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Regulation of the sperm-to-oocyte transition in Caenorhabditis briggsae hermaphrodites by the Cbr-met-2 and Cbr-fem-3 genes.

Aaron L BerensonScott Everet Baird
Published in: Molecular reproduction and development (2018)
In Caenorhabditis briggsae hermaphrodites, spermatogenesis begins in the L4 larval stage and persists into early adulthood. Oogenesis begins after spermatogenesis; the sperm-to-oocyte transition is irreversible. The timing of this transition is believed to have evolved in response to selection to maximize the intrinsic growth rate. Sperm-to-oocyte transitions occurred early in Cbr-met-2 and Cbr-fem-3 mutants. These early transitions resulted in reduced brood sizes, but had little or no impact on the intrinsic growth rate. In Cbr-met-2; Cbr-fem-3 doubly mutant hermaphrodites, the transition to oogenesis occurred even earlier and brood size was further reduced, indicating that Cbr-met-2 and Cbr-fem-3 regulate the sperm-to-oocyte transition through separate pathways. Mutations in Cbr-met-2 also resulted in an increase in the frequency of males in mutant populations. These increased male frequencies were not caused by increased rates of X nondisjunction during oogenesis in mutant hermaphrodites. Rather, increases in the rates of outcrossing in mutant populations likely were an indirect effect of reduced brood sizes derived from self-fertilization. Based on these observations, it is possible that the timing of the sperm-to-oocyte transition in C. briggsae evolved in response to sexual selection on hermaphrodites to limit rates of outcrossing. Mutations in the orthologous Caenorhabditis elegans gene, Cel-met-2, did not impact the timing of the sperm-to-oocyte transition, consistent with the independent evolution of hermaphroditic reproduction in these species. Although brood sizes were reduced in Cel-met-2 mutant strains, increased male frequencies were not observed. Cbr- and Cel-met-2 mutations also differed in terms of germline mortality, observed in C. elegans, but not in C. briggsae.
Keyphrases
  • tyrosine kinase
  • wild type
  • type diabetes
  • escherichia coli
  • cardiovascular disease
  • gene expression
  • dna methylation
  • dna repair
  • genetic diversity
  • copy number
  • aedes aegypti