Transcript Chapter 5
Chapter 5 Mendelian Selection in Populations: Selection and Mutation Population Genetics Integrates Darwin’s theory of evolution by natural selection with Mendelian genetics Changes in relative abundance of traits in a population can be tied to changes in relative abundance of alleles that influence them Case Studies CCR5-D32 Eugenics sterilization Cystic fibrosis Population Genetics CCR5-D32 allele Confers resistance to HIV-1 infection Buck vs. Bell U.S. Supreme Court upheld states’ mandatory sterilization laws for feebleminded people – Eugenics movement to remove feeblemindedness gene from population Cystic fibrosis Genetic disease that affects Caucasians Autosomal recessive Causes chronic infections of Pseudomonas aeruginosa – Severe lung damage Hardy-Weinberg Equilibrium Principle Must understand how alleles behave in populations to understand case studies Develop a null model for behavior of genes in populations Model specifies what will happen to frequencies of alleles and genotypes Applies to all diploid sexual organisms Hardy-Weinberg Equilibrium Principle Population = group of interbreeding individuals and their offspring Life Cycle Adults produce gametes Gametes combine to make zygotes Zygotes grow up to become next generation of adults Track fate of Mendelian genes across generations in a population Find out if particular alleles become more or less common over time Hardy-Weinberg Equilibrium Principle Imagine that mice have a particular locus A with two alleles: A and a Could also call them A1 and A2 or A and B All equivalent Track these alleles and follow them through one complete turn of the cycle to see if frequencies change Hardy-Weinberg Equilibrium Principle A numerical example Assume adults choose their mates at random – Matings are random within the gene pool Diploid organisms, so each has two alleles for A locus Meiosis caused one allele to be in each gamete for the A locus Hardy-Weinberg Hardy-Weinberg Equilibrium Principle A numerical example Imagine 60% of eggs and sperm received allele A and 40% received allele a Frequency of A allele in gene pool is 0.6, of a allele is 0.4 When egg and sperm meet, what proportion of genotypes will be AA? 60% egg will be A, 60% sperm will be A – 0.6 X 0.6 = 0.36 – 36% of zygotes will have genotype AA Hardy-Weinberg Equilibrium Principle A numerical example How many would be aa? – 0.4 X 0.4 = 0.16 How many would be Aa? – 0.6 X 0.4 X 2 = 0.48 Notice that 0.36 + 0.48 + 0.16 = 1 – All possible genotype frequencies will add up to one Hardy-Weinberg Hardy-Weinberg Equilibrium Principle If zygotes grow up, what will the frequency of A in the next generation be? AA is 36% – All gametes carry A Aa is 48% – Half will carry A, half will carry a aa is 16% – All gametes carry a Frequency of A in next generation will be: – 0.36 + (1/2)0.48 = 0.6 Frequency of a will be: – 0.16 + (1/2)0.48 = 0.4 Hardy-Weinberg Equilibrium Principle A numerical example 0.6 + 0.4 = 1 Allele frequencies are the same as in the first generation Allele frequencies are in equilibrium The population does not evolve If a population is in Hardy-Weinberg Equilibrium it will NEVER EVOLVE!!! – Regardless of starting frequencies Hardy-Weinberg Equilibrium Principle The General Case Imaginary population Single locus with A and B as the alleles Three possible diploid genotypes – AA, AB, BB Frequency of allele A is called p Frequency of allele B is called q p+q=1 Hardy-Weinberg Equilibrium Principle The General Case Let gametes make zygotes Four combinations – A + A = AA – A + B = AB – B + A = BA – B + B = BB p X p = p2 p X q = pq q X p = qp q X q = q2 p2 + 2pq + q2 = 1 – Genotype frequencies in Hardy-Weinberg Equilibrium General case General Case General case p2 + 2pq + q2 = 1 Next generation (zygotes grow and reproduce) What is the Allele freq of A? p2 + (½)2pq = p2 + pq Subst. (1-p) for q =p Hardy-Weinberg Equilibrium Principle Two fundamental conclusions Conclusion 1: the allele frequencies in a population will not change, generation after generation Conclusion 2: if the allele frequencies in a population are given by p and q, the genotype frequencies will be given by p2, 2pq, and q2 Hardy-Weinberg Equilibrium Principle Why do we use Hardy-Weinberg Equilibrium Principle? Shows evolution does not happen (Huh?) Gives specific set of testable assumptions If an assumption is violated, the Conclusions do not hold It is a null model that we can use to test for evidence of evolution occurring!!! Hardy-Weinberg Equilibrium Principle Assumptions of Hardy-Weinberg There is no selection – All members contribute equally to gene pool There is no mutation – No new alleles are created There is no migration – All alleles stay in gene pool There is a