike/constantnature confirmed on graph by them falling along line as time goes by neutral theory today: not all mol variation is neutral not all evol is driven by selection neutral theory as null model:if considering pseudogene □ ratio of nonsyn and syn mut should be 1 □ so under purely neutral evol dN/dS=1 when purifying(neg) selection elim deleterious nonsyn changes, ratio is less than one " positive selection pushing beneficial nonsyn changes to evol, ratio greater than 1 ex) BRCA1 gene- programmedcell death during neural devel □ human/chips have 3.1 and 2.6 ratio, indicates allele is under pos selection □ other orgs under neg selection mol clock hypoth- telling time since divergence by rate of accumulating netral subs branch lengths=amt of change in nucleotide subs, from nodes to tips time since divergence at one node is known from fossil record cautions when using mol clock: □ loci must be evolving in clocklikefashion □ species differ in ticking rates from diff in gen time/metrates which can affect accum of muts □ bottleneckselim genetic div, causing nucleotide subs that occurred to be missed contributions: □ favor neutrally evolving mol loci for recontruction of phylo relationships □ useful estimatesof when phylo divergences occurred whwen have no fossil records non random mating- indirect mech of ev ex) snails self fertilize (inbreeding) inc in relative of heteros causes genotype change but not allele freq inbreeding depression- results from exposure of deleteriousrecessive alleles to selection □ ex) AA- healthy(2 fx alleles) Aa- healthy (1 fx) aa- diseased (no fx alleles) inbreeding coeff(F)- how inbred an offspring would be □ multiply probs of same gene coming together in offspring □ mother and father off offspring have same mom □ inbreeding coeff is fitness of self-fertilized & outcrossedprogeny □ more inbred=morerecessive deleterious alleles exposed to selection □ mother and father off offspring have same mom □ inbreeding coeff is fitness of self-fertilized & outcrossedprogeny □ more inbred=morerecessive deleterious alleles exposed to selection
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