EVOLUTION Fall 2004: Review Key 1

This answer key was produced using the answers from the highest scoring tests.  Some answers are brilliant, others simply adequate.  But since there is no cumulative exam, I felt that it was not necessary to belabor minutia.

 

1.  Provide concise definitions for 25 of the following 26 terms.  (2 pts each)

a. Autosome: a non-sex-determining chromosome. 

b. Background selection: the idea that a mutation’s chance of being spread is dependent on the overall quality of the genome it arises in—a good mutation can kept from spreading due to being stuck in a low-fitness genome.  This is more important in asexual lineages because in sexual lineages recombination can to some extent overcome this pressure.

c. Background trapping: the idea that if a beneficial mutation arises in the living dead, it will not spread to fixation in a population.

d. Clonal interference: different beneficial mutations in different asexual lineages cannot combine, and so the beneficial mutations compete against each other to spread themselves, instead of combining as they would likely do in sexually reproducing lineages.

e. Coadapted gene complex: genes that work together.  They may or may not be closely linked.  Recombination often shuffles these genes, positive epistasis wants to keep these genes together.

f. Cost of males: in sexually reproducing species, males cannot give birth, but make up half the population, thereby cutting sheer number of those reproduced by one-half

g. Cost of meiosis: in meiosis only half of an organism’s genome ends up in the gamete.  Therefore, the offspring will only have .5 related to a parent, rather than the 1.0 relationship that an asexual lineage provides.

h. Eusocial: a type of social animal (such as honeybees, ants, and arguably naked mole rats) in which organisms are split into castes, one caste of which (the workers) do not reproduce.  This is frequently explained by haplodiploidy or other mechanisms that make it more advantageous for a worker to care for the breeder’s offspring than to produce her own. 

i. Frequency-dependent selection: selection that varies based on frequency of a given trait.  For example, in sex ratios, when frequency of males becomes high, selection favors females that produce females, when the females ratio becomes high, it favors females that produce males.  This can help to keep genetic variation in a species.

j. Genic capture: in the production of a sexually selected trait, a large proportion of the genome is involved; thus the phenotype displayed is an accurate representation of the entire genome of the individual.

k. Genomic imprinting: the non-Mendelian process in which it matters which parent gave you a gene. The copy of the gene the other parent passed on to you is turned off.

l. Good genes hypothesis: Sexual selection for “good genes” by a female.  Female selects male based on overall phenotype, with the effect that her progeny will possess those traits which have made the parner that she selected successful.

m. Haplodiploidy: in some organisms one sex (generally the male) is haploid, arising from an unfertilized egg, while the other sex is diploid.  In eusocial animals this can play into power conflicts and sex ratio conflicts.

n. Inclusive fitness: fitness of a given allele measured in terms of a particular individual and relatives,  offspring of the individual, and its relatives’ offspring.

o. Lek paradox: persistent female choice for particular male trait values should erode genetic variance in male traits and thereby remove the benefits of choice; and yet choice persists.

p. Linkage disequilibrium: the statistical tendency for alleles at different loci to occur together, thus departing from the frequency of combinations that would be expected from the overall frequencies of the alleles themselves in the popualtion 

q. Living dead: the portion of an asexual population whose accumulated deleterious mutations doom it to eventual dying out as selective sweep brings the advantageous genomes to fixation.  Even if an advantageous mutation arises in this population, it will die out because of background selection.

r. Meiotic drive: the tendency of a certain gene to show up more frequently than would be expected, indicative of some selfish genetic element (like a segregation distorter) attempting to pass itself on.

s. Muller’s rachet: the lineage with the fewest deleterious mutations in an asexual lineage is necessarily small.  It is therefore vulnerable to dying out through genetic drift and other random acts of chance. 

t. Mutation-selection balance: the idea that there is a balance between the frequency of mutations arising and the removal of variance in a population via selection.  If selection occurred faster than mutations, genes would often spread to fixation in a population.

u. Mutational load: the fitness reduction in a population due to accumulated deleterious mutations.

v. Progenitor tail: the small portion of an asexual population whose few deleterious mutations keep it from dying out with the living dead.  It then accumulates deleterious mutations of its own, and part of the progenitor tail eventually becomes part of the living dead itself as a new progenitor tail arises.

