EVOLUTION Fall 2004: Review Key 3
Spend
no more than 3.5 hours on this review.
Please type your answers on this review and email the whole thing back
to me by 11:59 pm Thursday night. Do not
put your name ANYWHERE on the review other than at the bottom of the last page
(your pledge). Pace yourself. I’ve enjoyed you guys and the experience of
making myself think about topics with which I was unfamiliar.
THIS
ANSWER KEY IS THE REVIEW OF THE STUDENT WHO MADE THE HIGHEST GRADE
1.
Describe where my office is located. (1 pt extra credit)
2.
What is a reaction norm and what relationship, if any, does it have to
canalization? (4 pts) A reaction norm is
the possible phenotypes that could emerge from a single genotype when it is
exposed to a range of environmental conditions.
Canalization can be considered to be the force which could limit the
range of possible reaction norms.
Canalization will be selected for when there is stabilizing selection on
a given allele (or multi-allelic trait) under a wide range of environmental
conditions. In other words, there is a
desirable phenotype (+/- a small amount of acceptable deviation from this
optimum) that exists under a wide variety of
environmental conditions. For example,
there is a great deal of stabilizing selection for neurons to function the way
that they do-even if you are born at high altitudes your neurons will be
similar, if not functionally identical, to low-altitude neurons. Thus, neuron-function could be considered to
be a highly canalized trait, and the reaction norm for this trait is
limited.
3. What is the benefit of developmental plasticity? (3 pts) Developmental plasticity allows for an
organism to produce a phenotype that is most closely matched to its
environment. This would allow for close
matching of phenotype to a given environment.
4. What is meant by a cost of developmental plasticity? (2 pts)
A cost of developmental plasticity is a cost, in terms of fitness (can
subdivide fitness into its components-survival, reproduction) which an organism
pays in order to either be plastic or
use its plasticity.
Provide 2 examples.
(4 pts) An example of the cost of being
plastic would involve when a developmentally fixed organism can produce a given
trait more efficiently than can a plastic organism. For instance, if two different races of
cladoceran produce a spike, and one always does and the other does in response
to predator presence, in an environment with predators, if producing the spike
plastically is more expensive, then the plastic organism would pay a cost for
being plastic. Another example of the
cost of plasticity involves when using a plastic trait the trait has negative
effects, by means of epistatic interactions, on a phenotype that is either
completely unassociated or only marginally associated with the plastic trait .
5. What is meant by a limit of developmental plasticity? (2 pts)
I think that both costs and limits of plasticity can only be determined
with respect to a fixed trait, and that limits of plasticity are necessarily
relative. A limit of developmental
plasticity is when the range of plastic phenotypes that can be produced is
somehow limited with respect to the range that can be achieved through fixed
development, or when the phenotype that can be produced plastically cannot
achieve the optimum phenotype as well as a developmentally fixed organism.
Provide 2 examples.
(4 pts) A limit of developmental
plasticity would be when in an extreme environment a plastic organism cannot
produce the phenotype that is optimum as well as a developmentally fixed
organism. Another limit of developmental
plasticity is due to information. An
organism must rely on information, and then process it, and then incorporate
this information as it develops the plastic trait. If information is limited, or if an organism
is correct initially but the environment changes, then the organism will be
unable to produce a phenotype that is correctly matched to the
environment.
6. “A given environment-dependent phenotypic change will be called
plasticity if it is believed to be adaptive, and lack of canalization if it is
not.” Explain. (4 pts)
Both canalization and plasticity implicitly imply that the phenomena are
adaptive. Plasticity allows for a
certain range of phenotypes to be expressed in accordance with the environment
that the organism is exposed to. Thus it
is assumed to be adaptive for an organism to allow for a “wide”-ranged reaction
norm, with reference to a specific trait or traits. When referring to another trait, one which
the investigator believes to be highly conserved across environmental gradients
due to strong stabilizing selection, variation or deviance from the “optimum”
is assumed to be non-adaptive, and thus could be characterized as a lack of
canalization. When a trait is considered
to be highly canalized, it is assumed that variation from the norm is
fitness-reducing, and canalization is the process by which a trait is produced
to be as close as possible to an optimum.
