©2002  by Gerard Wakefield
(This article may be copied for educational purposes only.)

"Still More Evidence for the Cost of Microevolution"

In two previous columns, [#1  #2]  I showed that microevolution (small improvements within species) does not result in new, improved life-forms, but entails a "fitness cost" by which creatures become disadvantaged in other aspects of their physiology. Fruit flies that developed resistance to parasitic wasps proved to be weaker, shorter-lived, and less able to compete for food than individuals that did not microevolve. Bumblebees that microevolved the ability to combat internal parasites experienced dramatic reductions in survival rates compared to non-microevolved bees. Birds that microevolved a greater immunity to tetanus and diphtheria produced fewer, weaker chicks than did non-microevolved birds. Humans in Africa who have microevolved a resistance to malaria have developed the painful but nonfatal disease sickle-cell anemia.

This phenomenon has even been observed in single-celled organisms. A team of French biologists cloned E. coli bacteria that had been modified to possess "mutator alleles" (gene sequences that increase the likelihood of mutation), and injected those bacteria into the intestines of germ-free mice. Also injected into the mice were wild E. coli that did not possess the increased capacity to mutate. After nine days, the "mutators" (the bacteria with the mutator alleles) outnumbered the wild germs by 800 to one (Giraud et al. 2606). This is clear evidence of microevolution at work: mutators have a distinct advantage over normal E. coli, an advantage that "depends on their ability to generate adaptive mutations" to new conditions faced in the unfamiliar environment of a mouse's intestine (Ibid. 2607).

This microevolutionary advantage, however, proved temporary. After 14 days, the number of wild E. coli caught up with the number of mutators. The biologists observed, "Once the most beneficial adaptive mutations have been generated, the advantage conferred by the mutator phenotype seems to have disappeared" (Ibid.). Even worse for the theory of macroevolution (changes allegedly resulting in brand-new species), the scientists declared "that, in addition to rare adaptive mutations, mutator bacteria rapidly accumulate numerous detrimental mutations" (Ibid.).

As it turns out, mutators accumulate mutations that cause them to lose robustness in the mouse's gut, and these mutations actually turn into DISadvantages in the natural world (Ibid. 2608). To confirm this, the researchers allowed germ-free mice to mingle freely with mice infected with mutators and with mice infected with wild E. coli. The results of the experiment showed that the wild E. coli were more efficient at colonizing the germ-free mice than were the mutators (Ibid.).

The biologists concluded, "The mouse model showed that the advantage of mutator bacteria when colonizing [a] new host [a mouse with bacteria in its gut] is due to their capacity to generate adaptive mutations rapidly, allowing them to exploit the ecosystem resources more quickly than wild-type bacteria. This advantage is reduced to little or nothing once adaptation is achieved. Moreover, if the mutation rate is not reduced…it leads progressively to loss of functions that are dispensable in the current environment BUT COMPROMISE THE LONG-TERM SURVIVAL OF MUTATOR CLONES. Our experiments also showed that bacterial migration between hosts is a potent factor in reducing the benefits of enhanced mutation rate…" (Ibid., emphasis added).

Once again, experimentation has shown that microevolution 1) does not produce a new species, and 2) carries a cost, because the microevolving creature becomes disadvantaged in one area despite being advantaged in another. The case of E. coli is exactly like the fruit flies, bumblebees, birds, and human beings discussed in earlier columns. Minor changes within species simply do not produce new species. [#4]


Giraud, Antoine, et al. (2001). "Costs and Benefits of High Mutation Rates: Adaptive Evolution of Bacteria in the Mouse Gut." Science 291, no. 5513.

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