{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T04:41:20Z","timestamp":1791348080153,"version":"4.3.1"},"reference-count":76,"publisher":"The Company of Biologists","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2003,1,1]]},"abstract":"<jats:p>Negative regulation of receptor tyrosine kinase (RTK)\/RAS signaling pathways is important for normal development and the prevention of disease in humans. We have used a genetic screen in C. elegans to identify genes that antagonize the activity of activated LET-23, a member of the EGFR family of RTKs. We identified two loss-of-function mutations in dpy-22,previously cloned as sop-1, that promote the ability of activated LET-23 to induce ectopic vulval fates. DPY-22 is a glutamine-rich protein that is most similar to human TRAP230, a component of a transcriptional mediator complex. DPY-22 has previously been shown to regulate WNT responses through inhibition of the \u03b2-catenin-like protein BAR-1. We provide evidence that DPY-22 also inhibits RAS-dependent vulval fate specification independently of BAR-1, and probably regulates the activities of multiple transcription factors during development. Furthermore, we demonstrate that although inhibition of BAR-1-dependent gene expression has been shown to require the C-terminal glutamine-rich region, this region is dispensable for inhibition of RAS-dependent cell differentiation. Thus, the glutamine-rich region contributes to specificity of this class of mediator protein.<\/jats:p>","DOI":"10.1242\/dev.00189","type":"journal-article","created":{"date-parts":[[2002,12,16]],"date-time":"2002-12-16T21:35:24Z","timestamp":1040074524000},"page":"57-69","source":"Crossref","is-referenced-by-count":53,"title":["A component of the transcriptional mediator complex inhibits RAS-dependent vulval fate specification in<i>C. elegans<\/i>"],"prefix":"10.1242","volume":"130","author":[{"given":"Nadeem","family":"Moghal","sequence":"first","affiliation":[{"name":"Howard Hughes Medical Institute, and Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul W.","family":"Sternberg","sequence":"additional","affiliation":[{"name":"Howard Hughes Medical Institute, and Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","reference":[{"key":"2021042611423480500_REF1","doi-asserted-by":"crossref","unstructured":"Aroian, R. and Sternberg, P. 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