期刊
ELIFE
卷 7, 期 -, 页码 -出版社
eLIFE SCIENCES PUBL LTD
DOI: 10.7554/eLife.35037
关键词
-
类别
资金
- China Postdoctoral Science Foundation
- National Institute on Aging [R01AG032435]
- National Institute of General Medical Sciences [R01GM117461]
- Pew Charitable Trusts
- American Diabetes Association [1-16-IBS-197]
- Alfred P. Sloan Foundation
- David and Lucile Packard Foundation
- Esther A. and Joseph Klingenstein Fund
- National Heart, Lung, and Blood Institute [R00HL116654]
How multicellular organisms respond to and are impacted by severe hypothermic stress is largely unknown. From C. elegans screens for mutants abnormally responding to cold-warming stimuli, we identify a molecular genetic pathway comprising ISY-1, a conserved uncharacterized protein, and ZIP-10, a bZIP-type transcription factor. ISY-1 gatekeeps the ZIP-10 transcriptional program by regulating the microRNA mir-60. Downstream of ISY-1 and mir-60, zip-10 levels rapidly and specifically increase upon transient cold-warming exposure. Prolonged zip-10 up-regulation induces several protease-encoding genes and promotes stress-induced organismic death, or phenoptosis, of C. elegans. zip-10 deficiency confers enhanced resistance to prolonged cold-warming stress, more prominently in adults than larvae. We conclude that the ZIP-10 genetic program mediates cold-warming response and may have evolved to promote wild-population kin selection under resource-limiting and thermal stress conditions.
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