SB201, 2014
Life History Evolution: Student Discussion Questions
Gustafsson et al 1988
The authors claim that they test three different ways of exploring this question – comparing between species,
comparing within populations, and experimental manipulation - but it appears as though they only tested the
first and last of those methods. This appears to hinge on their assertion that ‘there is no need for the pattern
between species or populations to correspond with the trade offs acting on an individual.’ Can we give
examples of when this statement might be true? Do the authors unfairly dismiss comparisons between species
or populations?
In the populations whose clutch size was manipulated experimentally, breeding females produced the highest
percentage of recruits at the natural clutch size, but the offspring of offspring performed best when the natural
clutch size was reduced by one. What can explain this discrepancy, or how might we design an experiment to
come up with an explanation?
Are there other environments (i.e., not Gotland) in which selective pressures are so strong that increased clutch
size would increase the number of recruits?
How can one rederive the formula (1) for the average fecundity of an adult female in terms of adult and juvenile
survival rates?
Pettifor et al, 1988
The individual optimization hypothesis implies that individual parental birds somehow ‘know’ how many eggs
they are most suited to raise, and that they then lay this number. How might the organism acquire such
knowledge? Are the influences on this trait intrinsic, extrinsic or both? … Given these potential mechanisms,
how are we to understand how evolution achieves the goal of clutch size optimization? I.e. what is the adaptive
substrate?
‘Individual optimization’ and ‘trade-off’ type mechanisms can be proposed for many distinct but related biological
processes. In nature these processes then only achieve broad biological tasks such as reproduction when
operating in combination. This feature of biology seems to allow us to chalk up very large numbers of
evolutionary explanations for particular natural phenomena such as clutch size variation. Worryingly, these
explanations seem able to fall under different classes of hypothesis. For example, a trade-off in nutrient
investment required for egg production might exist and appear to explain clutch size at one level, but we have
also just learned that individual optimization of clutch size with respect to recruitment explains the same
phenomena. Where does this leave evolutionary theory? It seems we are either faced with false dichotomies
between hypotheses, or are forced to severely limit the range of applicability for any given evolutionary
explanation... How might we move toward a more principled formulation of evolutionary ideas?
Gustafsson and Sutherland successfully identify reproductive trade-offs after experimentally increasing brood
size, in the form of reduced future fecundity of parents and their offspring (Gustafsson, 1988). Why might these
differences relative to the paper by Pettifor et al. arise? Do they highlight general issues for experimental
evolutionary biology?
The author used a generalized linear model with a first order term of clutch size, and a first and second order
term of the manipulation. While all three terms are statistically significant, the authors did not discuss whether
any other terms (such as the second order term of the clutch size) are statistically insignificant. The selection of
the variables could potentially change the conclusion, and would be important to justify.
Is there a common cause (e.g., the general health of the bird) that determines a larger size of the clutch and the
higher recruitment rate? Is the clutch size a constant feature of a bird throughout its reproduction ages or a
varying factor depending on the age and health of the bird?
Walsh & Reznick, 2010
Why didn’t the authors sample more frequent time points for the guppy introduction experiment? There aren’t
any tables that suggest that the populations were closely monitored once per year, for example. I would’ve been
interested to see a year-by-year breakdown of the key variables that they measure (e.g. Rivulus age/size at
maturity, reproductive effort, growth rate, amount of offspring).
How did the authors predict that the amount of food available to the Rivulus would be so closely tied to their
evolutionary behavior upon the addition of guppies? It seems that they were surprised by the experimental
results (of the guppy-introduction study), but tried to mirror these effects in the common garden experiment. As
an engineer (not an evolutionary biologist), I’m curious as to whether this is an obvious variable to adjust in
these studies, or if the conditions were tailored to this situation.
Why did the authors originally assume that increased guppy predation on young Rivulus would lead to delayed
maturation? If predators attack juveniles, wouldn’t the species evolve to mature faster to escape such attention?
How generalizable do you believe Walsh and Reznick's findings are? Their observations of killifish populations
suggest that indirect effects of juvenile predation seem to have meaningful impacts on phenotypic evolution,
would you expect this to be common or an exception in ecological conditions? More broadly, what do you think
evolutionary theory alone can tell us about organismal evolution in nature?
Lee et al, 2012
How are growth and senescence balanced in a molecular sense, and how plastic are these cellular changes
and tradeoffs? Do they allow room to adapt to environmental changes between breeding seasons?
A direction I would suggest for this work is to improve the quality of the hazard / mortality curves by having more
than 5 fish per batch. I'm particularly curious as to the *shape* of the curve: is growth rate simply scaling the
temporal axis (same shape), or is it fundamentally changing the population distribution (different shape)? The
effect could conceivably simply increase the death risk of a sub-population of fish, thereby changing the median
(i.e. the author's summary statistic) without necessarily implying the "energy allocation" scenario.
Which are the molecular mechanisms underneath this obervations? The authors describe about oxidative stress
and cellular damage caused by higher metabolic activity, but it is not the scope of this work to deal with those
issues.
To which extent can we extrapolate these results to other species? Is it a general result? Is it general just in
ectotherms, in fish, in this particul group or species?