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Lecture 13

# Notes Lecture 13.odt

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School
McGill University
Department
Biology (Sci)
Course
BIOL 202
Professor
Daniel Schoen
Semester
Winter

Description
Population genetics, part 2 (central part of population genetics==>Hardy Weinberg) • the effect of random mating alone on population genetic variation : Hardy Weinberg theory • applications of HW theory • Non-Random mating (inbreeding)? • Factos influencing allele frequencies (mutation and migration) • Factors influencing allele frequencies (genetic drift) How do we know the frequency of carriers of a rare recessive disease? (ex: cystic fibrosis) about 1/25 people are carriers for this mutation Another place where H&W have something to say: Not uncommon to find places that restrict people to give birth (forced sterilization). In the south, there was forced sterilization of appalachians. The idead that you can clean up the gene pool by not allowing recessive mutations to mate to eventually kill off that genetic line. This is more common in small populations. Ex: Retinitis pigmentosa=100x more common on the island of tristan de Cuhna, than in the general population of North america (Canada and the US) H&W asked: What happens to allele/gene frequencies in the absence of evolutionary forces? H&W principle: The constancy of allele frequencies when there are no acting evolutionary forces (Gen t= Gen t+1, same diploid genotypes as the parents) AFTER ONE GENERATION OF RANDOM MATING IN THEABSENCE OF THE EVOLUTIONARY FORCES, THE FREQUENCIES OF GENOTYPES ATADIALLELIC LOCUS WIL BE: f(A/A)=p^2 f(A/a)=2pq f(a/a)=q^2 easy to see using a punnets square AND FROM THEN ON, THESE FREQUENCIES WILL REMAIN UNCHANGED (provided there is continued random mating and the absence of evolutionary forces) *note:see the example on slides We dont choose our mates based on the basis of what carriers they are, so our frequencies are close to HW CF, caused by a recessive mutation. How can we dtmn frequency of carriers of CF in the population (about1/25 of the population are carriers, we knew this for a long time this carrier ratio, by applying HW) we knew the population of diseased in a population (q^2= 0.0004). so q=0.02. And p=1-0.02= 0.98. carriers=2pq=2(0.02)(0.28)=.392 which is ~1/25 If you take the possibility, and divide it by 4, you can predict the possibility of the offspring obtaining the disease from a carrier and a potential carrier. H&W theory (in eugenics**): When alleles are rare, they occur much more often in heterozygotes than in homozygotes (the graph is expected when looking at HW ratios) Take home message from the graph: when you have a rare condition, most of the rare alleles are in carriers, not in actually affected individuals H&W genotype frequencies are expected only when: 1)mating is random 2)no evolutionary forces are acting evolution requires variation. How does non random mating influence genotype frequencies? What about inbreeding (a form of non-random mating)? Kinds of throws things out of whack modification of HW: inbreeding due to cosanguinous (inbreeding) mating The textbook goes into quite a lot of detail on how to calculate the inbreeding coefficient, we don't have to know how to calculate the inbreeding coefficient from pedigrees.WE DO HAVE TO KNOW WHAT AN INBREEDING COEFFCIENT IS THOUGH F=inbreeding coefficient (0homozygotes are more common in inbreeding populations wild turkeys can self fertilize?s System of mating F Self-fertilization(most mammals can't do this, plants can) 1 Parent-offspring 1/2 Brother-Sister (some wasps do this) 1/4 First Cousins 1/16 2nd Cousins 1/64 imagine populations that have different systems of mating Smaller the population, larger the inbreeding coefficient (we create a lot of small populations by sectioning them geographicall. We are eroding genetic fitness of these populat
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