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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?
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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
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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.
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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?
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Random MatingIn Generation II, the allele frequencies are:
p =
q =
For a population in equilibrium:
F(AA) = F(Aa) = F(aa) =
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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
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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.
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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?
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HIV prevalence, 2009
http://wwwnc.cdc.gov/travel/yellowbook/2012/chapter-3-infectious-diseases-related-to-travel/hiv-and-aids.htm
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Numbers of people living with HIV/AIDS
WHO/UNAIDS
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HIV infection time course
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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
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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
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Origin of Genetic Variation: Mutation
• Point mutations
• Insertions/Deletions
• Inversions/Translocations
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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
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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.
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HIV infects T cells via CD4 and CCR5 cell surface receptors
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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?