large population size – No random events = genetic drift Panmixia – Mates are chosen randomly How we can violate H-W shows us how evolution can occur! Hardy-Weinberg Equilibrium Principle By having explicit assumptions, the violations of assumptions can be known to determine which forces are causing disequilibrium = evolution Example with CCR5-D32 Everyone survives equally No new D32 mutations arise No one moves between populations Populations are infinitely large People choose mates at random We can test for Hardy-Weinberg to see which assumptions are broken to understand cause of evolution and future of the D32 allele Selection Individuals with particular phenotypes survive to reproduce more than others Differential reproductive success Phenotypes must be heritable Can selection change the frequencies of alleles in the gene pool from one generation to the next? Can violation of the no-selection assumption violate Conclusion 1 of Hardy-Weinberg Equilibrium? The Hardy-Weinberg principle Given certain assumptions, whatever the initial genotype frequencies for two autosomal alleles may be, after one generation of random mating, the genotype frequencies will be p2:2pq:q2, and both these genotype frequencies and the allele frequencies will remain constant in succeeding generations. This means, as soon as Evolution stops occurring, the population will go back into H-W equilibrium within 1 generation! The Math N = total number of individuals n1 = number of A1A1 individuals n2 = number of A1A2 individuals n3 = number of A2A2 individuals p = frequency of the first allele q = frequency of the second allele The Math p = frequency of the first allele q = frequency of the second allele n2 (n1 ) 2 p N n2 (n3 ) 2 q N p + q = 1 always in a two allele system The Basic Symbols and their Meaning x = f(A1A1) = n1 / N y = f(A1A2) = n2 / N z = f(A2A2) = n3 / N p = x + ½ y q = z + ½ y Back door method: q = √q2 = √z Only works if the population is in H-W equilibrium Why is it so? p + q = 1 (p + q)2 = 12 p2 + 2pq + q2 = 1 f(A) f(a) f(A) f(a) f(AA) = f(A) x f(A) f(aA) = f(a) x f(A) f(Aa) = f(A) x f(a) f(aa) = f(a) x f(a) • p2 = f(AA) • pq + pq = 2pq = f(Aa) • q2 = f(aa) Three alleles p = f(A1) q = f(A2) r = f(A3) p + q + r = 1 (p + q + r)2 = 12 p2 +2pq + q2 + 2pr + 2qr + r2 = 1 f(A1A1) + f(A1A2) + f(A2A2) + f(A1A3) + f(A2A3) + f(A3A3) = 1 What’s it good for? Predicting genotype frequencies given allele frequencies Genotypes will approximate a binomial distribution – (p + q)2 = 1 – after 1 generation of random mating. If we know the allele frequencies in generation 1, we can predict the genotype frequencies in generation 2. Allele and genotype frequencies will not change as long as the assumptions are met. For example: Generation 1: f(AA) = 0.2, f(Aa) = 0.8, f(aa) = 0.0 What are the genotype frequencies in generation 2? First, find p and q: p = x + ½ y = 0.2 + (0.8 / 2) = 0.6 q = z + ½ y = 0.0 + (0.8 / 2) = 0.4 Generation 2: F(AA) = p2 = 0.36 F(Aa) = 2pq = 0.48 F(aa) = q2 = 0.16 Another example: Generation 1: f(AA) = 0.5, f(Aa) = 0.2, f(aa) = 0.3 What are the genotype frequencies in generation 2? First, find p and q: p = x + ½ y = 0.5 + (0.2 / 2) = 0.6 q = z + ½ y = 0.3 + (0.2 / 2) = 0.4 Generation 2: F(AA) = p2 = 0.36 F(Aa) = 2pq = 0.48 F(aa) = q2 = 0.16 Did you notice? We started with different genotype frequencies in each example, but the same allele frequencies (p & q). We ended (generation 2) with the same genotype frequencies in both examples. If all of the assumptions are met, what will be the genotype frequencies in generation 10? What else is it good for? Null hypothesis: H0: the population is in H-W equilibrium Ha: the population is not in H-W equilibrium Use a χ2 test to determine if the population is significantly different from H-W expectations If it is, one (or more) of the assumptions must be violated! Assumptions of H-W Equilibrium 1. 2. 3. 4. 5. 6. Random mating – panmixia Infinitely large population No gene flow – genes are not added from outside the population No mutation – genes do not change from one allelic state to another No natural selection – all individuals have equal probabilities of survival and reproduction Discrete generations – offspring do not mate with previous generations What happens if the assumptions are violated? Evolution! Evolution (in terms of H-W) is change in allele frequency over time. Allele frequencies do not change in a population in H-W equilibrium, therefore: A population in H-W equilibrium is not evolving. Violations of H-W assumptions Violations due to sampling error Drift Inbreeding Systematic changes Mutation Selection Gene flow / migration Violations of H-W assumptions Factors that increase variation Mutation Gene flow Factors that decrease