Transcript ppt
Lecture 25 : Tests of Neutrality April 14, 2014 Last Time Human origins Out of Africa hypothesis Neanderthal and Denisovan genomes Introgression into humans Signatures of selection Today Sequence data and quantification of variation Infinite sites model Nucleotide diversity (π) Sequence-based tests of neutrality Ewens-Watterson Test Tajima’s D Hudson-Kreitman-Aguade Synonymous versus Nonsynonymous substitutions McDonald-Kreitman The main power of neutral theory is it provides a theoretical expectation for genetic variation in the absence of selection. Equilibrium Heterozygosity under IAM 4N em q He = = 4N em +1 q +1 Frequencies of individual alleles are constantly changing Balance between loss and gain is maintained 4Neμ>>1: mutation predominates, new mutants persist, H is high 4Neμ<<1: drift dominates: new mutants quickly eliminated, H is low Effects of Population Size on Expected Heterozgyosity Under Infinite Alleles Model (μ=10-5) Rapid approach to equilibrium in small populations Higher heterozygosity with less drift Fate of Alleles in Mutation-Drift Balance Generations from birth to fixation Time between fixation events Time to fixation of a new mutation is much longer than time to loss Fate of Alleles in Mutation-Drift-Selection Balance Purifying Selection Which case will have the most alleles onHighest averageHat E?any given What will this depend upon? time? Neutrality Balancing Selection/Overdominance Assume you take a sample of 100 alleles from a large (but finite) population in mutation-drift equilibrium. What is the expected distribution of allele frequencies in your sample under neutrality and the Infinite Alleles Model? Number of Alleles A. B. C. 10 8 6 4 2 2 4 6 8 10 2 4 6 8 10 Number of Observations of Allele 2 4 6 8 10 Allele Frequency Distributions Black: Predicted from Neutral Theory White: Observed (hypothetical) Neutral theory allows a prediction of frequency distribution of alleles through process of birth and demise of alleles through time Comparison of observed to expected distribution provides evidence of departure from Infinite Alleles model Depends on f, effective population size, and mutation rate Hartl and Clark 2007 Ewens Sampling Formula 4 Ne Population mutation rate: index of variability of population: i Probability the i-th sampled allele is new given i alleles already sampled: Probability of sampling a new allele on the first sample: 0 Probability of observing a new allele after sampling one allele: . 1 1 Probability of sampling a new allele on the third and fourth samples: Expected number of different alleles (k) in a sample of 2N alleles is: E (k ) 2 N 1 i 1 i 0 1 2 ... 2N 1 Example: Expected number of alleles in a sample of 4: E (k ) 2 N 1 i i 0 3 i 0 i 1 1 2 3 He 2 3 Ewens Sampling Formula E ( n) 2 N 1 i i 0 1 1 2 ... 2N 1 where E(n) is the expected number of different alleles in a sample of N diploid individuals, and = 4Ne. 1 1 fe 4Ne 1 1 Predicts number of different alleles that should be observed in a given sample size if neutrality prevails under Infinite Alleles Model Small , E(n) approaches 1 Large , E(n) approaches 2N can be predicted from number of observed alleles for given sample size Can also predict expected homozygosity (fe) under this model Ewens-Watterson Test Compares expected homozygosity under the neutral model to expected homozygosity under Hardy-Weinberg equilibrium using observed allele frequencies Comparison of allele frequency distributions fe comes from infinite allele model simulations and can be found in tables for given sample sizes and observed allele numbers f HW p 2 i Ewens-Watterson Test Example Drosophila pseudobscura collected from winery Xanthine dehydrogenase alleles 15 alleles observed in 89 chromosomes fHW = 0.366 Hartl and Clark 2007 fe Generated fe by simulation: mean 0.168 How would you interpret this result? Expected Homozygosity fe Most Loci Look Neutral According to EwensWatterson Test Hartl and Clark 2007 DNA Sequence Polymorphisms DNA sequence is ultimate view of standing genetic variation: no hidden alleles Is this really true? What about back