title: The Caenorhabditis elegans ekl (enhancer of ksr-1 lethality) genes include putative components of a germline small RNA pathway.
abstract: A canonical Ras-ERK signaling pathway specifies the fate of the excretory duct cell during Caenorhabditis elegans embryogenesis. The paralogs ksr-1 and ksr-2 encode scaffolding proteins that facilitate signaling through this pathway and that act redundantly to promote the excretory duct fate. In a genomewide RNAi screen for genes that, like ksr-2, are required in combination with ksr-1 for the excretory duct cell fate, we identified 16 "ekl" (enhancer of ksr-1 lethality) genes that are largely maternally required and that have molecular identities suggesting roles in transcriptional or post-transcriptional gene regulation. These include the Argonaute gene csr-1 and a specific subset of other genes implicated in endogenous small RNA processes, orthologs of multiple components of the NuA4/Tip60 histone acetyltransferase and CCR4/NOT deadenylase complexes, and conserved enzymes involved in ubiquitination and deubiquitination. The identification of four small RNA regulators (csr-1, drh-3, ego-1, and ekl-1) that share the Ekl phenotype suggests that these genes define a functional pathway required for the production and/or function of particular germline small RNA(s). These small RNAs and the other ekl genes likely control the expression of one or more regulators of Ras-ERK signaling that function at or near the level of kinase suppressor of Ras (KSR).
authors.affiliation: Department of Medicine, McGill University , Montreal, Canada.
authors.forename: Christian E
authors.initials: CE
authors.lastname: Rocheleau
authors.forename: Kevin
authors.initials: K
authors.lastname: Cullison
authors.forename: Kai
authors.initials: K
authors.lastname: Huang
authors.forename: Yelena
authors.initials: Y
authors.lastname: Bernstein
authors.forename: Annina C
authors.initials: AC
authors.lastname: Spilker
authors.forename: Meera V
authors.initials: MV
authors.lastname: Sundaram
mesh_terms: D000818:Animals; D017173:Caenorhabditis elegans / Q000166:cytology / Q000201:enzymology / Q000235:genetics*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics*; D017124:Conserved Sequence; D004843:Epistasis, Genetic; D017353:Gene Deletion; D017238:Genes, Helminth; D005854:Germ Cells / Q000378:metabolism*; D051548:Histone Acetyltransferases / Q000378:metabolism; D007814:Larva; D008957:Models, Genetic; D009154:Mutation / Q000235:genetics; D011494:Protein Kinases / Q000378:metabolism; D034622:RNA Interference; D018510:RNA, Helminth / Q000235:genetics*; D034743:RNA-Induced Silencing Complex; D054875:Ubiquitination; D018631:ras Proteins / Q000378:metabolism
chemical_list: D029742:Caenorhabditis elegans Proteins; C529535:Ekl protein, c elegans; D018510:RNA, Helminth; D034743:RNA-Induced Silencing Complex; D051548:Histone Acetyltransferases; D011494:Protein Kinases; C097199:KSR-1 protein kinase; D018631:ras Proteins