variation Selection Drift Inbreeding Selection Example with mice B locus affects probability of survival Frequency of B1 = 0.6 Frequency of B2 = 0.4 After random mating, genotype frequencies are 0.36, 0.48, and 0.16 Will use a population of 1000 individuals – B1B1 = 360 individuals – B1B2 = 480 – B2B2 = 160 Selection Example with mice Incorporate selection All B1B1 individuals survive 75% B1B2 individuals survive 50% B2B2 individuals survive Now 800 adults left – 360 B1B1 (360) – 360 B1B2 (480) – 80 B2B2 (160) Selection Example with mice Frequencies of genotypes are: – B1B1 360/800 = 0.45 – B1B2 360/800 = 0.45 – B2B2 80/800 = 0.1 When they produce gametes – B1 = 0.45 + (1/2)0.45 = 0.675 – B2 = (1/2)0.45 + 0.1 = 0.325 – Allele frequencies Frequency of B1 rose by 7.5% Frequency of B2 fell by 7.5% Selection Population evolved in response to selection Rarely is selection so strong Usually requires many generations to change allele frequencies much Selection Empirical example with Drosophila Cavener and Clegg Two alleles for alcohol dehydrogenase locus – AdhF and AdhS – Break down alcohol at different rates Maintained two populations of flies spiked with alcohol and two controls without alcohol At each generation took random sample of flies and determined their genotypes Selection Empirical example with Drosophila Control populations appeared to be in HardyWeinberg Equilibrium – Allele frequencies did not change Populations under selection pressure (alcohol) showed a decline in AdhS allele Hardy-Weinberg Conclusion 1 did not hold in experimental populations The populations evolved because of selection for better ability to break down alcohol Selection How does selection affect Conclusion 2? Can we still calculate genotype frequencies by multiplying allele frequencies Sometimes Conclusion 2 is violated Allele frequencies do not change but genotype frequencies cannot be calculated by HardyWeinberg equation Can use Chi Square test to determine if genotype frequencies vary significantly from Conclusion 2’s expectations Selection CCR5-D32 Will the frequency of the allele increase in response to HIV epidemic? Three potential models – Model 1 Frequency of allele 20% 1/4 of people with genotype +/+ or +/D32 die before reproducing All D32/D32 individuals survive After 40 generations (1000 years) the D32 allele is nearly 100% Selection CCR5-D32 Model 2 – Frequency of allele 20% – HIV infection rate less than 1% – All D32/D32 individuals survive – After 40 generations (1000 years) the D32 allele is still at 20% – Selection is too weak to cause a large change in allele frequencies Selection CCR5-D32 Model 3 – Frequency of allele 1% – 1/4 of people with genotype +/+ or +/D32 die before reproducing – All D32/D32 individuals survive – After 40 generations (1000 years) the D32 allele is still at 1% – Most copies of D32 would be heterozygotes and hidden from selection Patterns of Selection Dominant and Recessive alleles (Directional selection) Flour beetles with l locus Two alleles: + and l – Individuals with genotype +/+ or +/l are normal – Individuals with genotype l/l do not survive Recessive lethal allele Dawson started colonies with heterozygotes – Allele frequencies 0.5 for each Patterns of Selection Flour beetles with l locus Because l/l have lower fitness, expect population to evolve to lower l frequencies Measured allele frequency over 12 generations Frequency of l allele dropped to 0.25 but was not eliminated Dominance and allele frequency interact – If recessive is common, evolution is rapid – When recessive is rare, evolution is very slow – When rare, recessive allele is usually hidden from selection Patterns of Selection Selection coefficient w = fitness of an allele s = strength of selection on an allele w++, w+l, wll – w++ = 1, w+l = 1, wll = 1 + s – s gives strength of selection on homozygous recessive phenotype Positive s is selection in favor of allele Negative s is selection against allele Patterns of Selection Selection coefficient Selection on dominant allele w++ = 1 + s, w+l = 1 + s, wll = 1 – Positive s is selection in favor of allele – Negative s is selection against allele Adaptive landscapes of fitness Patterns of Selection Selection on heterozygotes and homozygotes (Balancing selection) When one allele is dominant and one is recessive, heterozygote fitness is equal to that of one kind of homozygote Other scenarios possible Often fitness is intermediate to two homozygotes – Changes rate of evolution – Eventually one allele may become fixed and the other lost Patterns of Selection Sometimes fitness of heterozygote is superior or inferior to either homozygote Different evolutionary outcomes produced Example with Drosophila melanogaster Single locus – Homozygotes for