Abstract:
: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.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Caruso ME,Jenna S,Bouchecareilh M,Baillie DL,Boismenu D,Halawani D,Latterich M,Chevet Edoi
10.1128/MCB.02252-07subject
Has Abstractpub_date
2008-07-01 00:00:00pages
4261-74issue
13eissn
0270-7306issn
1098-5549pii
MCB.02252-07journal_volume
28pub_type
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