Mutations in genes encoding extracellular matrix proteins suppress the emb-5 gastrulation defect in Caenorhabditis elegans.
The second division of the gut precursor E cells is lethally accelerated during Caenorhabditis elegans gastrulation by mutations in the emb-5 gene, which encodes a presumed nuclear protein. We have isolated suppressor mutations of the temperature-sensitive allele emb-5(hc61), screened for them among dpy and other mutations routinely used as genetic markers, and identified eight emb-5 suppressor genes. Of these eight suppressor genes, at least four encode extracellular matrix proteins, i.e., three collagens and one proteoglycan. The suppression of the emb-5 gastrulation defect seemed to require the maternal expression of the suppressors. Phenotypically, the suppressors by themselves slowed down early embryonic cell divisions and corrected the abnormal cell-division sequence of emb-5 mutant embryos. We propose an indirect stress-response mechanism to be the main cause of the suppression because: (1) none of these suppressors is specific, either to particular temperature-sensitive emb-5 alleles or to the emb-5 gene; (2) suppressible alleles of genes, reported here or elsewhere, are temperature sensitive or weak; (3) the suppression is not strong but marginal; (4) the suppression itself shows some degree of temperature dependency; and (5) none of the extracellular matrix proteins identified here is known to be expressed in oocytes or early embryos, despite the present observation that the suppression is maternal.
Nishiwaki
K
K
Fundamental Research Laboratories, NEC Corporation, Miyukigaoka, Tsukuba, Japan.
Miwa
J
J
D000483:Alleles; D000818:Animals; D017173:Caenorhabditis elegans / Q000196:embryology* / Q000235:genetics*; D029742:Caenorhabditis elegans Proteins; D002455:Cell Division / Q000235:genetics; D003094:Collagen / Q000235:genetics; D004625:Embryo, Nonmammalian / Q000502:physiology; D016326:Extracellular Matrix Proteins / Q000235:genetics* / Q000502:physiology*; D005775:Gastrula / Q000378:metabolism / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental; D005796:Genes / Q000235:genetics*; D016153:Genes, Suppressor / Q000235:genetics*; D005838:Genotype; D005934:Glucagon / Q000235:genetics; D052216:Glucagon-Like Peptide 1; D015801:Helminth Proteins / Q000235:genetics*; D018832:Molecular Chaperones / Q000502:physiology; D009154:Mutation; D010446:Peptide Fragments / Q000235:genetics; D010641:Phenotype; D011498:Protein Precursors / Q000235:genetics; D011509:Proteoglycans / Q000235:genetics; D013696:Temperature; D014157:Transcription Factors / Q000235:genetics*
D029742:Caenorhabditis elegans Proteins; C100928:Emb-5 protein, C elegans; D016326:Extracellular Matrix Proteins; D015801:Helminth Proteins; D018832:Molecular Chaperones; D010446:Peptide Fragments; D011498:Protein Precursors; D011509:Proteoglycans; D014157:Transcription Factors; D052216:Glucagon-Like Peptide 1; D003094:Collagen; D005934:Glucagon