one allele viable – Homozygotes for other allele not viable Used heterozygotes to start two populations – Initial allele frequencies 0.5 each Frequency of viable allele increased rapidly at first Rate slowed and viable allele reached equilibrium at 0.79 Patterns of Selection Example with Drosophila melanogaster Started new populations with viable allele at 0.975 Frequency of viable allele dropped to 0.79 Patterns of Selection Example with Drosophila melanogaster How did selection maintain a lethal allele at 0.21? Heterozygote superiority = overdominance Heterozygotes have higher fitness than either homozygote Overdominance maintains genetic diversity Patterns of Selection Second example with Drosophila Heterozygotes may have lower fitness than either homozygote Fruit flies with compound chromosomes – Homologous chromosomes that have swapped entire arms – During meiosis, compound chromosomes may not segregate – Four types of gametes can be produced Both homologous chromosomes Just one member of pair Just other member of pair Neither member of pair Patterns of Selection Second example with Drosophila When two compounds mate, 1/4 of zygotes have correct chromosome dose and are viable – Other 3/4 have too many or too few pieces and are not viable When compound flies mate with normal flies, no zygotes are viable Patterns of Selection Second example with Drosophila Established populations with some founders with compound chromosomes, C(2), and some with compound chromosomes, C(3) – Treat chromosomes as alleles – C(2)C(2) and C(3)C(3) genotypes Fitnesses of mixed populations – wC(2)C(2) = 0.25 – wC(2)C(3) = 0 – wC(3)C(3) = 0.25 Genotypes exhibit underdominance Patterns of Selection Algebraic treatment predicts that genetic equilibrium will be achieved if both allele are at 0.5. The equilibrium is unstable if either allele freq. goes above or below 0.5 It will quickly rise to 1 if above 0.5 and go to 0 if below 0.5 Patterns of Selection Patterns of Selection Second example with Drosophila Established populations with some founders with compound chromosomes, C(2), and some with normal chromosomes, N(2) – Treat chromosomes as alleles – C(2)C(2) and N(2)N(2) genotypes Fitnesses of mixed populations – wC(2)C(2) = 0.25 – wC(2)N(2) = 0 – wN(2)N(2) = 1 Genotypes exhibit underdominance Patterns of Selection Second example with Drosophila Set up mixed 13 populations with initial C(2) frequencies ranging from 0.71 to 0.96 Populations with higher initial C(2) frequency, C(2) rose to fixation Populations with lower C(2) frequency, C(2) was lost Unstable equilibrium reached at 0.9 C(2) Heterozygote inferiority reduces genetic diversity within populations by pushing alleles to fixation It can help to maintain genetic diversity among populations Frequency-Dependent Selection So far we have assumed selection is constant over time Direction of selection may fluctuate One allele favored and then the other Elderflower orchids Persist in two colors, yellow and purple Flowers attract bumble bees but they get no reward Alternate between colors Frequency-Dependent Selection Bee visits one color 1st, no reward, alternates to other color, no reward. This keeps going until the bee leaves Bees tend to visit equal numbers of flowers Thus, more rare color is visited more often per plant Frequency-Dependent Selection If pollinator visits equal reproductive success, then rare-color has advantage Selection by bees favors yellow until it becomes too common, then switch to purple. Frequency-Dependent Selection Experiment, 10 experimental arrays of 50 plants each Freq. of yellow flowers varied among arrays with 2 arrays at 0.1,0.3,0.5,0.7 and 0.9 Monitored orchids for removal of pollinaria, deposition of pollinaria and fruit set Frequency-Dependent Selection Freq of yellow morph Frequency-Dependent Selection Fitnesses change each generation with freq. of allele (yellow flower) Move toward equilibrium freq. Frequency-Dependant selection can maintain genetic diversity Compulsory Sterilization Evolutionary consequences of eugenics sterilization Reduce fitness of feeblemindedness genotype to zero to reduce frequency of alleles responsible for feeblemindedness Defined as: “One who is capable of earning his living under favorable circumstances, but is incapable from mental defect existing from birth or from an early age. . .” Feeblemindedness thought to behave as a simple Mendelian recessive trait Compulsory Sterilization Remember that recessive genetic diseases are not easily eliminated from populations Rare recessives decline slowly Scientists thought feeblemindedness was very common and increasing At least 1% of population: ff If q is frequency of recessive allele f: q = √0.01 = 0.1 wff = 0 if all are sterilized