Actually I am rephrasing a notion of Jonathan Losos in the book 'The Princeton Guide to Evolution' (PUP,2013), in which he states that "[T]he ability of a single genotype to produce different phenotypes when exposed to different environments - may itself be adaptive."
Of course, unlimited phenotypic plasticity is an idealization, one which inspired comic book writers to conceive fictional humans capable of biomimicry. Concerning real world science though, I can imagine a future biomimetic trend in (human) synthetic biology.
It is evident that adaptivity to different environments is a highly valuable capability, thus the adaptivity of phenotypic plasticity would be a most impressive feature of living organisms.
So far, 'only' technology allowed us humans to bypass 'slow' genetic differentiation, and even enabled us to populate a small orbital space station.
Returning to the initial question, do you know of any (non-phenomenological) research on phenotypic plasticity in mammals, apart from behaviour?
There is for example evidence that famine induces up-regulation of protective and repair enzyme mechanisms, which may vary among populations. Does this represent an adaptivity of phenotypic plasticity? If so, is it limited, because environmental conditions favor reproduction?
The general answer to the question of why phenotypic plasticity is limited is that there are costs of maintaining plasticity, which requires mechanisms that sample internal or external cues that have ancestrally predicted variable world states. Thus, the evolution and ontogenetic maintenance of phenotypic plasticity is only expected to the degree that the improved match between phenotypic strategy and individual circumstance produces fitness benefits that outweigh the inherent costs of palsticity.
see http://rspb.royalsocietypublishing.org/content/early/2011/04/05/rspb.2011.0055
I'd say go further back to your Fisher, Falconer and additive genetic variance. Add in that much of phenotypic plasticity can be associated with traits related to fitness, e.g., egg number due to body size, and then there's just only so much of a selection differential that can be effective.
I would say the phenotypic plasticity must have meet not only the functional requirement (or constraint) but also the development constraints. That is the evolving form must have the basic functions, but the different types of forms that different organisms can develop are limited. George MeGhee says in his book "convergent evolution" that "size of the form set in not infinite, and the functional constraints of physics and geometry to be the same throughout the universe and to be extrinsic with respect to biology".
Great discussion!
my 10 cents: one rather counterintuitive consequence of phenotypic plasticity for evolution has recently been pointed out by Draghi and Whitlock: DOI: 10.1111/j.1558-5646.2012.01649.x. To make a long story short, it helps diverse genotypes to live through environmental fluctuations which otherwise would have wiped them out. As a result, plasticity might facilitate (rather than slow down) ecological genetic differentiation! Pretty cool.
(It all depends on the frequency and magnitude of environmental disturbances, though)
I regret that I have lost the reference, though you might look at (surprisingly) one of the volumes of "the Science of Discworld" ( Cohen, Stewart, Pratchett) who refer to the fact that amphibians have far more DNA per nucleus than mammals, arguably because they have to function in a much wider range of internal conditions, especially temperature. The argument is that a greater range of enzymes etc is needed. I realise that this is in a sense the opposite of your question: here we try to explain phenotypic stability in the face of radically different conditions, but I have a gut feeling that the issues are related
There's a recent paper pertaining to salamander genome size in Genome Biology and Evolution by Drs. Cheng Sun, José R. Lopez Arriaza and Rachel Lockridge Mueller from Colorado State University. Full text is available at http://gbe.oxfordjournals.org/content/4/12/1340.full
Don't forget that a significant amount of phenotypic plasticity can be mediated by maternal and paternal effects. Thus, parental 'condition' can exert a transgenerational influence on phenotype development. These may be either positive (e.g., effects on developmental rate, final body size) or negative (e.g. fetal alcohol syndrome).
Just as selection requires variance, selection for plasticity requires GXE interaction (Via and Lande, 1985. Evolution, 39(3):505). In other words, there must be variation in norms of reaction. If this component of variation is small, plasticity will evolve only slowly.
Evolution is a balance between robustness and adaptivity. Unlimited 'adaptivity' would be counter productive. In order to survive, systems need to be robust. If any environmental challenge could knock out an entire system, we wouldn't survive. Gene and molecular networks are scale free. They are not connected like old fashioned Christmas tree lights, where one error can knock out the whole network. We get mutations regularly because of all the transcription going on but we have DNA repair mechanisms to repair them - replace base pairs, repair tears, etc.
This question has occupied researchers since Darwin. There's a classic review that's still worth reading to get an idea of the key issues people have thought about: http://www.sciencedirect.com/science/article/pii/S0169534797012743
There's plenty still being done on this in evolutionary ecology (checking out the recent papers that cite this review would be a good place to start getting a handle on where the field is at).
http://www.sciencedirect.com/science/article/pii/S0169534797012743
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