Document Detail


Wolfram syndrome 1 gene negatively regulates ER stress signaling in rodent and human cells.
MedLine Citation:
PMID:  20160352     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Wolfram syndrome is an autosomal-recessive disorder characterized by insulin-dependent diabetes mellitus, caused by nonautoimmune loss of beta cells, and neurological dysfunctions. We have previously shown that mutations in the Wolfram syndrome 1 (WFS1) gene cause Wolfram syndrome and that WFS1 has a protective function against ER stress. However, it remained to be determined how WFS1 mitigates ER stress. Here we have shown in rodent and human cell lines that WFS1 negatively regulates a key transcription factor involved in ER stress signaling, activating transcription factor 6alpha (ATF6alpha), through the ubiquitin-proteasome pathway. WFS1 suppressed expression of ATF6alpha target genes and repressed ATF6alpha-mediated activation of the ER stress response element (ERSE) promoter. Moreover, WFS1 stabilized the E3 ubiquitin ligase HRD1, brought ATF6alpha to the proteasome, and enhanced its ubiquitination and proteasome-mediated degradation, leading to suppression of ER stress signaling. Consistent with these data, beta cells from WFS1-deficient mice and lymphocytes from patients with Wolfram syndrome exhibited dysregulated ER stress signaling through upregulation of ATF6alpha and downregulation of HRD1. These results reveal a role for WFS1 in the negative regulation of ER stress signaling and in the pathogenesis of diseases involving chronic, unresolvable ER stress, such as pancreatic beta cell death in diabetes.
Authors:
Sonya G Fonseca; Shinsuke Ishigaki; Christine M Oslowski; Simin Lu; Kathryn L Lipson; Rajarshi Ghosh; Emiko Hayashi; Hisamitsu Ishihara; Yoshitomo Oka; M Alan Permutt; Fumihiko Urano
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-02-15
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  120     ISSN:  1558-8238     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-04     Completed Date:  2010-03-31     Revised Date:  2012-04-25    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  744-55     Citation Subset:  AIM; IM    
Affiliation:
Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA 01605-2324, USA.
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MeSH Terms
Descriptor/Qualifier:
Activating Transcription Factor 6 / genetics,  metabolism
Animals
COS Cells
Calmodulin-Binding Proteins / genetics,  metabolism*
Cell Line, Tumor
Cercopithecus aethiops
Endoplasmic Reticulum / genetics,  metabolism,  pathology
Gene Expression Regulation / genetics
Humans
Insulin-Secreting Cells / metabolism*,  pathology
Membrane Proteins / genetics,  metabolism*
Mice
Proteasome Endopeptidase Complex / genetics,  metabolism
Rats
Signal Transduction*
Trans-Activators / genetics,  metabolism
Ubiquitin / genetics,  metabolism
Ubiquitin-Protein Ligases / genetics,  metabolism
Ubiquitination / genetics
Unfolded Protein Response*
Wolfram Syndrome / genetics,  metabolism*,  pathology
Grant Support
ID/Acronym/Agency:
5 P30 DK32520/DK/NIDDK NIH HHS; R01 DK067493/DK/NIDDK NIH HHS; R01 DK067493/DK/NIDDK NIH HHS; R01 DK067493-07/DK/NIDDK NIH HHS; R01 DK067493-08/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/ATF6 protein, human; 0/Activating Transcription Factor 6; 0/Atf6 protein, mouse; 0/Calmodulin-Binding Proteins; 0/Membrane Proteins; 0/Trans-Activators; 0/Ubiquitin; 0/WFS1 protein, rat; 0/wolframin protein; EC 3.4.25.1/Proteasome Endopeptidase Complex; EC 6.3.2.-/HRD1 protein, mouse; EC 6.3.2.19/SYVN1 protein, human; EC 6.3.2.19/Ubiquitin-Protein Ligases; EC 6.3.2.19/synoviolin protein, rat
Comments/Corrections

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