Q & A: Evolution Makes Do

Evolutionary biologist Andreas Wagner argues that many evolutionary innovations may have non-adaptive origins.

By | July 14, 2013

SANTA FE INSTITUTE, NICOLAS RIGHETTITraits that initially confer a selective advantage often later become beneficial in some unrelated—and often surprising—way. A classic example of a so-called pre-adaptive trait, or exaptation, is the feather, which originated for a purpose other than flight. Although numerous anecdotal examples of exaptations litter the evolutionary biology literature, it is unclear how commonplace they are. Research published today (July 14) on simulated metabolic networks, however, suggests that exaptations may in fact outnumber adaptations several-fold.

“The paper is an important effort to characterize the frequency of exaptation as an evolutionary mechanism,” Richard Blob, an evolutionary biologist at Clemson University who was not involved in the study, said in an email. “The authors have identified an effective system to begin approaching this question in a systematic way.”

Leading the research was Andreas Wagner, an evolutionary biologist at the University of Zurich, who studies evolutionary innovation across many levels of biological organization, from genes to organisms to communities. Publishing in Nature with coauthor Aditya Barve, Wagner described the ubiquity of exaptations in metabolism, one of the most critical—and ancient—systems common to all multicellular organisms. To address this question, Wagner created sophisticated simulations of thousands of metabolic networks, each with a set of chemical reactions that allow for the synthesis of biomass from one of 50 different carbon sources—glucose, for example. Reflecting real-life metabolic networks, the simulated networks were also endowed with a modest number of random chemical reactions. Wagner found that all of the networks showed exaptations for the ability to utilize other carbon sources—as many as 20 different sources in some networks.

The Scientist chatted with Wagner about exaptations, their apparent ubiquity, and what they mean for the study of evolutionary biology.

The Scientist: Where did the notion of exaptations come from?

Andreas Wagner: Stephen Jay Gould first coined the term to describe traits that may be simple by-products of other traits. Also, Darwin said in his Origin of the Species back in 1859 that organs that serve a particular purpose may have originated for a completely different purpose. So even Darwin was aware that exaptations exist, although they didn’t have that word at the time.

TS: What are your favorite examples of exaptation?

AW: The origin of feathers, which help with stabilization during flight. But they probably originated for completely different reasons such as thermal insulation or waterproofing. There are also these fascinating proteins in our eye lens called crystallins, which originated from metabolic enzymes. At high concentrations they retain transparency, allowing nature to build lenses with high refractive indices, which are well suited to focus light.

TS: How did you become interested in the transition from pre-adaptive to adaptive traits?

AW: I consider this to be the last frontier in evolutionary biology. Natural selection we’ve known about for more than 150 years. So, we know a lot about how evolutionary innovations spread through populations, but we know very little about how they originate.

TS: Can all adaptive traits be traced to an exaptive origin?

AW: I would say the answer is yes. Gould argued very much in favor that [exaptive traits are] very frequent. And he was attacked from all sides because the common wisdom was that all traits originated for the same reason that they are still being kept around today. Nowadays, most people agree that exaptations occur and are fairly frequent, but we didn’t know whether they are more frequent than regular adaptations.

TS: What conclusions can you draw from your simulations of metabolic networks?

AW: Our work shows that exaptations exceed adaptations several-fold. Mere examples of exaptations [could not] address this question. You really need this kind of systematic approach where you study a sample of all possible metabolisms and what typical properties they have.

TS: So, evolution creates a pool of possible adaptations, only a few of which are expressed at a time?

AW: Exactly. Imagine we find a novel microbe that is able to survive on some carbon source, say citrate. Reflexively, a microbiologist would say, because citrate is an important carbon source in the microbe’s environment, that this ability is an adaptation. What our work tells us is this need not be the case. This could simply be the by-product of the ability to live on some other carbon source that we may not even have identified yet.

TS: What does this mean for the field of evolutionary biology?

AW: This opens a huge can of worms for evolutionary biologists because it becomes very hard to distinguish adaptation from exaptation.

TS: Why does it matter to have a clear delineation?

AW: If exaptations are pervasive, then natural selection—which few doubt is critical for the preservation and spreading of traits—may not be that important for the origin of innovations in life’s history.


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Avatar of: James V. Kohl

James V. Kohl

Posts: 453

July 15, 2013

Thermodynamically controlled exaptations that beneift organism-level thermoregulation link the development of antibiotic resistance in E. Coli to nutrient-dependent pheromone-controlled survival of species from microbes to man via conserved molecular mechanisms. In my model, this establishes Natural Selection for nutrients as the driving force behind the exaptations that enable adaptive evolution, which is controlled by the metabolism of nutrients to species-specific pheromones. Exaptations become adaptations when the benefit to organism-level thermoregulation is fixed via chromatin remodeling and alternative splicings, but only after seemingly futile cycles of protein biosynthesis and degradation have occurred. The result of the 'futile' cycles, which actually exemplify epigenetic 'fine-tuning' at the cellular level, is de novo creation of olfactory receptor genes that enable additional receptor-mediated acquisition of the nutrient that was initially beneficial. That benefit is 'signaled' to conspecifics via nutrient-dependent species-specific pheromone production, which enables nutrient-dependent species diversification in accordance with what is known about the physiology of ecological, social, neurogenic, and socio-cognitive niche construction. The examples I used from model organisms of the epigenetic tweaking of immense gene networks via a single nutrient-dependent amino acid substitution follow, in part, from from Dr. Wagner's lead in Rapid detection of positive selection in genes and genomes through variation clusters. The examples include a human population that adaptively evolved in central China during the past ~30,000 years. Human / non-human primate orthologues can be examined in the context of how nutrients alter the microRNA / messenger RNA balance from the bottom up, and how pheromones control the 'balance' of life from the top down, as is consistent with Darwin's 'conditions of life' that precede Natural Selection.

Avatar of: mightythor


Posts: 80

July 15, 2013

What's new here besides the vocabulary?  Is this anything besides a variation on the old "mutation proposes, selection disposes"?

Avatar of: Curculio


Posts: 55

July 15, 2013

My middle ear bones can't hear you!

Avatar of: John Edser

John Edser

Posts: 24

July 15, 2013


The key points as I see them: parts of organisms are necessarily selected to work together for a singular adult organism fitness maximand (a fitness value that is without a single exception, maximised). Selecting together must also apply to so called "selfish genes" placing heritable epistasis at the centre of preadaptation. Yet, Hamilton's outdated gene centric model continues to dominate Neo Darwinism allowing competing genes to make war against the organism they only a part of. Fisher's proclamation made over a century ago, that statistical epistasis (e) is not heritable so e is to be regarded as not selectable, absolutely removed e from Hamilton's Rule removing the necessary complexity to be able to provide a credible mechanism for exaptation. The net result is that Hamilton's Inclusive Fitness model has been misused on an ongoing way as a bona fide theory. Oversimplified models of theories are not theories and cannot replace the theory they were oversimplified from.     John Edser   Moderated discussion:  sci.bio.evolution

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