high rate of mutation founder effect bottleneck effect

a) High rate of mutationb) Founder effectc) Bottleneck effectd) Cats with extra toes are

better at catching micee) Extra toes are sexually

appealing to female catsf) ?

Q: A high proportion of the cats on Key West have extra toes (polydactyly). The most likely explanation is:

How will this population evolve in the future?

Evolutionary Mechanisms

Biological evolution: change in genetic composition of a population over time

• How can the gene pool of a population be characterized quantitatively?

• What happens to the gene pool of a sexually reproducing population over generations?

• What mechanisms cause evolutionary change?– Model systems to study evolutionary

mechanisms

Quantifying genetic variation in sexually reproducing populations

Fig. 21.03

The gene pool is the sum of all alleles

Only locus X is shown,with three alleles (X1, X2 , and X3 )

Genetic structure is the frequency of the different genotypes in the population.

Allele frequencies

Cystic fibrosis is a recessive genetic disease. Among Northern Europeans, the incidence of CF is 1 per 2500 live births.

Q1: What is the frequency of the CF allele in the Northern European population?

Q2: What proportion of the population are carriers of the CF allele?

Random MatingIn Generation II, the allele frequencies are:

p =

q =

For a population in equilibrium:

F(AA) = F(Aa) = F(aa) =

Q3 - equilibriumIn both populations shown below, p = 0.6 and q =

0.4; which population(s) are in Hardy-Weinberg equilibrium?Population A

36 red (CRCR), 48 roan (CRCr), and 16 white (CrCr).

Population B32 red (CRCR), 56 roan (CRCr), 12 white (CrCr).

a. Population Ab. Population B

c. Both A and Bd. Neither A nor B

Hardy-Weinberg (H-W) Equilibrium

• Assumptions.

• If the H-W assumptions are met, then allele frequencies will not change from one generation to the next.

HIV infection

• Is there genetic variation among HIV virus particles in an infected individual?

• Is there significant mortality in the virus population of an infected individual?

• Does genetic variation make a difference in survival and reproduction of HIV virus?

HIV prevalence, 2009

http://wwwnc.cdc.gov/travel/yellowbook/2012/chapter-3-infectious-diseases-related-to-travel/hiv-and-aids.htm

Numbers of people living with HIV/AIDS

WHO/UNAIDS

HIV infection time course

Q4: 3TC resistant viruses

a. Arose by mutations induced by 3TC

b. Arose from a small pool of mutant viruses already resistant to 3TC

c. Arose by gradual adaptation of viruses to 3TC

Campbell & Reece 7th ed. p. 448

PatientNo. 1

Patient No. 2

Patient No. 3

Per

cen

t of

HIV

res

ista

nt

to 3

TC

Weeks

Figure 22.13 Evolution of Drug Resistance in HIV

Why do anti-HIV drugs become ineffective?

Huang et al., 1998, Science 282:1669

• Structure of HIV reverse transcriptase & resistance mutations

• Blue = AZT resistance

• Lt. Blue = ddI, ddC, 3TC

• Violet = both AZT + ddI

Origin of Genetic Variation: Mutation

• Point mutations

• Insertions/Deletions

• Inversions/Translocations

Q6: How many times did SIV make the jump to human hosts to become HIV?

a. Once

b. Twice

c. 3 times

d. 4 times

e. 5 or more

Q7: What anti-HIV therapies are informed by the theory of natural selection?

A. Multiple-drug cocktails

B. Drug treatment immediately after exposure

C. Stopping drug treatment when resistance emerges

D. All of the above.

E. None of the above.

HIV infects T cells via CD4 and CCR5 cell surface receptors

Frequency of CCR5-delta32 allele in different human populations

• Northern Europe 10%• Central Asia 2%• Asia, Africa 0%

Why is the CCR5-delta 32 allele so frequent among Northern Europeans? Propose at least two alternative hypotheses.

What percentage of people in each region are expected to be resistant to HIV infection?