期刊
SCIENCE
卷 367, 期 6476, 页码 436-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaz6896
关键词
-
资金
- NIH [F32 AG051355, F31 AG060660, AG042679, AG059566]
- EMBO Long-Term Fellowship [462-2017]
- NSF [DGE1752814]
- Thomas and Stacey Siebel Foundation
- Howard Hughes Medical Institute
The ability of the nervous system to sense cellular stress and coordinate protein homeostasis is essential for organismal health. Unfortunately, stress responses that mitigate disturbances in proteostasis, such as the unfolded protein response of the endoplasmic reticulum (UPRER), become defunct with age. In this work, we expressed the constitutively active UPRER transcription factor, XBP-ls, in a subset of astrocyte-like glia, which extended the life span in Caenorhabditis elegans. Glial XBP-ls initiated a robust cell nonautonomous activation of the UPRER in distal cells and rendered animals more resistant to protein aggregation and chronic ER stress. Mutants deficient in neuropeptide processing and secretion suppressed glial cell nonautonomous induction of the UPRER and life-span extension. Thus, astrocyte-like glial cells play a role in regulating organismal ER stress resistance and longevity.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据