mutation? Signatures of past evolution are contained in DNA sequence Neutral theory presents null model Departures due to: Selection Demographic events - Bottlenecks, founder effects - Population admixture Sequence Alignment Necessary first step for comparing sequences within and between species Many different algorithms Tradeoff of speed and accuracy Quantifying Divergence of Sequences Nucleotide diversity (π) is average number of pairwise differences between sequences where N pi p j ij N 1 ij N is number of sequences in sample, pi and pj are frequency of sequences i and j in the sample, and πij is the proportion of sites that differ between sequences i and j Sample Calculation of π 5 10 15 20 25 30 35 A B C A->B, 1 difference A->C, 1 difference B->C, 2 differences N pi p j ij N 1 ij 3 (0.33)(0.33)(1 / 35) (0.33)(0.33)(1 / 35) (0.33)(0.33)(2 / 35) 2 0.01867 On average, there are 18.67 polymorphisms per kb between pairs of haplotypes in the population Tajima’s D Statistic Infinite Sites Model: each new mutation affects a new site in a sequence E ( ) m m where m is length of sequence, and 4 Ne Expected number of polymorphic sites in all sequences: E(S ) a1 S 1 S S a1 a1 i 1 i n 1 where n is number of different sequences compared Sample Calculation of S 5 10 15 20 25 30 A B C Two polymorphic sites S=2 n 1 1 1 1 a1 1.5 1 2 i 1 i S 2 S 1.33 a1 1.5 0.01867 m (0.01867)(35) 0.65 35 Tajima’s D Statistic Two different ways of estimating same parameter: S m S a1 Deviation of these two indicates deviation from neutral expectations d S d D V (d ) where V(d) is variance of d Tajima’s D Expectations D=0: Neutrality D>0 d S Balancing Selection: Divergence of alleles (π) increases OR Bottleneck: S decreases D<0 Purifying or Positive Selection: Divergence of alleles decreases OR Population expansion: Many low frequency alleles cause low average divergence Balancing Selection Balancing selection ‘balanced’ mutation Neutral mutation d S Slide adapted from Yoav Gilad Should increase nucleotide diversity () Decreases polymorphic sites (S) initially. D>0 Recent Bottleneck d S Rare alleles are lost Polymorphic sites (S) more severely affected than nucleotide nucleotide diversity () D>0 Standard neutral model Positive Selection and Purifying Selection sweep S Advantageous mutation Neutral mutation d S Slide adapted from Yoav Gilad recovery s s Time Should decrease both nucleotide diversity () and polymorphic sites (S) initially. S recovers due to mutation recovers slowly: insensitive to rare alleles D<0 Rapid Population Growth will also result in an excess of rare alleles even for neutral loci Rapid population size increase Time Standard neutral model Often two main haplotypes, some rare alleles Slide adapted from Yoav Gilad Most alleles are rare 4 Ne Most alleles are rare Nucleotide diversity () depressed Polymorphic sites (S) unchanged or even enhanced : 4Neμ is large D<0 d S How do we distinguish these two forms of divergence (selection vs demography)? Hudson-Kreitman-Aguade Test Divergence between species should be of same magnitude as variation within species Provides a correction factor for mutation rates at different sites Complex goodness of fit test Perform test for loci under selection and supposedly neutral loci Hudson-Kreitman-Aguade (HKA) test Neutral Locus Polymorphism Divergence 8 3 20 8 Polymorphism: Variation within species Divergence: Variation between species Slide adapted from Yoav Gilad Test Locus A 8/20 ≈ 3/8 Hudson-Kreitman-Aguade (HKA) test Neutral Locus Polymorphism Divergence Test Locus B 8 3 20 19 8/20 >> 3/19 Conclusion: polymorphism lower than expected in Test Locus B: Selective sweep? Slide adapted from Yoav Gilad http://www.nsf.gov/news/mmg/media/images/corn-and-teosinte_h1.jpg Teosinte Maize Maize w/TBR mutation http://www.nsf.gov/news/mmg/media/images/corn-and-teosinte_h1.jpg Mauricio 2001; Nature Reviews Genetics 2, 376 HKA Example: Teosinte Branched Lab exercise: test Teosinte-Branched Gene for signature of purifying selection in maize compared to Teosinte relative Compare to patterns of polymorphism and diversity in Alchohol Dehydrogenase gene