Our research is focused on mechanisms of evolution at the gene, genomic, cellular, and phenotypic levels, with special attention being given to the roles of mutation, random genetic drift, and recombination. For these purposes, we are currently utilizing several model systems, most notably the microcrustacean Daphnia, the ciliate Paramecium, and numerous additional unicellular eukaryotes and prokaryotes. In addition, comparative analyses of completely sequenced genomes are being performed to shed light on issues concerning the origins of genomic, gene-structural, and cellular diversity. Most of our empirical work is integrated with the development and use of mathematical theory in an effort to develop a formal understanding of the constraints on the evolutionary process. Evolution is a population-level process, and the underlying philosophy of our research is that "nothing in evolution makes sense except in the light of population genetics."
As one of the few cellular traits that can be quantified across the tree of life, DNA-replication fidelity provides an excellent platform for understanding fundamental evolutionary processes. Furthermore, because mutation is the ultimate source of all genetic variation, clarifying why mutation rates vary is crucial for understanding all areas of biology. A potentially revealing hypothesis for mutation-rate evolution is that natural selection primarily operates to improve replication fidelity, with the ultimate limits to what can be achieved set by the power of random genetic drift. This drift-barrier hypothesis is consistent with comparative measures of mutation rates, provides a simple explanation for the existence of error-prone polymerases and yields a formal counter-argument to the view that selection fine-tunes gene-specific mutation rates.
Genetic drift, selection and the evolution of the mutation rate
Sexual recombination provides a powerful means for producing multi-locus genotypes with high fitness, but also has the negative side-effect of breaking apart coadaptive complexes of alleles. A great deal of theory has been developed to help explain the phylogenetic distribution of recombination, but the key biological observations for testing the various hypotheses remain to be developed. To help provide a mechanistic understanding of the causes and consequences of the loss of recombination, we are studying the microcrustacean Daphnia pulex, which consists of both sexual and asexual races of various evolutionary ages. Specific projects now include: the isolation and characterization of the genes responsible for meiosis suppression in obligate asexuals; quantification of the rate of accumulation of deleterious mutations in asexual vs. sexual lineages; estimation of the rate and tempo of allele and genotype turnover in natural populations; and the quantification of the influence of recombination on the activity of mobile genetic elements. The asexual lineages in this species complex are remarkably young (often