A Biochemical Mechanism for Nonrandom Mutations and Evolution
Barbara E. Wright*
Author Affiliations
Division of Biological Sciences, The University of Montana, Missoula, Montana
Abstract
As this minireview is concerned with the importance of the environment in directing evolution, it is appropriate to remember that Lamarck was the first to clearly articulate a consistent theory of gradual evolution from the simplest of species to the most complex, culminating in the origin of mankind (71). He published his remarkable and courageous theory in 1809, the year of Darwin's birth. Unfortunately, Lamarck's major contributions have been overshadowed by his views on the inheritance of acquired characters. In fact, Darwin shared some of these same views, and even Weismann (106), the father of neo-Darwinism, decided late in his career that directed variation must be invoked to understand some phenomena, as random variation and selection alone are not a sufficient explanation (71). This minireview will describe mechanisms of mutation that are not random and can accelerate the process of evolution in specific directions. The existence of such mechanisms has been predicted by mathematicians (6) who argue that, if every mutation were really random and had to be tested against the environment for selection or rejection, there would not have been enough time to evolve the extremely complex biochemical networks and regulatory mechanisms found in organisms today. Dobzhansky (21) expressed similar views by stating “The most serious objection to the modern theory of evolution is that since mutations occur by ‘chance’ and are undirected, it is difficult to see how mutation and selection can add up to the formation of such beautifully balanced organs as, for example, the human eye.”
The most primitive kinds of cells, called progenotes by Woese (108), were undoubtedly very simple biochemically with only a few central anabolic and catabolic pathways. Wächterhäuser (103) theorizes that the earliest metabolic pathway was a reductive citric acid cycle by which carbon fixation occurred (64). At that point in time, some four billion years ago, how did the additional, more complex metabolic pathways found in even the simplest prokaryotes evolve? For that matter, how are they evolving today? As pointed out by Oparin (79), it is inconceivable that a self-reproducing unit as complicated as a nucleoprotein could suddenly arise by chance; a period of evolution through the natural selection of organic substances of ever-increasing degrees of complexity must intervene. Horowitz (40) suggests a plausible scheme by which biosynthetic pathways can evolve from the successive depletion and interconversion of related metabolites in a primitive environment, as the rich supply of organic molecules is consumed by a burgeoning population of heterotrophs. Thus, a possible scenario begins with the starvation of a self-replicating unit for its precursor, metabolite A, utilized by enzyme 1 encoded by gene 1. When metabolite A is depleted, a mutation in a copy of gene 1 gives rise to gene 2 and allows enzyme 2 to use metabolite B by converting it to metabolite A. Then metabolite B is depleted, obtained from metabolite C, and so on, as an increasingly complex biochemical pathway evolves. In fact, there are examples in which a similar series of events can actually be observed in the laboratory, for example, involving enzymes that are “borrowed” from existing pathways, via regulatory mutations, to establish new pathways (75).
The starvation conditions that may initiate a series of events such as those described above target the most relevant genes for increased rates of transcription, which in turn increase rates of mutation (111). Transcriptional activation can result from the addition of a substrate or from the removal of a repressor or an end product inhibitor. The latter mechanism, called derepression, occurs in response to starvation for an essential substrate or for an end product that represses its own synthesis by feedback inhibition. Since evolution usually occurs in response to stress (41), transcriptional activation via derepression is the main focus of this minireview.
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