A SPERM-SUPPLIED PRODUCT ESSENTIAL FOR INITIATION OF NORMAL EMBRYOGENESIS IN CAENORHABDITIS-ELEGANS IS ENCODED BY THE PATERNAL-EFFECT EMBRYONIC-LETHAL GENE, SPE-11
A SPERM-SUPPLIED PRODUCT ESSENTIAL FOR INITIATION OF NORMAL EMBRYOGENESIS IN CAENORHABDITIS-ELEGANS IS ENCODED BY THE PATERNAL-EFFECT EMBRYONIC-LETHAL GENE, SPE-11
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DOI:
10.1016/0012-1606(89)90138-3
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发表时间:
1989-11-01
影响因子:
2.7
通讯作者:
STROME, S
中科院分区:
文献类型:
--
作者:
HILL, DP;SHAKES, DC;STROME, S
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 for 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 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.