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A Reader Asks: Can Microevolutionary Changes Add Up to Macroevolutionary Change?

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After my recent article on microevolutionary changes in lizard toepads, a reader wrote to us here to ask whether there is any real distinction between microevolution and macroevolution. It’s a reasonable question. In other words, could thousands upon thousands of small microevolutionary changes accumulate and add up to “macroevolution”? In response, I pointed out that there are good reasons to understand that many biological features cannot be built simply by adding up small changes.

I assume that if one reader took the trouble to ask about this, then others must be wondering, despite our having addressed the issue many times in the past. So please let me explain.

Darwinian evolution can work fine when one small step (e.g., a single point mutation) along an evolutionary pathway gives an advantage. The theory of intelligent design has no problem with this.

But what about cases where many steps, or many mutations, are necessary to gain some advantage? Evolutionary biologist Jerry Coyne affirms this when he states: “It is indeed true that natural selection cannot build any feature in which intermediate steps do not confer a net benefit on the organism.”1 Darwin wrote much the same thing in the Origin of Species:

If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.

For natural selection, the problem comes when a feature cannot be built through “numerous, successive, slight modifications” — that is, when a structure requires lots of mutations to be present before providing any advantage for natural selection to select.

As proponents of intelligent design show, the data suggest that many structures in biology indeed require many mutations to be present before granting an advantage.

In 2004, biochemist Michael Behe co-published a study in Protein Science with physicist David Snoke demonstrating that if multiple mutations were required to produce a functional bond between two proteins, then “the mechanism of gene duplication and point mutation alone would be ineffective because few multicellular species reach the required population sizes.”2

Writing in 2008 in the journal Genetics, Behe and Snoke’s critics tried to refute them, but failed. The critics found that, in a human population, to obtain only two simultaneous mutations via Darwinian evolution “would take > 100 million years,” which they admitted was “very unlikely to occur on a reasonable timescale.”3 It’s becoming increasingly clear that many such “multi-mutation features,” which would require multiple mutations before providing any benefit, are unlikely to be produced by unguided evolutionary mechanisms.

In a 2010 peer-reviewed study, molecular biologist Douglas Axe demonstrated the inability of Darwinian evolution to produce multi-mutation features. Axe calculated that when a “multi-mutation feature” requires more than six mutations before giving any benefit, it is unlikely to arise even in the whole history of the Earth.4 He provided empirical backing for this conclusion from experimental research he earlier published in the Journal of Molecular Biology. He found there that only one in 1074 amino-acid sequences yields a functional protein fold.5 That implies that protein folds in general are multi-mutation features, requiring many amino acids to be fixed before the assembly provides a functional advantage.

Another study by Axe and Ann Gauger found that merely converting one enzyme into a closely related enzyme — the kind of conversion that evolutionists claim can happen easily — would require a minimum of seven simultaneous changes,6 exceeding the probabilistic resources available for evolution over the Earth’s history, as calculated by Axe in his 2010 paper.4 This data imply that many biochemical features are so complex that they would require many mutations before providing any advantage to an organism, and would thus be beyond the limit of what Darwinian evolution can do.

An empirical study by Gauger and biologist Ralph Seelke similarly found that when merely two mutations along a stepwise pathway were required to restore function to a bacterial gene, even then the Darwinian mechanism failed.7 The reason the gene could not be fixed was because it got stuck on a local fitness maxima, where it was more advantageous to delete a weakly functional gene than to continue to express it in the hope that it would “find” the mutations that fixed the gene. What this means is that multiple mutations were necessary to provide an advantage, and therefore Darwinian evolution couldn’t do it.

That in turn corroborates a 2010 review paper by Michael Behe in Quarterly Review of Biology. He found that when bacteria and viruses undergo adaptations at the molecular level, they tend to lose or diminish molecular functions.8 This is because evolving an entirely new function requires many mutations before you get an advantage — something very unlikely to happen by Darwinian evolution. It’s a lot easier just to break things, which requires far fewer mutations.

The problem here, again, is that many features require multiple mutations before providing an advantage. These cannot be produced by Darwinian evolution, because intermediate stages provide no advantage and thus cannot be selected for.

And indeed, ID proponents are not the only ones who find that such features exist. Evolutionary biologist Michael Lynch writes in Proceedings of the National Academy of Sciences that Darwinian evolution fails when “multiple mutations must be acquired to confer a benefit”:

[A] broad subset of adaptations cannot be accommodated by the sequential model, most notably those in which multiple mutations must be acquired to confer a benefit. Such traits, here referred to as complex adaptations, include the origin of new protein functions involving multiresidue interactions, the emergence of multimeric enzymes, the assembly of molecular machines, the colonization and refinement of introns, and the establishment of interactions between transcription factors and their binding sites, etc. The routes by which such evolutionary novelties can be procured include sojourns through one or more deleterious intermediate states.9

Though Lynch himself is a critic of ID, this is exactly what ID proponents are saying and finding in nature.

The ID movement is producing both empirical and theoretical research showing that when multiple mutations are required before conferring any advantage on an organism, the “waiting time” for those mutations is often beyond the time available over the history of the Earth. There are good reasons to expect that random mutations cannot build many complex features we see in biology. Some non-random process that can “look ahead” and find complex advantageous features is necessary. That process is intelligent design.

References Cited

  1. Jerry Coyne, “The Great Mutator,” The New Republic (June 14, 2007).
  2. Michael Behe and David Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues,” Protein Science 13 (2004): 2651-2664.
  3. Rick Durrett and Deena Schmidt, “Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution,” Genetics 180 (2008):1501-1509.
  4. Douglas Axe, “The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations,” BIO-Complexity, 2010 (4): 1-10.
  5. Douglas Axe, “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds,” Journal of Molecular Biology, 341 (2004):1295-1315; Douglas Axe, “Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors,” Journal of Molecular Biology, 301 (2000): 585-95.
  6. Ann Gauger and Douglas Axe, “The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway,” BIO-Complexity, 2011 (1): 1-17.
  7. Ann Gauger, Stephanie Ebnet, Pamela F. Fahey, and Ralph Seelke, “Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,” BIO-Complexity, 2010 (2): 1-9.
  8. Michael Behe, “Experimental Evolution, Loss-of-Function Mutations, and the ‘First Rule of Adaptive Evolution’,” The Quarterly Review of Biology, 85(4) (December, 2010).
  9. Michael Lynch, “Scaling expectations for the time to establishment of complex adaptations,” Proceedings of the National Academy of Sciences USA, 107 (38): 16577-16582 (August 11, 2010).

Casey Luskin

Associate Director and Senior Fellow, Center for Science and Culture
Casey Luskin is a geologist and an attorney with graduate degrees in science and law, giving him expertise in both the scientific and legal dimensions of the debate over evolution. He earned his PhD in Geology from the University of Johannesburg, and BS and MS degrees in Earth Sciences from the University of California, San Diego, where he studied evolution extensively at both the graduate and undergraduate levels. His law degree is from the University of San Diego, where he focused his studies on First Amendment law, education law, and environmental law.