1. A study finds thatguppies bred in an aquarium have only 10% the rate of extrinsic mortalitycompared to guppies living in the wild. Imagine that a population of guppieswas bred in the aquarium environment for hundreds of generations. How would youexpect this difference in extrinsic mortality to affect the rate of senescence(i.
e., how quickly senescence happens with age) in captive guppies compared totheir wild relatives? The aquarium guppies have a lower extrinsic mortality thantheir wild relatives because the wild relatives face more harsh conditions,such as predation, disease, and competition when resources are scarce. As aresult, mutations and adaptations that promote early reproductive maturity andsuccess in wild guppies are favored by natural selection. Aquarium guppies, onthe other hand, do not have the environmental pressure to mature early, so alonger life span is favored by natural selection.
In addition, there is a tradeoff between age of sexual maturation and life span because energy and nutrientsneed to be invested in both. Aquarium guppies will have a longer life span, andtherefore a slower rate of senescence, due to a higher age of onset for sexualmaturation; there is more investment in prolonging life. Wild guppies would haveshorter life spans, and therefore a higher rate of senescence, due to a lowerage of onset for sexual maturation; there is more investment in earlymaturation and reproduction. 2.
A study finds that increased pollution in a lake causedtwo fish species to merge into a single species. Give a reasonable explanationfor how pollution might have caused this change in reproductive isolation. Possible explanation:The two fish species evolved from one species that divergedthrough sympatric speciation. The sympatric speciation resulted from therebeing a difference in resources and conditions on opposite sides of the lake,which would have led to selection for different traits and mutations, localadaptation to these conditions, and eventually, the two species of fish.However, this also resulted in hybrids, as there was no barrier preventingmigration and contact between the sides of lake.
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Though these hybrids have theability to mate with other hybrids and both distinct fish species, they did notthrive. This is because of their inability to adapt effectively to either sideof the lake (before pollution), and therefore, they were low in populationsize. However, after pollution was introduced to the lake, the hybrids hadadvantageous traits and were able to survive and mate (with other hybrids andboth distinct fish species) at a higher frequency than the distinct fishspecies did with themselves. Over time, this would have lowered the populationsize of the two distinct fish species, and caused the fish species to mergeinto one species that was much like the hybrids. 3. Imagine that a new medical treatment completely removesany negative effects of being a heterozygote for the mutant allele that causeHuntington’s disease; however, homozygotes for the defective alleles stilldevelop the disease with its normal consequences.
Assume everyone who needs itis able to get this treatment. How would you expect the frequencies of theHuntington’s allele and the disease itself to change over a long periodfollowing the introduction of this treatment. Huntington’s disease is a progressive neurological disorderthat is caused by an autosomal dominant mutation in the HTT gene. There will be no change in the allelefrequencies because this treatment only has an effect on the phenotype, not thegenotype; it does not change the mutant allele into a normal allele.
Thefrequencies of the mutant allele could have potentially gone up if the onset ofdisease was early in life, because this would then cause heterozygotes to live longenough to reproduce and mate, thereby increasing its allelic frequency.However, onset is usually in the thirties or forties, so the frequencies of theHuntington’s allele will stay the same because those with the Huntington’sallele(s) most likely would have had children before or around the time ofonset. However, the frequency of thedisease itself will go down because heterozygotes would now have the chance toreceive treatment to remove the negative effects of being a heterozygote forHuntington’s disease. The phenotypic frequency will now be like the phenotypicfrequency of a recessive disease. This is because the mutant allele isautosomal dominant, meaning only one mutant allele is necessary to exhibit thedisease (without this treatment), as opposed to autosomal recessive, where bothalleles (homozygosity) are necessary to exhibit the disease. However, with thetreatment, it will be necessary to be homozygous to exhibit the disease, as itis with recessive diseases. Citation:1.
“Huntington disease – Genetics Home Reference.” U.S.National Library of Medicine, National Institutes of Health, 6 Dec. 2017,ghr.nlm.nih.gov/condition/huntington-disease.
4. Imagine that the majority of the population startsreceiving the flu vaccine each year. Give one reasonable argument why thismight select for increased virulence of the virus, and one argument why thismight have the opposite effect on the evolution of virulence. Increased Virulence: If the majority of the population started receiving the fluvaccine each year, this might increase virulence.
This is because the viruswill evolve under the vaccinated host’s conditions, due to selection for a morevirulent flu virus. These viruses can afford the cost of higher virulencebecause their vaccinated hosts have a higher resistance to their virulence.This will make these flu viruses even more dangerous to those who areunvaccinated because these virulent viruses will use more of the host’sresources and cause more damage to the host. Decreased Virulence: If the majority of the population started receiving the fluvaccine each year, this might decrease virulence. This is because the viruswill evolve within the vaccinated host, due to the selective pressure to beless virulent. If the vaccinated host is less susceptible to infection to thevirus, then viruses that decrease virulence and lay “dormant” in the host willbe more efficient at transmitting to unvaccinated hosts. Citation:Mackinnon, M.J.
, S. Gandon, and A.F. Read. “VirulenceEvolution in Response to Vaccination: The Case of Malaria.
” Vaccine26.48-5 (2008): C42–C52. PMC. Web. 12 Dec. 2017.
