Adaptation, constraint, and scientific progress

Yesterday I read an academic paper reviewing something called “phenotypic integration”. I’ll spare you most of it, but the basic idea is that an organism’s different functional traits (roughly meaning “features that do something”, like a bird’s bill or its oxygen-carrying red blood cells) can covary, or only be found in particular combinations of measurements. How they covary can tell us something interesting about their underlying biology—about intrinsic constraints on evolutionary processes, for example.

Among the things that struck me in the paper, written by Massimo Pigliucci, was its cogent explanation of how the way we commonly talk about such constraints can be misleading and unproductive. The idea of constraints has a long and storied history in evolutionary biology, a topic which cannot be discussed without at least briefly mentioning a famous paper by Stephen Jay Gould and Richard Lewontin, succinctly titled “The Spandrels of San Marco and the Panglossian Paradigm: A Critique of the Adaptationist Programme”.

In “Spandrels”, Gould and Lewontin push back on the common idea that an organism’s traits have been directly shaped by natural selection—that the pointyness of a bird’s bill is necessarily related to success at extracting nectar from flowers. Instead, particular forms or values of traits might only exist because there are a limited range of options given the existing values of other traits. (A spandrel is an architectural feature found between the top of an arch and a rectangular frame; just because the spandrels in a cathedral are ornately patterned doesn’t mean they serve a functional purpose or are anything more than a byproduct of the rules of construction, the metaphor goes.)

Their paper was important and necessary and launched a thousand academic ships. But it also entrenched a certain way of thinking about the relationship between adaptation and constraint—that they are somehow opposites; that it’s an either / or proposition. Summarizing work from the philosophy of science literature for a journal whose readership might not be familiar with it, Pigliucci suggests that this is a mistake, and that everything we typically talk about as a constraint on adaptation (“the genetic-developmental mileu”) is actually the raw material of adaptive evolution itself:

Think of it this way: the rule of Mendelian inheritance may be thought of as ‘constraining’ the occurrence of certain phenotypes in a population. Yet, if inheritance were, say, blended (as Darwin thought), natural selection would soon run out of fuel and could not play the role of constructive causative agent that the modern theory of evolution asserts it plays (p. 266)

There’s a lot here—especially if you haven’t taken biology in a few years—so let’s unpack it. Mendelian inheritance is a model for how genes are separated and independently grouped as they are passed on from parents to offspring, initially proposed by friar-biologist Gregor Mendel (think Punnett squares and peas). Though Mendel’s “Experiments on Plant Hybridization” was published only a few years after Origin of Species, Darwin was unaware of his work. This was too bad, because it eventually helped solve a major weakness in Darwin’s original theory: how trait variation sticks around in populations, rather than being blenderized into a homogeneous slurry by interbreeding. Natural selection wouldn’t work with a slurry—it needs variation as “fuel”—and so Pigliucci’s point is that while it’s tempting to think of Mendel’s discovery as yet another set of rules that limit the possibilities of what forms life can take, it actually provides the very substrate for a creative, generative process.

I think this counterintuitive framing of adaptation and constraint is an example of how the real coup in science can be to understand the rules of the particular world you’re studying, and figure out how to ask questions of it on its own terms. In conservation biology, for instance, we often think of small populations as imperiled because of inbreeding. Without sufficient genetic variation, the argument goes, recessive genetic diseases that would be “masked” by dominant gene copies of healthy versions of traits can run rampant. To combat this, wildlife biologists often augment isolated populations with individuals from larger, healthier populations elsewhere.

Yet as one of my favorite recent studies discovered, this tactic doesn’t always work, because large “source” populations may have more harmful gene copies in the first place. These harmful gene copies can then be exposed by inbreeding when mating choices are limited. The study’s breakthrough came from first treating the world of small populations as operating differently from the world of large populations, and then trying to figure out how and why. I wish it were an easier approach to emulate.