7. Why might some people argue that characters for which asymmetry
largely affects fitness might exhibit less fluctuating asymmetry than other
traits. (4 pts) Well, for one thing, ideally symmetrical
characters, such as wing structure and shape, will deteriorate in function as
they become less symmetrical. So from a
purely functional standpoint (and consequently fitness-a lop-sided bird isn’t
able to control flight and catch as many insects and won’t have as much time to
sing, attract mates, and protect a territory), symmetry leads to more precise
function. With respect to characters
such as sexual traits, in which symmetry is selected for as because it is
indicative of overall quality, symmetry is a signal of developmental
coordination and efficiency. If a male
cardinal is symmetrical, one could speculate that he has good genes which allow
him to be symmetrical. Females will
choose him because his symmetry is indicative of his overall quality. So don’t stray from the symmetry.
8. Like predators, parasitoids must kill their hosts. So how is it that they can be said to vary in
virulence? (4 pts) It can be said that they vary in virulence by
describing the proportion of the hosts which they effectively colonize and
kill. A 100% virulent parasitoid would
never be encapsulated and destroyed by the host insect—it would always
effectively use the host’s resources to grow and eventually destroy the host as
it developed. A certain parasitoid will
vary in its virulence with respect to different hosts, and a single host race
will vary in the virulence that different parasitoids demonstrate. Also affecting parasitoid virulence are
environmental conditions, such as host condition and the temperature to which
the host/parasitoid system is exposed.
Here, variation in temperature can either increase or decrease
parasitoid virulence.
9. How might the sex ratio produced by a female insect infected by
Wolbachia be affected by a short-term
exposure to high temperatures? Briefly explain. (3 pts) A female
insect which was exposed for a short time to high temperatures would be more
likely to produce an even sex ratio. Wolbachia influences female insects to
only lay female eggs, because, like mitochondria, endosymbionts are only passed
on in the female germ line. Thus, males
do not contribute to the fitness of the Wolbachia
strain. When a female is exposed to high
temperatures, she might clear herself of her Wolbachia load, as the endosymbiont has a lower LTmax than most
insects (perhaps not a Grylloblatid, a crazy little insect that lives in
glacier fields and far above treeline).
10. Briefly explain the three characteristics of H. floresensis
that make this find ”among the most outstanding discoveries in
palaeoanthropology for half a century”?
(6 pts) It’s very small size- the Flores
man was apparently little more than a meter tall, and had a brain case much
smaller than modern humans. It’s
apparent persistence until almost 18,000 (?) years ago, only 8,000 years before
H. sapiens showed up in
Indonesia. And it’s apparent use of
tools and weapons, suggesting a high degree of technological sophistication-on
the site were found what were believed to be rudimentary weapons and the bones
of komodo dragons and extinct pygmy elephants, suggesting that H. floriensis was a social and
coordinated hunter (which may mean that it even had language, but this will
most likely never be known).
11. One of these characteristics is the reason why the remains on
Flores have been called “the most extreme example ever found of human
adaptation.” That’s a very bold
statement. Explain. (3 pts)
This statement is referring to the small size of the hominids found on
Flores. Along with pygmy elephants and
massive lizards, they are an example of the strange forces that islands can
work on the evolution of organisms. Due
to some sort of constraint, be it resources or something else, H. floriensis became much smaller than
its likely ancestor H. erectus. So human-like creatures can be as flexible as
the next type of critter, getting smaller due to environmental
constraints.
12. What is the African Replacement Model of human evolution? (4 pts)
The African replacement model is that H. sapiens evolved in Africa and migrated to replace the rest of
the hominid species that had arisen and migrated around the earth. This model assumes that there was little or
no interbreeding/hybridization between the H.
sapiens and neandertalensis or erectus.
Homo sapiens came to
eventually swamp the rest of the hominid species.
13. In our discussions, we mentioned fever as a non-specific
response. That was an over-statement. Explain what’s going on in the following
(real) scenarios:
Species A exhibits a high fever when attacked by pathogen X and
recovers. (2 pts) Species A is either a) attempting to destroy
directly the pathogen by means of heating it beyond its LTmax, or b) attempt to
affect its own immune system in a way that will allow it to overcome the
pathogen. Either a) or b) or an
interaction between the two processes is successful and Species A is able to
recover.
