Why Sexual Reproduction?
In protists, for example, sexual reproduction involves conjugation (fusion of cells) and meiosis (doubling of parental DNA, recombination between homologous chromosomes, and their segregation through subsequent divisions). Asexual (mitotic) propagation is simpler and faster, taking only one round of DNA replication and cell doubling. Why then is the costly process of sex not outcompeted by mitotic division? Why sex is so widespread across the eukaryotic tree of life? Since Darwin’s time, such questions have been repeatedly posed, with no satisfactory answer so far.
Certainly meiotic recombination generates genetic variability, and sex may thereby influence “evolvability”. For example, shuffling of alleles by meiosis may create new traits that help sexuals escape parasitism or adapt faster than asexuals to heterogeneous ecological niches. Accordingly, in experiments with yeast and the alga Chlamydomonas reinhardtii, advantages of sexuals over asexuals in novel or variable environments have been identified. How does genomic shuffling influence such adaptability? The conventional Fisher–Muller hypothesis proposes that in asexuals, beneficial mutations accumulate only one at a time in separate lineages that compete with each other (by clonal interference). In contrast, in sexuals, beneficial mutations in different organisms can be brought together by mating, recombination, and cosegregation in the offspring. Sex would thereby speed evolution whenever mutation rates and population size are large enough to supply and combine many new adaptive alleles. Another view is that meiotic recombination can purge deleterious mutations by either segregating an offspring clean of deleterious parental alleles or fatally joining deleterious mutations in a daughter cell that dies and extinguishes both alleles from the population. In contrast, accumulation of deleterious mutations in clonal lines can be purged only if the population size is large enough to favor purifying selection over the ratchet of mutation accumulation.
It is further suggested that sex may influence overall genome evolution by altering its nucleotide composition, content, modular organization, size, and rates of nonreciprocal recombination between repetitive elements. Genomic redundancy is contributed mainly by transposable elements (TEs) that propagate via sex from one host to another. In contrast, sex may suppress TE spreading if purifying selection predominates. In asexuals, depending on population size, propagation of TEs may overload a host genome, leading to its extinction. The complex and ambiguous dynamics of TEs in both sexual and asexual organisms awaits a better understanding. Overall, the problem of the evolution of sex is still controversial and insufficiently supported by empirical data. This defect is evident in many experimental protocols that focus almost exclusively on comparative phenotypic adaptations of sexuals versus asexuals while disregarding actual genetic variations, in the form of DNA mutations, underlying fitness gains. This neglect is remarkable, considering that understanding genetic variability may be crucial to explaining sex. However, there is a reason for the neglect. Technology that allows detecting fine DNA variations on a genome- and population-wide scale has only recently become available. Here we propose to make use of Next Generation Sequencing to create a fine catalog of the genetic variations observed in sexual lines compared to asexual yeast populations. Learn more about our Project Goals...
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