w. Selective sweep: the selective process that leads to the fixation of a positive trait in a population.  It is responsible for the living dead’s disappearance in asexual populations.

x. Sexy son hypothesis: closely related to the Fisher process, this hypothesis states that if a female with a preference for a trait mates with a male with a trait, their offspring will have the trait and a preference for that trait.  The trait may not provide any selective advantage, but females will want to mate with males that have the trait, particularly if the preference for that trait is widespread, because the trait will be passed on to their sons, who will then have higher reproductive success and spread more genes.

y. Twiggy distribution: the majority of asexual lineages show up as relatively new additions, to sexual lineages, on phylogenetic trees.  This twiggy distribution indicates that asexual lineages do not have high long-term fitness and do not tend to speciate into other lineages.

z. Worker policing: workers in some eusocial organisms will kill the eggs of other workers (which they can identify by chemical differences from the queen’s eggs).  This occurs because they are more related to their brothers than they will be to their nephews, particularly if a queen was multiply mated.  Hence, although it is advantageous for each worker to sneak in eggs of her own (since she’ll be more related to her son than her brother), it is advantageous for the other workers to kill eggs that are not the queen’s (or their own.)  Oddly enough, this happens even in slave ants, when the slaves should have no genetic reason to get rid of non-queen eggs (since they’re not related to any of the ants in the colony.)

 

2. Referring to the provisioning of jellyfish babies with stinging cells from mom: “if these vertically transmitted cnidocytes are capable of de-differentiating into multipotent cells, then parental cell lineages could compete for access to their offspring’s germ line.”  Explain. (3 pts) 

This quote refers to the prevalence of a unicellular propagule.  It both shows how parental provisioning can help overcome some of the disadvantages associated with the creation of a unicellular propagule (the stinging cells should prevent predators from eating all the propagules) and how the commonly held ideas about why there are unicellular bottlenecks (specifically that the creation of a unicellular propagule reduces competition among the cells of the organism) are confounded sometimes.  In this instance, the maternal cells are not only provisioning the propagule, but also competing to reproduce again by becoming part of the propagule germ line. 

 

3. Some intracellular parasitic bacteria feminize males.  Some ladybugs have a parasitic endosymbiont bacteria that causes male embryos to die.  When females hatch, they gorge on the eggs of their dead brothers.  Why is cannibalism important in this system? (3 pts)

            The ‘goal’ of the parasitic elements is to increase the likelihood that they will be passed onto the next generation. In order to be passed on their hosts must survive. The female ladybugs stand a better chance of survival if they are well-nourished enough to live until they reproduce. Eating the male embryos thus gives the females, and the parasites a better chance at surviving to reproductive age.  Although feminizing males might be a better way to increase the fitness of this selfish bacteria, providing infected females with a hearty first meal is a pretty savvy strategy.

 

4. It was long thought that the loss of eyes in cave fish was due to either lack of selection for eyes OR selection for lack of eyes. 

a.       Briefly explain the difference. (3 pts) 

If there was a lack of selection for eyes, the loss of eyes in cave fish would occur because there was no selection against mutations in genes that coded for eyes.  Deleterious mutations simply weren’t selected against, added up, and the eyes were lost.  If there was a selection for lack of eyes, it would indicate that the lack of eyes would somehow be advantageous for the organism, and therefore any mutation that created lack of eyes would be selected for and spread through the population.

b.      Then explain the selection pressures now known to have resulted in eye loss in Mexican tetras (3 pts)

It appears that the gene coding for eyes in Mexican tetras is connected to the genes for lateral lines.  A mutation that was advantageous to the lateral lines was deleterious to the eyes.  However, this loss of eye function wasn’t deleterious in this instance because the eyes could do little in the environment anyway, so the gene was not selected against on that account.  The improved lateral lines, on the other hand, offered a distinct advantage, and so the gene was selected for.  In some ways, the eye loss in cave fish can be seen as being both a lack of selection for eyes, because the mutation that caused eye loss was not selected against because of lack of need for eyes, and selection against eyes, because the advantageous affects on the lateral lines necessitated lack of eyes.

