A sperm-supplied product essential for initiation of normal embryogenesis in Caenorhabditis elegans is encoded by the paternal-effect embryonic-lethal gene, spe-11

Dev Biol. 1989 Nov;136(1):154-66. doi: 10.1016/0012-1606(89)90138-3.

Abstract

Loss-of-function mutations in the spe-11 gene in Caenorhabditis elegans result in a paternal-effect embryonic-lethal phenotype: fertilization of wild-type oocytes by sperm from homozygous spe-11 mutant males leads to abnormal zygotic development, whereas oocytes from homozygous spe-11 hermaphrodites when fertilized by wild-type sperm develop normally. Embryos fertilized by sperm from homozygous spe-11 worms fail to complete meiosis and show defects in eggshell formation, mitotic spindle orientation, and cytokinesis. Genetic analysis suggests that the spe-11 gene is expressed before the completion of spermatogenesis and that the wild-type locus encodes a product that is present in sperm and participates, directly or indirectly, in initiating the correct program of early events in C. elegans embryos. Such an ontogenetic role of the spe-11+ gene product in early embryogenesis distinguishes spe-11 mutations from the two paternal-effect mutations identified in Drosophila, ms(3)K81 and pal, which primarily affect chromosome behavior. Analysis of spe-11 provides the first step toward genetic dissection of the functions of the sperm in early embryogenesis in C. elegans.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Caenorhabditis / embryology*
  • Caenorhabditis / genetics
  • Cell Division
  • Cytoplasmic Granules / physiology
  • Disorders of Sex Development
  • Fertilization / physiology
  • Genes, Lethal / physiology*
  • Homozygote
  • Male
  • Meiosis
  • Microscopy, Electron
  • Mutation
  • Phenotype
  • Spermatozoa / physiology*
  • Spermatozoa / ultrastructure
  • Spindle Apparatus / physiology
  • Zygote / physiology