The Caenorhabditis elegans ekl (Enhancer of ksr-1 lethality) genes include putative components of a germline small RNA pathway
Christian E Rocheleau 1*, Kevin Cullison 2, Kai Huang 2, Yelena Bernstein 2, Annina C Spilker 3 and Meera Sundaram 2
1 McGill University
2 University of Pennsylvania School of Medicine
3 Institute of Biochemistry, ETH Zurich
* To whom correspondence should be addressed. E-mail: christian.rocheleau{at}mcgill.ca.
Submitted on November 14, 2007
Revised on December 21, 2007
Accepted on 4 January 2008
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Abstract |
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A canonical Ras - ERK signaling pathway specifies the fate of the excretory duct cell during C. 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 genome-wide 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 de-ubiquitination. 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 KSR.
Key Words:
C. elegans, Ras signaling, gene expression, small RNAs
