Disease relevance of emo-1

• RNA interference of tropomyosin or troponin C caused sterility by inhibiting ovarian contraction that is required for expelling mature oocytes into the spermatheca where fertilization takes place, thus causing accumulation of endomitotic oocytes in the ovary [1].

High impact information on emo-1

• We propose that the emo-1 gene product acts in the transport of secreted and transmembrane proteins in C. elegans oocytes, and is necessary for both oogenesis and the coupling of ovulation with meiotic maturation [2].
• Genetic mosaic analysis using the oz1 allele indicates that emo-1(+) expression in germ cells is required for fertility [2].
• emo-1(oz1) is a member of a class of hermaphrodite sterile mutations in Caenorhabditis elegans that produce endomitotic oocytes in the gonad arm [2].
• Specifically, the strongest of these new alleles was characterized by the absence of lin-26 expression in the somatic gonad, the presence of endomitotic oocytes, decreased germline proliferation, a protruding vulva and a less penetrant absence of gonad arms [3].
• Defective ovulation can result in the formation of endomitotic oocytes in the gonad, the formation of haploid embryos, and reversals in embryonic polarity. ceh-18 mutant oocytes exhibit defects prior to nuclear envelope breakdown, suggesting that they are physiologically different from the wild type [4].

Biological context of emo-1

• To phenocopy daf-21 mutations, we impaired the daf-21 function by RNA interference (RNAi), and found that oocytes skipped the diakinesis arrest and displayed a defective diakinesis arrest, which led to the production of endomitotic oocytes with polyploid chromosomes (Emo phenotype) [5].

References