Sunday, March 12, 2006


Mutation and adaptation: the directed mutation controversy in evolutionary perspective

[Lenski & Sniegowski, Annual Review of Systematics, Nov '95]


A central tenet of evolutionary theory is that mutation is random with respect to its adaptive consequences for individual organisms; that is, the production of variation precedes and does not cause adaptation. Several recent experimental reports have challenged this tenet by suggesting that bacteria (and yeast) ''may have mechanisms for choosing which mutations will occur'' (6, p. 142). The phenomenon of nonrandom mutation claimed in these experiments was initially called ''directed mutation'' but has undergone several name changes during its brief and controversial history. The directed mutation hypothesis has not fared well; many examples of apparently directed mutation have been rejected in favor of more conventional explanations, and several reviews questioning the validity of directed mutation have appeared (53, 54, 59-61, 79, 80). Nonetheless, directed mutation has recently been reincarnated under the confusing label ''adaptive mutation'' (5, 23, 24, 27, 35, 74). Here we discuss the many experimental and conceptual problems with directed/adaptive mutation, and we argue that the most plausible molecular models proposed to explain ''adaptive mutation'' are entirely consistent with the modern Darwinian concept of adaptation by natural selection on randomly occurring variation.

In the concluding section of the paper, we discuss the importance of an informed evolutionary approach in the study of the potential adaptive significance of mutational phenomena. Knowledge of the molecular bases of mutation is increasing rapidly, but rigorous evolutionary understanding lags behind. We note that ascribing adaptive significance to mutational phenomena (for example, ''adaptive mutation'') is beset with some of the same difficulties as ascribing adaptive significance to features of whole organisms (29). We consider some examples of mutational phenomena along with possible adaptive and nonadaptive explanations. [Evolution]

Also available at:,%20ARES,%20Sniegowski%20&%20Lenski.pdf

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Directed mutation is NOT intelligent design, nor does it imply any kind of long-term planning for a goal or for conditions that have not yet appeared. It just implies that lifeforms ghange their own genome to adapt instead of waiting for random mutations and dying if the right mutations do not come. A scientific site should not conflate such different concepts just because they go under the same name. And it is wrong to call tclaim that all mutations are random "a central tenet of evolutionary theory" as if there were only one possible mechanism of evolution. The ENCODE project have shown that at least 80% of the human genome is functionally active. Some try explaining it away by claiming that most of the activity is insignificant, but that away-explanation ignores several factors. One is that reading DNA is a job done by energy-expensive reading molecules, making any major amount of meaningless DNA activity extremely unlikely. Another factor is the missing heredity: protein-coding genes can only explain a minor fraction of the heredity shown by twin studies. Some explain away discoveries of functions in non-coding DNA by claiming that they are a minority case and that the vast majority is still junk, theoretically "supporting" it by reference to limitations of how many mutations natural selection can purge per generation. But they are overlooking the fact that hereditary diseases that cannot be explained by protein-coding DNA outnumbers those that can 20 to 1. That is patently not a "minor border revision". Rather, it is a massive expansion of the amount of functionally important genome that makes directed mutations necessary to avoid that literally everybody dies from genetic diseases. A possible mechanism for the directing is that working groups of proteins "feel" when one particular protein in the group does not do its job properly, and sends a signal that triggers unscrambling of the responsible parts of the genome. Experiments that supposedly prove that mutations are random, are in fact victims of false generalizations. Those experiments are really about introducing diseases or poisons that kills too fast for the organisms to have time to direct mutations. John Cairns experiments supporting directed mutations in the 1980s, on the other hand, were about malnutrition (only giving the bacteria food they lacked the genes to digest, in this case giving E.coli only lactose to eat), which gives more time to direct mutations. Not only must there be time to signal the error and change the gene(s), there must also be time to get the production of the modified protein up and going and distribute it to the relevant working groups of proteins. Several molecules are known to interact directly with specific locations in the genome, molecules chemically resembling ones known to affect the risk of cancer when intaken more diffusely. That mechanism should be able to locally alter mutation probabilities. Mechanical changes of the structure of the DNA spiral, a known part of epigenetics, also almost certainly affects the vulnerability of the DNA by making it more or less exposed. And as shown in "Bacteria evolved way to safeguard crucial genetic material", there is evidence that mutation rates do differ between parts of the genome, falsifying the dogma of mutation rates only being able to change over the whole genome and not locally. Epigenetics crosses over from soma to germline, and the is no reason to assume that mutation-directing complaints is anyhow unable to cross with it. Weissman's so-called "barrier" is a false generalization, assuming that the stop must be between soma and germline when it may just as well be between macroanatomy and cell behavior instead. See Pure science Wiki, the pages "Self-organization" and "Inheritance of acquired characteristics".

Martin J Sallberg
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