 

5. Interpopulation crosses can provide extremely interesting data.

a. When an eyeless female Mexican tetra from cave A was crossed with an eyeless male from cave B, the offspring had semi-developed eyes.  Explain. (3 pts) 

      The eyelessness of the tetra parents must have arisen during separate evolutionary events and arise from mutations on different genes.  The offspring tetra will have inherited a good copy of each gene from one of the parents, while getting the mutated copy of each gene from the other parent, allowing it to have more-developed eyes than either of its parents.

 

b. Females fruit flies mated with males from a different population died younger than did females mated with males of their own population.  Explain. (3 pts)

      The male fruit fly has probably been undergoing sexually antagonistic evolution with the females from his species.  He has evolved some way to mix fluids in his seminal fluid that kill other sperm.  However, this is toxic to the female.  In his species, the female has evolved ways to negate the toxicity of this fluid.  However, the female from the other species, having been under no such evolutionary pressure, has not developed resistances and is vulnerable to the full toxicity of the fluid.

 

c. Interpopulation crosses in some insects with even sex ratios produce female-biased broods.  Explain. (3 pts)

      It is likely here that there is some selfish genetic element at work (perhaps a bacteria) that kills the male embryos, or biases sex ratios in favor of the female.  However, members of the sex with the selfish element at work have developed compensatory mutations that allow them to keep their sex ratios even.  Crossing with members of another species, which doesn’t have this compensatory mutation, however, allows the selfish genetic element to rear its ugly head and express itself in a female-biased ratio.

 

d. Mixed strains of slime molds possess higher spore:stalk ratios, even though the parental strains show no bias.  Explain. (3 pts)

            The likelihood here is that one of the strains of slime mold is a cheater, which manages to infiltrate into the spores more often than it should (advantageous since this allows that strain to reproduce itself to the detriment of the other strain).  However, the cheater trait is fixed in the population, and so is not apparent when only that strain is present, because all the organisms in that strain are cheaters, and cheaters can’t cheat unless there is a naïve strain.  When mixed with a naïve strain, however, the cheater trait reemerges as it takes advantage of the vulnerable strain, leading to a higher spore:stalk ratio.  Also it is possible that the strains are both cheaters, who cheat in a different ways, which would lead to hugely high spore:stalk ratios as each strain tried to put their organisms into the stalk. 

 

6. In flowering plants, pollen lands on the stigma, “germinates”, and a pollen tube grows down through the style and into the ovary for fertilization of an individual ovule.  Because many sperm may land on the stigma during its receptive phase, there is intense selection on the growth rate of the pollen tube.  In fact, the strength of this selection is reflected in the fact that pollen tubes are the fastest growing tissue in the world (deer antlers are the fastest non-cancerous mammalian tissue). 

  1. Would a mutation that increases the growth rate of pollen tubes at the expense of later seed production spread through a population?  Why or why not? (3 pts)

Such a mutation would spread throughout the population because it acts to cause advantage earlier in the life cycle than seed production.  If the growth rate of pollen tubes increases, the chances of the sperm out-competing others to fertilize the egg increases, and selection favors mutations that provide an advantage early on, even to the detriment of later life.  However, if the affect on seed production was too high (i.e. such a mutation caused almost no seeds to develop) the mutation would not spread because it affects reproductive fitness too highly.

 

  1. When the pollen tube reaches the ovary, 2 sperm nuclei emerge.  One fertilizes the ovary, the other “fertilizes” what will become the endosperm (a 3N tissue that acts as nutriment for the growing embryo).  Describe the conflict taking place at this time. (3 pts)

Each sperm nucleus wants to reproduce, and get its genes into the germ line for the next generation.  Unless the sperm nuclei are identical genetically, there will be competition of some kind between the two sperm nuclei over fertilizing the egg.  Both want to make it into the germ line, neither wants to be stuck in the endosperm where it will be unable to reproduce itself.  Any mutation that allowed for a sperm to have better success at fertilizing the egg would be selected for.

 

7. Why would a clade with a high propensity to generate high fitness asexual lineages go extinct more quickly than clades that do not? (3 pts)

            High fitness asexual lineages can out-reproduce and outcompete sexual lineages in the short term (because beneficial genes are passed on intact, not shuffled up in recombination and because there are no males, allowing more reproduction.)  The sexual lineages will end up dying out, and eventually the asexual lineages will accumulate too many mutations and die out too.  Therefore, the clade that tends to produce high fitness asexual lineages will go extinct via outcompetition of sexual species and increased mutational load.  On the other hand, clades that tend to produce lower quality asexuals do not see their sexual lineages die out because of competition with asexuals, and so have no problems when the asexual lineages eventually die out.

