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Resources » Paper

Christian E Rocheleau et al. (2005) International Worm Meeting "Chromatin remodeling and RISC-like complexes cooperate with Ras signaling to specify the excretory duct cell fate"

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  • Comments on Christian E Rocheleau et al. (2005) International Worm Meeting "Chromatin remodeling and RISC-like complexes cooperate with Ras signaling to specify the excretory duct cell fate" (0)

  • Overview

    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00025483

    Christian E Rocheleau, Yelena Bernstein, & Meera V Sundaram (2005). Chromatin remodeling and RISC-like complexes cooperate with Ras signaling to specify the excretory duct cell fate presented in International Worm Meeting. Unpublished information; cite only with author permission.

    Ras signaling is required for multiple cell fate decisions during C. elegans development including specification of the excretory duct cell. Strong mutations in let-60 ras result in a distinct rod-like larval lethal phenotype due to a loss of the excretory duct cell. Mutations in Ras pathway scaffolds ksr-1 and ksr-2 display little or no rod-like lethality (<1%), but ksr-2; ksr-1 double mutants display >90% rod-like larval lethal phenotype. To identify positive regulators of Ras signaling, we are performing a RNAi screen for enhancers of ksr-1 rod-like lethality (ekls). Based on their molecular identities, most of the ekls fall into two functional groups. The first group are components of a chromatin remodeling complex; some of these are Synmuv genes that antagonize Ras signaling during vulval cell fate specification. The second group are either required for RNAi or related to genes required for RNAi; these include an Argonaute, a RNA-directed RNA Polymerase, and a Dicer-related helicase. Interestingly, one of the chromatin remodeling complex components is also required for RNAi suggesting that both groups function together to promote Ras signaling during excretory duct cell fate specification. The RISC-like complex may be distinct from that required for RNAi or miRNA function as a number of genes required for these processes are not ekl genes. The ekls may be promoting Ras signaling by affecting the chromatin state (and hence transcription) of genes in the Ras pathway or genes that are transcriptional targets of the Ras pathway. ksr-2 is an excellent candidate target because, like all the ekls tested, ksr-2 strongly enhances ksr-1 mutants, but not mutations in other components of the Ras pathway. However, this would imply that the RISC-like complex is positively regulating ksr-2.

    Affiliation:
    - Dept Genetics, Univ Pennsylvania, Philadelphia, PA.


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