1. A study finds that
guppies bred in an aquarium have only 10% the rate of extrinsic mortality
compared to guppies living in the wild. Imagine that a population of guppies
was bred in the aquarium environment for hundreds of generations. How would you
expect this difference in extrinsic mortality to affect the rate of senescence
(i.e., how quickly senescence happens with age) in captive guppies compared to
their wild relatives?
The aquarium guppies have a lower extrinsic mortality than
their wild relatives because the wild relatives face more harsh conditions,
such as predation, disease, and competition when resources are scarce. As a
result, mutations and adaptations that promote early reproductive maturity and
success in wild guppies are favored by natural selection. Aquarium guppies, on
the other hand, do not have the environmental pressure to mature early, so a
longer life span is favored by natural selection. In addition, there is a trade
off between age of sexual maturation and life span because energy and nutrients
need to be invested in both. Aquarium guppies will have a longer life span, and
therefore a slower rate of senescence, due to a higher age of onset for sexual
maturation; there is more investment in prolonging life. Wild guppies would have
shorter life spans, and therefore a higher rate of senescence, due to a lower
age of onset for sexual maturation; there is more investment in early
maturation and reproduction.
2. A study finds that increased pollution in a lake caused
two fish species to merge into a single species. Give a reasonable explanation
for how pollution might have caused this change in reproductive isolation.
The two fish species evolved from one species that diverged
through sympatric speciation. The sympatric speciation resulted from there
being a difference in resources and conditions on opposite sides of the lake,
which would have led to selection for different traits and mutations, local
adaptation to these conditions, and eventually, the two species of fish.
However, this also resulted in hybrids, as there was no barrier preventing
migration and contact between the sides of lake. Though these hybrids have the
ability to mate with other hybrids and both distinct fish species, they did not
thrive. This is because of their inability to adapt effectively to either side
of the lake (before pollution), and therefore, they were low in population
size. However, after pollution was introduced to the lake, the hybrids had
advantageous traits and were able to survive and mate (with other hybrids and
both distinct fish species) at a higher frequency than the distinct fish
species did with themselves. Over time, this would have lowered the population
size of the two distinct fish species, and caused the fish species to merge
into one species that was much like the hybrids.
3. Imagine that a new medical treatment completely removes
any negative effects of being a heterozygote for the mutant allele that cause
Huntington’s disease; however, homozygotes for the defective alleles still
develop the disease with its normal consequences. Assume everyone who needs it
is able to get this treatment. How would you expect the frequencies of the
Huntington’s allele and the disease itself to change over a long period
following the introduction of this treatment.
Huntington’s disease is a progressive neurological disorder
that is caused by an autosomal dominant mutation in the HTT gene. There will be no change in the allele
frequencies because this treatment only has an effect on the phenotype, not the
genotype; it does not change the mutant allele into a normal allele. The
frequencies of the mutant allele could have potentially gone up if the onset of
disease was early in life, because this would then cause heterozygotes to live long
enough to reproduce and mate, thereby increasing its allelic frequency.
However, onset is usually in the thirties or forties, so the frequencies of the
Huntington’s allele will stay the same because those with the Huntington’s
allele(s) most likely would have had children before or around the time of
onset. However, the frequency of the
disease itself will go down because heterozygotes would now have the chance to
receive treatment to remove the negative effects of being a heterozygote for
Huntington’s disease. The phenotypic frequency will now be like the phenotypic
frequency of a recessive disease. This is because the mutant allele is
autosomal dominant, meaning only one mutant allele is necessary to exhibit the
disease (without this treatment), as opposed to autosomal recessive, where both
alleles (homozygosity) are necessary to exhibit the disease. However, with the
treatment, it will be necessary to be homozygous to exhibit the disease, as it
is with recessive diseases.
1. “Huntington disease – Genetics Home Reference.” U.S.
National Library of Medicine, National Institutes of Health, 6 Dec. 2017,
4. Imagine that the majority of the population starts
receiving the flu vaccine each year. Give one reasonable argument why this
might select for increased virulence of the virus, and one argument why this
might have the opposite effect on the evolution of virulence.
If the majority of the population started receiving the flu
vaccine each year, this might increase virulence. This is because the virus
will evolve under the vaccinated host’s conditions, due to selection for a more
virulent flu virus. These viruses can afford the cost of higher virulence
because their vaccinated hosts have a higher resistance to their virulence.
This will make these flu viruses even more dangerous to those who are
unvaccinated because these virulent viruses will use more of the host’s
resources and cause more damage to the host.
If the majority of the population started receiving the flu
vaccine each year, this might decrease virulence. This is because the virus
will evolve within the vaccinated host, due to the selective pressure to be
less virulent. If the vaccinated host is less susceptible to infection to the
virus, then viruses that decrease virulence and lay “dormant” in the host will
be more efficient at transmitting to unvaccinated hosts.
Mackinnon, M.J., S. Gandon, and A.F. Read. “Virulence
Evolution in Response to Vaccination: The Case of Malaria.” Vaccine
26.48-5 (2008): C42–C52. PMC. Web. 12 Dec. 2017.