Q: A high proportion of the cats on Key West have extra toes (polydactyly). The most likely explanation is: a) High rate of mutation b) Founder effect c) Bottleneck effect d) Cats with extra toes are better at catching mice e) Extra toes are sexually appealing to female cats f) ?
How will this population evolve in the future?

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
Only locus X is shown, with three alleles
(X
1
, X
2
, and X
3
)
The gene pool is the sum of all alleles
Genetic structure is the frequency of the different genotypes in the population.
Fig. 21.03

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 Mating
In Generation II, the allele frequencies are: p = q =
For a population in equilibrium:
F(AA) =
F(Aa) =
F(aa) =

Q3 - equilibrium
In both populations shown below, p = 0.6 and q =
0.4; which population(s) are in Hardy-Weinberg equilibrium?
Population A
36 red (C R C R ),
48 roan (C R C r ), and
16 white (C r C r ).
Population B
32 red (C R C R ),
56 roan (C R C r ),
12 white (C r C r ). a. Population A b. Population B c. Both A and B d. Neither A nor B

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

• 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-totravel/hiv-and-aids.htm

Numbers of people living with HIV/AIDS
WHO/UNAIDS

HIV infection time course

Q4: 3TC resistant viruses
Patient
No. 1
Patient No. 2
Patient No. 3 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
Weeks
Figure 22.13 Evolution of Drug Resistance in HIV
Campbell & Reece 7 th ed. p. 448

Why do anti-HIV drugs become ineffective?
• Structure of HIV reverse transcriptase & resistance mutations
• Blue = AZT resistance
• Lt. Blue = ddI, ddC, 3TC
• Violet = both AZT + ddI
Huang et al., 1998, Science 282:1669

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
• Central Asia
• Asia, Africa
10%
2%
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?