Over 250 generations frequency declines from 0.01 to 0.0025 Compulsory Sterilization Is this decrease good? Most copies of allele are in heterozygotes and hidden from selection Compulsory Sterilization Problems with the practice Feeblemindedness is not a recessive allele Caused by many heritable and nonheritable factors People were classified based on hearsay Eugenics movement not based on sound population genetics understanding Mutation How do deleterious alleles like cystic fibrosis remain at high frequencies in population? Heterozygote superiority? Introduced anew by mutation? Mutation introduces new alleles into a population How effective is mutation as a force of evolution? Can mutation violate Conclusions of HardyWeinberg Equilibrium Principle? Mutation Mutation alone is not a potent evolutionary force Model mice population Locus A Frequency of allele A = 0.9 Frequency of allele a = 0.1 a is recessive loss of function mutation Copies of A are converted to a at a rate of 1 copy per 10,000 generations – Very high mutation rate Mutation Model mice population Back mutations to A are negligible Assume all mutations happen in gametes in gene pool Adult genotype frequencies – – – – AA = 0.81 Aa = 0.18 aa = 0.01 In Hardy-Weinberg proportions Alleles in gametes are still 0.9 and 0.1 Mutation Model mice population Now 1 of 10,000 A alleles mutates to a New frequency of A (p) is old frequency minus fraction lost to mutation – p = 0.9 - (0.0001)(0.9) New frequency of a (q) is old frequency plus fraction gained by mutation – q = 0.1 + (0.0001)(0.9) When gametes make zygotes – AA = 0.80984 – Aa = 0.18014 – aa = 0.01002 Mutation Model mice population New allele and genotype frequencies are almost identical to old frequencies Mutation had virtually no effect Over many generations, mutation could change allele frequencies After 1000 generations, frequency of A would be 0.81 Mutation can cause evolution, but it is usually does so slowly Mutation and Selection Mutation alone cannot cause great changes in allele frequencies but it is still important in evolution In combination with selection, mutation can be a potent evolutionary force Lenski’s E. coli study Studied a strain incapable of conjugation Mutation is only form of genetic variation Grew 12 colonies in minimal salts medium Mutation and Selection Lenski’s E. coli study After growing billions of cells, they removed approximately 5 million cells from each and transferred them to new medium Daily transfers for 1500 days – 10,000 generations At intervals, researchers froze samples of transferred cells – Can freeze E. coli and revive it later Could directly measure differential fitness of descendant populations in competition at the same time Also monitored cell size Mutation and Selection Lenski’s E. coli study During study fitness and cell size increased in response to natural selection Fitness increases occurred in jumps Beneficial mutations swept through population to fixation Mutations caused bacteria to divide faster and increase in size Mutation is ultimate source of genetic variation Mutation-Selection Balance Most mutations are deleterious Selection eliminates these mutations Mutations are created anew When rate of deleterious alleles being eliminated by selection equals rate of creation by mutation: Mutation-Selection Balance Mutation-Selection Balance Deleterious recessive allele is at equilibrium when: ^ = /m q √ s m = mutation rate s = selection coefficient – Between 0 and 1 expressing strength of selection If selection is small and mutation is high, equilibrium frequency of allele will be high If selection is high and mutation is low, equilibrium frequency will be low Mutation-Selection Balance Is cystic fibrosis maintained by mutation-selection balance? Recessive loss-of-function allele on locus on chromosome 7 Cystic fibrosis transmembrane conductance regulator (CFTR) CFTR normally destroys Pseudomonas aeruginosa – Cause chronic lung infections Few affected people survive to reproductive age or are infertile Mutation-Selection Balance Cystic fibrosis Frequency q = 0.02 in people with European ancestry s=1 q = 0.02 Therefore, m = 4 X 10-4 Actual mutation rate is 6.7 X 10-7 Mutation rate is not causing high frequency of the recessive allele Mutation-Selection Balance Cystic fibrosis Researchers discovered that the high frequency is maintained by heterozygote superiority Heterozygotes were partially resistant to typhoid fever infection Cystic fibrosis maintained by mutation and heterozygote superiority Hardy-Weinberg Equilibrium Have examined how selection and mutation violate the Conclusions of the HardyWeinberg Equilibrium Principle Will next examine the other three forces: Migration Genetic Drift Nonrandom mating