Literature DB >> 28381586

Asexual but Not Clonal: Evolutionary Processes in Automictic Populations.

Jan Engelstädter1.   

Abstract

Many parthenogenetically reproducing animals produce offspring not clonally but through different mechanisms collectively referred to as automixis. Here, meiosis proceeds normally but is followed by a fusion of meiotic products that restores diploidy. This mechanism typically leads to a reduction in heterozygosity among the offspring compared to the mother. Following a derivation of the rate at which heterozygosity is lost at one and two loci, depending on the number of crossovers between loci and centromere, a number of models are developed to gain a better understanding of basic evolutionary processes in automictic populations. Analytical results are obtained for the expected neutral genetic variation, effective population size, mutation-selection balance, selection with overdominance, the spread of beneficial mutations, and selection on crossover rates. These results are complemented by numerical investigations elucidating how associative overdominance (two off-phase deleterious mutations at linked loci behaving like an overdominant locus) can in some cases maintain heterozygosity for prolonged times, and how clonal interference affects adaptation in automictic populations. These results suggest that although automictic populations are expected to suffer from the lack of gene shuffling with other individuals, they are nevertheless, in some respects, superior to both clonal and outbreeding sexual populations in the way they respond to beneficial and deleterious mutations. Implications for related genetic systems such as intratetrad mating, clonal reproduction, selfing, as well as different forms of mixed sexual and automictic reproduction are discussed.
Copyright © 2017 by the Genetics Society of America.

Keywords:  automixis; central fusion; mutation–selection balance; neutral genetic variation; overdominance; parthenogenesis

Mesh:

Year:  2017        PMID: 28381586      PMCID: PMC5499200          DOI: 10.1534/genetics.116.196873

Source DB:  PubMed          Journal:  Genetics        ISSN: 0016-6731            Impact factor:   4.562


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