A change across generations in the frequency of alleles

Why is it important to establish a null model for how gene frequencies (like the ▲32 CCR5 allele) should behave in populations?

We need to compare the behavior of the allele in the actual population to its behavior under normal conditions to see if evolution is taking place.

1

For a diploid species, how many gene copies does an adult have for any particular gene in question?

2

13AA, 28Aa, 9aa   270 carrying A, 230 carrying a; Allele frequencies: .54 A, .46 a

Did your simulated population in question 6 evolve?

Yes

Genetic Drift

.2916 AA, .4968 Aa, .2116 aa

1

1/8

That allele frequencies of 0.5 and 0.5 represented the only possible equilibrium state for a two-allele system.

P²

What is the frequency of the pq heterozygote in the next generation?

2pq

q

What are the two fundamental conclusions from the Hardy-Weinberg calculations?

1) The allele frequencies in a population will not change, generation after generation

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   

What are the 5 assumptions of the Hardy-Weinberg calculations?

1) There is no selection

2) There is no mutation

3) There is no migration

4) There are no chance events (population size is infinitely large)

5) Individuals choose their mates at random

None of the assumptions hold true        .  

Is it safe to assume that selection acts directly on the genotype?  Why or why not?

Only when the phenotypes fall into discrete classes that appear to be determined strictly by genotypes. Otherwise, most phenotypic traits are not determined strictly by genotype.

In populations, what amplifies even small changes in survivorship between genotypes (small selection differentials).

Selection continuing over generations

What is the ADH allele and how are alleles of this gene identified (by Cavener and Clegg)?  

ADH is an enzyme that breaks down ethanol. AdhF moves fast through a gel and AdhS moves slow through a gel. 

Cavener and Clegg took random populations of flies and spikes the food source of 2 and 2 were controls. After several generations, they determined ADH genotypes. Control had no frequency change of AdhF, experimental pops had a big and rapid frequency change of ADHF.          

Design a complementary experiment that might support the work of Cavener and Clegg on ADH in Drosophila.  

Cleanse the food source of the experimental group of ethanol (no rotting fruit).

Original: 13AA, 28Aa, 9aa   270 carrying A, 230 carrying a; Allele frequencies: .54 A, .46 a

6AA, 28Aa, 4aa; 200 carrying A, 180 carrying a; Allele Freq: .53 A, .47 a

A fatal neurological disorder known only from an epidemic that struck the Fore people. It is a spongiform encephalopathy caused by a prion protein which warps the forms of other proteins. Can get it by contamination or ingestion of infected tissue.

What gene can limit progression of Kuru in humans and how does this gene vary between the two dominant allele types, and which allele type confers disease resistance?

The PrP gene on Chromosome 20. The alleles differ in the amino acid found at position 129 (valine or methionine). Heterozygotes are restistant.          

How did the genotype frequencies of the older women compare with those predicted from the allele frequencies?  

What conditions would be necessary for the ▲32 CCR5 allele to go to high frequency in the human population?  Are these scenarios likely?  Why or why not.  

The initial freq is 20%, ¼ of the individuals with genotype +/+ or +/Δ32 contract AIDS and die without reproducing whereas all of the Δ32/Δ32 survive. Not likely because HIV is more prevalent than the Δ32 allele. Also, people will reproduce even if they are infected, the initial frequency is not 20%

How did Dawson experimentally verify the Hardy-Weinberg principle.

Studied flour beetles. Homozygous recessive l/l was lethal. He expected to see lower and lower frequencies of the l allele, but via computer analysis found that the l alleles decreases in frequency but not completely.   

How was the experiment by Mukai and Burke similar to that of Dawson and how were the results different and why?

They both measured allele frequency changes in flies in which l/l was lethal. Mukai and Burke used heterozygotes as population founders. They saw the dominant allele frequency increased fast at first, but reached equilibrium at .79, and the recessive allele reached equilibrium at .21.   

2 more experimental pops. Initial freq of viable allele at .975. The freq of the viable allele fell and reached equilibrium at .79         

What is a compound chromosome?

Homologous chromosomes that have swapped entire arms.   

          Neither of the alleles is dominant or the heterozygote is lethal

Why is compulsorily sterilization a misguided principal aside from the fact that is morally indefensible?

We can’t determine what feeble mindedness is or if it is hereditary. There is probably no allele for it so it wouldn’t change allele frequencies.

Because of heterozygote superiority, and rate of mutation is high.

Is mutation a rapid force of evolution by itself?

No, mutation is not rapid enough. Recombination and independent assortment amplifies mutation affects.

Why did cell size increase in jumps in Lenski’s experiments with bacteria?

          There has been a new beneficial mutation that swept through the population, then there was a period of stasis.

Describe the mutation selection-balance?

When the rate of deletion of deleterious alleles is the same as the rate of production of new alleles.

No, instead there is heterozygote superiority in which the heterozygotes are more likely to survive typhoid fever.

How did Pier and colleagues test the hypothesis in question 47?

Cell cultures with a CFTR mutation were grown. Typhoid fever was less likely to progress in heterozygotes.