The Caenorhabditis elegans ekl (enhancer of ksr-1 lethality) genes include putative components of a germline small RNA pathway

Genetics. 2008 Mar;178(3):1431-43. doi: 10.1534/genetics.107.084608. Epub 2008 Feb 3.

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).

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caenorhabditis elegans / cytology
  • Caenorhabditis elegans / enzymology
  • Caenorhabditis elegans / genetics*
  • Caenorhabditis elegans Proteins / genetics*
  • Conserved Sequence
  • Epistasis, Genetic
  • Gene Deletion
  • Genes, Helminth*
  • Germ Cells / metabolism*
  • Histone Acetyltransferases / metabolism
  • Larva
  • Models, Genetic
  • Mutation / genetics
  • Protein Kinases / metabolism
  • RNA Interference
  • RNA, Helminth / genetics*
  • RNA-Induced Silencing Complex
  • Ubiquitination
  • ras Proteins / metabolism

Substances

  • Caenorhabditis elegans Proteins
  • Ekl protein, c elegans
  • RNA, Helminth
  • RNA-Induced Silencing Complex
  • Histone Acetyltransferases
  • Protein Kinases
  • KSR-1 protein kinase
  • ras Proteins