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J. Biol. Chem., Vol. 276, Issue 38, 35909-35916, September 21, 2001

This Article Full Text Full Text (PDF) All Versions of this Article: 276/38/35909    most recent M105779200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Raymond, K. Articles by Fauvarque, M.-O. Search for Related Content PubMed PubMed Citation Articles by Raymond, K. Articles by Fauvarque, M.-O. Social Bookmarking                      What's this?

The Rac GTPase-activating Protein RotundRacGAP Interferes with Drac1 and Dcdc42 Signalling in Drosophila melanogaster^*

Karine Raymond, Evelyne Bergeret, Marie-Claire Dagher, Rock Breton^§¶, Ruth Griffin-Shea, and Marie-Odile Fauvarque

From the  Département de Biologie Moléculaire et Structurale, CEA-CNRS-UJF, UMR 5092, 17 rue des Martyrs, Grenoble 38054, and the ^§ Institut de Biologie Structurale CEA-CNRS-UJF, UMR 5075, 41 rue J. Horowitz, Grenoble 38054, France

RhoGTPases are negatively regulated by GTPase-activating proteins (GAPs). Here we demonstrate that Drosophila RotundRacGAP is active in vitro on Drac1 and Dcdc42 but not Drho1. Similarly, in yeast, RotundRacGAP interacts specifically with Drac1 and Dcdc42, as well as with their activated V12 forms, showing a particularly strong interaction with Dcdc42V12. In the fly, lowering RotundRacGAP dosage specifically modifies eye defects induced by expressing Drac1 or Dcdc42 but not Drho1, confirming that Drac1 and Dcdc42 are indeed in vivo targets of RotundRacGAP. Furthermore, embryonic-directed expression of either RotundRacGAP, or dominant negative Drac1N17, transgenes induces similar defects in dorsal closure and inhibits Drac1-dependent cytoskeleton assembly at the leading edge. Expression of truncated forms of RotundRacGAP shows that the GAP domain of RotundRacGAP is essential for its function. Unexpectedly, transgenes encoding Drac1N17, Dcdc42N17, or RotundRacGAP do not affect the c-Jun N-terminal kinase-dependent gene expression of decapentaplegic and puckered, indicating that another Drac1-independent signal redundantly activates this pathway. Finally, in a situation where Drac1 is constitutively activated, RotundRacGAP greatly reduces the ectopic expression of decapentaplegic, possibly by negatively regulating Dcdc42.

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