ER stress protects from retinal degeneration

作者:Mendes Cesar S; Levet Clemence; Chatelain Gilles; Dourlen Pierre; Fouillet Antoine; Dichtel Danjoy Marie Laure; Gambis Alexis; Ryoo Hyung Don; Steller Hermann; Mollereau Bertrand*
来源:The EMBO Journal, 2009, 28(9): 1296-1307.
DOI:10.1038/emboj.2009.76

摘要

The unfolded protein response (UPR) is a specific cellular process that allows the cell to cope with the overload of unfolded/misfolded proteins in the endoplasmic reticulum (ER). ER stress is commonly associated with degenerative pathologies, but its role in disease progression is still a matter for debate. Here, we found that mutations in the ER-resident chaperone, neither inactivation nor afterpotential A (NinaA), lead to mild ER stress, protecting photoreceptor neurons from various death stimuli in adult Drosophila. In addition, Drosophila S2 cultured cells, when pre-exposed to mild ER stress, are protected from H(2)O(2), cycloheximide-or ultraviolet-induced cell death. We show that a specific ER-mediated signal promotes antioxidant defences and inhibits caspase-dependent cell death. We propose that an immediate consequence of the UPR not only limits the accumulation of misfolded proteins but also protects tissues from harmful exogenous stresses. The EMBO Journal (2009) 28, 1296-1307. doi: 10.1038/emboj.2009.76; Published online 2 April 2009

  • 出版日期2009-5-6