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Molecular and Cellular Biology, July 2008, p. 4261-4274, Vol. 28, No. 13
0270-7306/08/$08.00+0     doi:10.1128/MCB.02252-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

GTPase-Mediated Regulation of the Unfolded Protein Response in Caenorhabditis elegans Is Dependent on the AAA⁺ ATPase CDC-48 ^,

Marie-Elaine Caruso,¹ Sarah Jenna,^1, Marion Bouchecareilh,² David L. Baillie,³ Daniel Boismenu,⁴ Dalia Halawani,⁵ Martin Latterich,⁵ and Eric Chevet^1,2,6*

Department of Surgery, McGill University, Montreal, QC, Canada,¹ INSERM, U889, Team Avenir, Bordeaux, France,² Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC, Canada,³ McGill University and Génome Quebec Innovation Centre, Montreal, QC, Canada,⁴ Faculty of Pharmacy, University of Montreal, Montreal, QC, Canada,⁵ University Bordeaux 2, Bordeaux, France⁶

Received 20 December 2007/ Returned for modification 7 January 2008/ Accepted 10 April 2008

When endoplasmic reticulum (ER) homeostasis is perturbed, an adaptive mechanism is triggered and named the unfolded protein response (UPR). Thus far, three known UPR signaling branches (IRE-1, PERK, and ATF-6) mediate the reestablishment of ER functions but can also lead to apoptosis if ER stress is not alleviated. However, the understanding of the molecular mechanisms integrating the UPR to other ER functions, such as membrane traffic or endomembrane signaling, remains incomplete. We consequently sought to identify new regulators of UPR-dependent transcriptional mechanisms and focused on a family of proteins known to mediate, among other, ER-related functions: the small GTP-binding proteins of the RAS superfamily. To this end, we used transgenic UPR reporter Caenorhabditis elegans strains as a model to specifically silence small-GTPase expression. We show that the Rho subfamily member CRP-1 is an essential component of UPR-induced transcriptional events through its physical and genetic interactions with the AAA⁺ ATPase CDC-48. In addition, we describe a novel signaling module involving CRP-1 and CDC-48 which may directly link the UPR to DNA remodeling and transcription control.

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* Corresponding author. Mailing address: Team Avenir, INSERM U889, Université Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux, France. Phone: 33 (0)5 57 57 92 53. Fax: 33 (0)5 56 51 40 77. E-mail: eric.chevet{at}u-bordeaux2.fr

Published ahead of print on 5 May 2008.

Supplemental material for this article may be found at http://mcb.asm.org/.

Present address: Dept. of Chemistry, UQAM, Montreal, QC, Canada.

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Molecular and Cellular Biology, July 2008, p. 4261-4274, Vol. 28, No. 13
0270-7306/08/$08.00+0     doi:10.1128/MCB.02252-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

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