Species A exhibits a mild fever when attacked by pathogen Y and
recovers. (4 pts) I’m not sure that I understand what the
difference would be between a mild fever and severe fever, other than the
intensity of the infection which must be overcome. When there is a serious infection, such as
the flu or Streptococcus pneumoniae,
the immune response will be greater than when there is an infection of the
common cold, simply because there is a greater risk in allowing the flu
pathogen to persist in the body. So
apparently, pathogen Y is not as severe of an infection, and that the
interactive attack of the immune system on the pathogen does not require as
significant of a fever response in order to be effective. A fever condition is a risky condition to be
in, as it will limit an organism’s ability to forage and otherwise fend for
itself. So if the pathogen is not as
great of a potential risk, an optimum fever response would be milder than in
the case of attack by a highly virulent pathogen.
Species A exhibits a mild fever when attacked by pathogen Z and
does not recover. (4
pts) This seems the trickiest to
me. Apparently, for some reason,
Species’ A immune response could be considered ill-matched to the nature of the
pathogen and the risk that it posed.
Perhaps, although this seems unlikely, mild fever benefited the pathogen
and increased its replication rate. Or
A’s immune system believed that the highly virulent and risk-posing pathogen
was more like a little cold pathogen, and did not respond to the threat
strongly enough. This response by A
would have to be deliberately induced by pathogen Z in order for this low
fever/death sequence to be evolutionary beneficial for Z. If it was not adaptive, this would represent
a dead end for species Z. This seems
likely because low fever would usually indicate low pathogen virulence and
hence low rate of pathogen replication and consequently a low rate of pathogen
transmission. If a pathogen has a low
rate of pathogen transmission, it would be adaptive to keep the host alive so
that the host can interact with a large number of potential hosts. (As I was answering question 17, I realized
that species A could also be ectothermic, and is unable to raise its
temperature sufficiently to overcome the pathogen because of environmental
constraints).
14. If a parasite/pathogen is locally adapted, infectivity rates
will be higher in sympatric hosts vs. allopatric hosts. Does the same relationship hold for
virulence? Explain your answer. (4 pts)
Not
necessarily. Optimum virulence is
adaptive in the sense that infectivity is maximized. Infectivity can be maximized by a variety of
different optimum virulence strategies.
Each particular optimum virulence strategy is a function of local host
ecology. The conditions of host habitat
influence pathogen virulence. Pathogen
virulence will often be greater in poor-condition habitats, due to high host
mortality. The behavioral ecology
(social, eusocial, not social- interaction frequency) of the host will also
influence parasite virulence. In highly
social or gregarious animals, high virulence could be selected for. Related to this is local variation in
pathogen dispersal mechanism. If
pathogen dispersal mechanisms vary spatially, optimum virulence will vary
according to the dispersal mechanism.
15. In the data paper about the wasps and Drosophila, if several
generations of selection changed encapsulation rates from 10% to 60% and if
encapsulation prevents mortality, why were encapsulation rates only 10% in the
first place? (and please define encapsulation). (3 pts)
Encapsulation is a surrounding of parasitoid egg in insects by haemocyte
attack. Haemocytes attack the egg, and
either destroy it by direct attack or asphyxiate it. There will be selection for the ability to
encapsulate the egg. Host defenses in
the first generation were ill-prepared for the threat that the parasitoid, at
least most of them. Those flies who had
some sort of beneficial variation from the majority in immune response were
able to encapsulate the egg (this incidence seems like good empirical evidence
of the Red Queen hypothesis). These
flies lived to reproduce and a larger proportion than 10% of their offspring
inherited the allelic combination which proved to be effective against the parasitoid. This process repeated until encapsulation
rates achieved 60% (the same process will occur, but in reverse, as parasitoid
eggs are selected for their ability to overcome host defenses).
16. You’re a biocontrol expert working for the UN in southern
Africa. In spring you test a new fungus
for its ability to infect and kill locusts.
It works fabulously, so you move to implement it as a biocontrol agent
as quickly as possible. By summer you’ve
jumped through all sorts of bureaucratic and industrial hoops and you start
infecting plagues of locusts. But it
doesn’t work. Why not? (3 pts)
It must be related to the seasonal changes which the question makes
explicit. Spring is cooler than summer
and the angle at which the sun strikes the earth makes thermoregulation less
effective, so the locust is unable to raise its internal temperature
sufficiently to overcome the pathogen.
But by late summer, thermoregulatory opportunities are greater and
ambient temperatures are much higher, so that the locust is able to raise its
temperature sufficiently to overcome the parasite. Parasites on ectothermic animals often have
temperature preference and tolerance curves that are shifted towards the cold
side, respective of the host organism.
