Most angiosperms are thought to share strict maternal inheritance of both plastids and mitochondria. Exceptions have been described and analysed, especially for plastids. However, the lack of phenotypic markers and the use of RFLPs on small samples may have biased the prevailing view of organelle inheritance by underestimating the occurrence of low-frequency paternal transmission of organelles. According to Muller's Ratchet, some recombination among organelle genomes is required, which would necessitate at least occasional biparental transmission. Uniparental inheritance can reduce the spread of selfish genetic elements and maintain good combinations of alleles. However, this does not explain why organelles transmitted by both parents have not invaded populations with uniparental inheritance. A link between outcrossing reproductive systems and the occurrence of biparental transmission suggests that plastids may play more of a genetic role in their inheritance than is usually assumed. Their prevailing non-Mendelian mode of inheritance thus remains to be convincingly explained.

Mutator genotypes with increased mutation rates may be especially important in microbial evolution if genetic adaptation is generally limited by the supply of mutations. In experimental populations of the bacterium Escherichia coli, the rate of evolutionary adaptation was proportional to the mutation supply rate only in particular circumstances of small or initially well-adapted populations. These experiments also demonstrate a "speed limit" on adaptive evolution in asexual populations, one that is independent of the mutation supply rate.

Although seed plants and multicellular animals are predominantly diploid, the prominence of diploidy varies greatly among eukaryote life cycles, and no general evolutionary advantage of diploidy has been demonstrated. By doubling the copy number of each gene, diploidy may increase the rate at which adaptive mutations are produced. However, models suggest that this does not necessarily accelerate adaptation by diploid populations. We tested model predictions regarding rates of adaptation using asexual yeast populations. Adaptive mutations were on average partially recessive. As predicted, diploidy slowed adaptation by large populations but not by small populations.

Sex is a general feature of the life cycle of eukaryotes. It is not universal, however, as many organisms seem to lack sex entirely. The widespread occurrence of sex is puzzling, both because meiotic recombination can disrupt co-adapted combinations of genes, and because it halves the potential rate of reproduction in organisms with strongly differentiated male and female gametes. Most attempts to explain the maintenance of sexuality invoke differences between parents and sexual offspring. These differences may be advantageous in novel or changing environments if new gene combinations are favoured from time to time. Sex would then serve to concentrate beneficial mutations that have arisen independently into the same line of descent. But in a stable environment sex might serve to concentrate deleterious mutations, so that they will be more effectively purged from the population by selection. We have studied the effect of sex on mean fitness in experimental populations of the budding yeast Saccharomyces cerevisiae. Our results show that sex increases mean fitness in an environment to which the populations were well adapted, but not in an environment to which new adaptation occurred, supporting the hypothesis that the advantage of sexuality lay in the removal of deleterious mutations.

The somatic accumulation of defective mitochondria causes human degenerative syndromes, senescence in fungi, and male sterility in plants. These diverse phenomena may result from conflicts between natural selection at different levels of organization. Such conflicts are fundamental to the evolution of cooperating groups, from cells to populations. We present a model in which defective mitochondrial genomes accumulate because of a within-cell replication advantage when among-cell selection for efficient respiration is relaxed. We tested the model by using experimental populations of the yeast Saccharomyces cerevisiae. We constructed yeast strains that were heteroplasmic for mitochondrial mutations that destroy the ability to respire (the petite phenotype) and followed the accumulation of mitochondrial defects in cultures with different effective population sizes. As predicted by the model, the inability to respire evolved only in small populations of S. cerevisiae, where among-cell selection favoring cells that can respire was reduced relative to within-cell selection favoring parasitic mitochondria. In a control experiment, mitochondrial point mutations that confer resistance to chloramphenicol showed no tendency to change in frequency under any culture conditions. The accumulation of some mitochondrial defects is therefore an evolutionary process, involving multiple levels of selection. The relative intensities of within-and among-cell selection may also explain the tissue specificity of human mitochondrial defects.

In small or repeatedly bottlenecked populations, mutations are expected to accumulate by genetic drift, causing fitness declines. In mutational meltdown models, such fitness declines further reduce population size, thus accelerating additional mutation accumulation and leading to extinction. Because the rate of mutation accumulation is determined partly by the mutation rate, the risk and rate of meltdown are predicted to increase with increasing mutation rate. We established 12 replicate populations of Saccharomyces cerevisiae from each of two isogenic strains whose genomewide mutation rates differ by approximately two orders of magnitude. Each population was transferred daily by a fixed dilution that resulted in an effective population size near 250. Fitness declines that reduce growth rates were expected to reduce the numbers of cells transferred after dilution, thus reducing population size and leading to mutational meltdown. Through 175 daily transfers and approximately 2900 generations, two extinctions occurred, both in populations with elevated mutation rates. For one of these populations there is direct evidence that extinction resulted from mutational meltdown: Extinction immediately followed a major fitness decline, and it recurred consistently in replicate populations reestablished from a sample frozen after this fitness decline, but not in populations founded from a predecline sample. Wild-type populations showed no trend to decrease in size and, on average, they increased in fitness.

Chromosomes exhibiting elevated levels of differentiation are termed hypervariable but no proposed mechanisms are sufficient to account for such enhanced evolutionary divergence.

There is currently limited empirical and theoretical support for the prevailing view that adaptation typically results from the fixation of many mutations, each with small phenotypic effects. Recent theoretical work suggests that, on the contrary, most of the phenotypic change during an episode of adaptation can result from the selection of a few mutations with relatively large effects. I studied the genetics of adaptation by populations of budding yeast to a culture regime of daily hundredfold dilution and transfer in a glucoselimited minimal liquid medium. A single haploid genotype isolated after 2000 generations showed a 76% fitness increase over its ancestor. This evolved haploid was crossed with its ancestor, and tetrad dissections were used to isolate a complete series of six meiotic tetrads. The Castle-Wright estimator of the number of loci at which adaptive mutations had been selected, modified to account for linkage and variation among mutations in the size of their effect, is 4.4. The estimate for a second haploid genotype, isolated from a separate population and with a fitness gain of 60%, was 2.7 loci. Backcrosses to the ancestor with the first evolved genotype support the inference that adaptation resulted primarily from two to five mutations. These backcrosses also indicated that deleterious mutations had hitchhiked with adaptive mutations in this evolved genotype.