 

8. What is the general purpose genotype hypothesis? (3 pts)

            Successful asexual lineages tend to have genotypes that are not too specific.  They tend to work for a niche in a generalist community, and to be able to survive temporal changes, and also tend to incorporate some form of phenotypic plasticity and a low mutation rate.  These lineages may be boring, but they are able to stick around for long periods of time by not specializing so much that they will be greatly affected by minor environmental change.

 

9. What did Morgan, Fisher, and Muller all realize about recombination and the co-occurrence of beneficial mutations (in other words, why are multiple beneficial mutations more likely to be present in the same individual in sexual populations than in asexual populations)? (3 pts)

            In sexual populations recombination can lead to beneficial mutations being in the same gamete.  This gamete can combine with another gamete with its own beneficial mutations.  Asexuals can’t share genes in this way, and so beneficial mutations must arise independently, a rather rare occurrence.  Moreover, the asexual lineages undergo clonal interference as different lineages with beneficial mutations try to compete with each other to be the lineage to “win,” reproduce, and become part of the progenitor tail.  Essentially, they are competing rather than working together to create an even more successful organism.

 

10. We said that lunglessness in plethodontid salamanders and asexuality in aphids are unlikely ever to be reversed but winglessness in stick insects has been reversed multiple times.  Explain. (4 pts)

            In stick insects the muscles and developmental pathways that produce wings are still being used for similar activities, therefore mutations will not pile up due to lack of selection.  Also, the same (or very similar) pathways are there, easing the way for any reversion mutation.  In the salamander example, the pathways that used to lead to lung development are now being used for a projectile tongue, a different path from the original.  Any reversion back to the ancestral lunged state would mean losing the useful projectile tongue, and would probably never work because the salamanders have gone too far down another developmental path.  In aphids, the genes that are responsible for sexual pathways are unused, and it is probable that mutations have built up due to lack of selection against deleterious mutations.

 

11. Explain the informational basis of power asymmetries in gamergate ants. (3 pts)

            In gamergate ants the gamergate knows that her rival is laying haploid eggs, and that those haploid eggs are chemically different from her own.  Therefore she can kill off the beta’s eggs, which are less related to her than her own sons, with little cost to herself.  The beta, on the other hand, knows the gamergate’s eggs are chemically different than her own, but can’t tell which are male and unwanted and which are female, which she does want because she’s very related to them.  When the gamergate’s eggs hatch the beta can tell the difference between male and female, but the chemical signal is gone and she might kill her own kids.  So the gamergate has more information than the beta, allowing her to control reproduction of the beta at very little cost to herself and bolstering her own position, thus proving that knowledge is indeed power.

 

12. New Zealand researchers, in an attempt to bolster the reproductive success of the kakapo (a flightless lekking nocturnal parrot), provided extra food for the females.  But to their surprise, the females didn’t make more babies; they made more of one sex.  Which sex?  Explain. (3 pts)

            According to the Trivers-Willard model, the sex who has to compete for reproductive success will benefit more from having more resources, because in this instance the higher resources mean a higher quality kid, more likely able to compete successfully and have many kids.  Most likely in this situation it’ll be the males, because lekking tends to be about strong male-male competition.

 

13. Briefly describe the costs and benefits of a unicellular bottleneck. (4 pts)

            The costs of a unicellular bottleneck are that it creates a smaller, vulnerable propagule which needs either parental care or provisioning.  There is also a loss of specialized tissue, which leads to a longer development time for the propagule as it rebuilds the specialized tissues lost in the unicellular bottleneck.  However, a unicellular bottleneck also allows for the expedited purging of deleterious mutations, since a cell with serious mutations cannot hide among less-mutated cells like it could in a multicellular propagule.  This purging keeps highly mutated cells from getting into another germ line and reproducing again.  Also, the unicellular bottleneck causes all cells in one organism to have the same genome.  This is beneficial because it prevents competition between differing lineages to get into the germ line, probably preventing cheater cells from taking over an organism’s germ line.

           

By typing your name at the end of the review, you are pledging it.

 

 Return to Review Keys