17. Not all reductions in host fitness are due to pathogen multiplication. How does this pose a problem for the
trade-off hypothesis? (4
pts) The trade-off hypothesis assumes
that reductions in host fitness and survival are the product of a trade-off
between parasite replication and parasite transmission, and that there is
selection for the parasite to achieve some sort of optimum virulence, suited to
its particular mode of transmission.
Thus, host fitness in this hypothesis is decreased in relation to the
virulence (pathogen multiplication) exhibited by a particular parasite. The tradeoff hypothesis could fail to explain
observed phenomena when evolutionary forces fail to act upon a particular
strain or colony of pathogen. For instance,
polio normally affects the gastro-intestinal trait, and has oral/fecal route of
transmission. But when polio enters the
CNS, there is no selection for optimal levels of virulence, and the virus
replicates beyond bounds suitable for optimum transmission.
18. This first paper we read this time said “One of the most
important advances achieved through the evolutionary synthesis is the
consideration of phenotypic variation as a quantity of interest, whereas,
according to the classic typological view, it is considered a nuisance.” Nonetheless, most biologists are still guilty
of some sort of tunnel vision. Explain
why one biologist might legitimately study host-parasite relationships by
ignoring variation among pathogens and instead injecting her subjects with
sheep red blood cells… and explain why another biologist assumes all her
subjects are equivalent and is interested only in the variation produced by
injecting them with an allopatric pathogen vs. a sympatric one. (4 pts)
The first scientist is testing for strength of host response while
controlling for pathogen- specific interactions with the host. By injecting sheep red blood cells, she can
take measurements such as antibody production or T-cell count. She is attempting to quantify or describe induced
non-specific response to a
pathogen. The second scientist is
attempting to quantify variation in induced specific
response to a pathogen by eliminating the variability in
host-condition. She is attempting to
isolate the effects that parasite/host local coevolution have on the nature of
disease. Controlling for variable is a
necessary measure to obtain information.
By stripping down or assuming away levels of complexity we are more
easily able to generalize, draw conclusions, and test those conclusions at
different levels of scale and complexity (see Simon Levin in Ecology McArthur
Lecture from about 10 years back).
19. “Virulence is not necessarily a constant, nor simply an
inherent property of the parasite alone”
Explain how each of the following are expected to affect
virulence:
Delay between transmission and mortality (4 pts)
As
the delay between the time-period in which transmission is possible and
mortality increases, virulence is expected to increase. The author of the paper in which this idea
was discussed made the analogy of disease to organismal life history and the
evolution of senescence. The same is
true in organisms, when the mortality costs of a given reproductive effort are
delayed, the more that a high level of reproductive effort will be selected
for. The same in the parasite; when
mortality costs of a given level of virulence (and hence rate of transmission
and transmission potential) are felt way down the line, possibly nearing the
end of the time-frame in which transmission is possible, there will be
selection for high levels of virulence.
Mortality rate of uninfected individuals (3 pts)
When
there is a high level of background mortality in the host population, there
will be selection for a high level of virulence (if I’m not mistaken, I don’t
think this point was cut and dry clarified in the paper, but I’ll do my best
with logic). If wombats are dropping
left and right wombat parasites will be selected for a high level of virulence,
because rapid exploitation (high virulence) of host resources will lead to greater
transmission than low levels of host exploitation. If you are a highly virulent strain, there is
a greater likelihood that you will transmit to a new host before your host
dies, which he is likely to do at any second, infection or no infection.
20.
Like HIV, malaria has a high mutation rate that allows the plasmodium to evade
our efforts at vaccines. We said that
condoms would not only slow the spread of HIV, but also select for less
virulent forms. Why would providing
mosquito-netting for malaria patients (rather than for healthy persons)
accomplish the same thing? (4 pts) There
is an evolutionary cycle that occurs in which those strains that are capable of
rapid transmission are selected for high virulence, and those strains which are
incapable of rapid transmission (due to the behavioral/spatial ecology of the
host), are selected for low virulence.
