MUTATION, DRIFT, AND THE ORIGIN OF SUBCELLULAR FEATURES
Michael Lynch is a Distinguished Professor of Biology at Indiana University, Bloomington. He earned his Ph.D. from the University of Minnesota
Although natural selection may be the most powerful force in the biological world, it is not all powerful. As a consequence, many aspects of evolution of the molecular level can only be explained by the inability of natural selection to operate. This general principle, which explains a lot about the diversity of genome architectures across species, also appears to extend to numerous higher-level features of cells. This is surprising, as the latter is closer to the phenotype and presumably more accessible to natural selection.
Understanding the mechanisms of evolution and the degree to which phylogenetic generalities exist requires information on the rate at which mutations arise and their effects at the molecular and phenotypic levels. Information on spontaneous mutations obtained from whole-genome sequencing of mutation-accumulation lines implies an inverse scaling of the mutation rate (per nucleotide site) with the effective population size of a species, with 1000-fold differences across the Tree of Life. This pattern is thought to arise naturally as natural selection pushes the mutation rate down to a lower limit set by the power of random genetic drift rather than by intrinsic molecular limitations on repair mechanisms or by selection for an optimum mutation rate.
If this drift-barrier hypothesis is correct, the population-genetic environment imposes a fundamental constraint on the level of perfection that can be achieved by any adaptation at the molecular and cellular level. Additional examples will be drawn from recent observations on the transcription-error rate, the evolution of the multimeric states of proteins, and the bioenergetic costs of maintaining and expressing genes.