lin-35 Rb Acts in the Major Hypodermis to Oppose Ras-Mediated Vulval Induction in C. elegans
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TL;DR
The results indicate that lin-35 activity is required in the major hypodermal syncytium and not in the VPCs to inhibit vulval fates, and LIN-35 Rb may inhibit vulVal fates by regulating a signal from hyp7 to the V PCs or the physiological state of hyp7.
Abstract
Specification of vulval precursor cell (VPC) fates in C. elegans has served as an important signal transduction paradigm. Genetic studies have indicated that a large group of synthetic multivulva (SynMuv) genes, including the Rb ortholog lin-35, antagonizes the activity of the EGF receptor-Ras-MAP kinase pathway during VPC specification. A prevalent view has been that Rb-mediated transcriptional regulation and chromatin remodeling activities act in the VPCs to antagonize Ras activation through effects on promoters of target genes of the EGF receptor-Ras-MAP kinase pathway that promote vulval fates. Here, we have investigated the cellular focus of lin-35 using conventional genetic mosaic analysis and tissue-specific expression. Our results indicate that lin-35 activity is required in the major hypodermal syncytium and not in the VPCs to inhibit vulval fates. LIN-35 Rb may inhibit vulval fates by regulating a signal from hyp7 to the VPCs or the physiological state of hyp7.