This is so because high virulent strains decrease the timeframe of
opportunity for transmission in “hopes” of accelerating the rate of
transmission; low-virulence strains will evolve when the behavioral ecology or
spatial structuring of the host prevents rapid transmission. By preventing patients that have malaria from
spreading the disease (via Anopheline mosquitoes), you are effectively slowing
the rate of transmission, and thus selecting for low-virulence strains that
will persist within the host for longer, and allow him/her to be able to walk
around and get bitten by a skeeter.
21.
So… you are HIV positive and an intravenous drug user (a junkie).
Why
would you not want to share a needle with another junkie? (3 pts) He could have a different strain of HIV, and
by sharing needles you could develop a “super-infection,” or an infection
consisting of multiple strains. When
this occurs, the strains will compete with each other to obtain resources from
the host. When this happens,
“evolutionary stable” levels of virulence will be thrown out the window, and
the virulence of the infection will dramatically increase, and the user/HIV +
will be made extremely sick.
Why
would you especially not want to share a needle with another junkie
who’s AIDS has progressed to an advanced state? (3 pts) First of all, by saying that he has AIDS
means that his HIV has progressed to a degree where his T-cell count is very
low, and thus he is very likely to have other infections besides AIDS
(pneumonia, flu), which could have severe effects on you in your weakened HIV+
state. Also, selection is not as strong
on “old” infections to maintain an optimal level of virulence. Thus, you could potentially contract one of
these “pie-eating” strains of HIV, which would lead to rapid deterioration of
your health.
22.
Explain Red Queen dynamics, what they have to do with host specificity, why
they are invoked to explain the maintenance of sexual reproduction, and why
they are invoked to explain the maintenance of heritable variation of fitness
related traits. (8 pts) So the Red Queen
says to Alice, “You’ve got to keep running all the time just to stay in the
same place.” I’m paraphrasing from Lewis
Carroll, who is the source of the name for the biological phenomenon. Describes the dynamic, at times cyclical,
process of coevolution of parasites and hosts.
Rare host genotypes that are capable of overcoming parasite attack are
selected for and become more common—rare parasite genotypes that are able to
overcome the now common host genotype’s defenses achieve high fitness and drive
the common host genotype to extinction or very close to it. This process continues ad infitum, which invokes
the running in place but never getting anywhere image.
Host
specificity- Red Queen dynamics will tend to create extensive host/parasite
coevolution. The parasite will become
very specialized at overcoming host defense mechanisms, so specialized that its
approach would not be effective against different types of hosts. Since immune response is such a highly
coordinated and sophisticated system, a parasite can’t be some blundering yokel
sort of parasite, walking in thinking it’s gonna take over the joint. It would get shot down in a second by the
coordinated host immune system. Thus,
parasites will tend to become increasingly specialized to over come a
particular host’s defenses.
Sexual
reproduction has the potential to generate genetic diversity in one
generation. Asexual reproduction is only
capable of generating genetic diversity by means of mutation and with high
levels of mutation subsequently follow high levels of deleterious
mutation. Sexual reproduction generates
the rare host genotypes, relatively free of deleterious mutations, which will
be the next generation of rare defense-capable host organisms.
Heritable
variation of fitness related traits- As I stated above, there are rare host
genotypes who are able to overcome parasite attack. These genotypes will achieve high fitness and
have lots of offspring. These
offspring, at least until parasite attack mechanisms catch up, will have high
fitness.
23.
Explain Sewell Wright’s adaptive landscape model (4 pts) Sewell Wright’s adaptive landscape model
describes a series of fitness peaks, a sort of topographical map of
adaptiveness. I am not quite sure of the
limitations of the model, and how one would actually quantify the position of a
particular (extant) species on the landscape (it seems possible that one could
outline historical positions, and demonstrate how an organism showed at Time A
that it had high fitness, and was moving upwards, but an environmental
disturbance at Time B knocked it from its adaptive peak). Nevertheless, it is a useful model as it
puts into a visual/graphical perspective the consequences of certain genetic,
evolutionary, and environmental mechanisms on the fitness of a particular
species. When an organism is in an
adaptive valley, it is in trouble. There
will be selection for the organism to achieve high fitness, perhaps arising
through the evolutionary mechanism which achieves a positive instantaneous
fitness derivative through the easiest route (it will hit an upward slope the
quickest or with the least resistance—although does not have to be the case,
high fitness could be achieved when an organism is “knocked around” on the
landscape). The adaptive landscape model
also highlights that multiple paths to high fitness are possible, with multiple
potential peaks in the landscape.
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