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热休克恢复需要秀丽隐杆线虫中的 microRNA 途径。

Recovery from heat shock requires the microRNA pathway in Caenorhabditis elegans.

机构信息

Division of Biology, University of California, San Diego, La Jolla, California, United States of America.

Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.

出版信息

PLoS Genet. 2021 Aug 5;17(8):e1009734. doi: 10.1371/journal.pgen.1009734. eCollection 2021 Aug.

DOI:10.1371/journal.pgen.1009734
PMID:34351906
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8370650/
Abstract

The heat shock response (HSR) is a highly conserved cellular process that promotes survival during stress. A hallmark of the HSR is the rapid induction of heat shock proteins (HSPs), such as HSP-70, by transcriptional activation. Once the stress is alleviated, HSPs return to near basal levels through incompletely understood mechanisms. Here, we show that the microRNA pathway acts during heat shock recovery in Caenorhabditis elegans. Depletion of the miRNA Argonaute, Argonaute Like Gene 1 (ALG-1), after an episode of heat shock resulted in decreased survival and perdurance of high hsp-70 levels. We present evidence that regulation of hsp-70 is dependent on miR-85 and sequences in the hsp-70 3'UTR that contain target sites for this miRNA. Regulation of hsp-70 by the miRNA pathway was found to be particularly important during recovery from HS, as animals that lacked miR-85 or its target sites in the hsp-70 3'UTR overexpressed HSP-70 and exhibited reduced viability. In summary, our findings show that down-regulation of hsp-70 by miR-85 after HS promotes survival, highlighting a previously unappreciated role for the miRNA pathway during recovery from stress.

摘要

热休克反应（HSR）是一种高度保守的细胞过程，可促进应激期间的存活。HSR 的一个标志是通过转录激活快速诱导热休克蛋白（HSPs），如 HSP-70。一旦应激减轻，通过尚未完全了解的机制，HSPs 恢复到接近基础水平。在这里，我们表明 microRNA 途径在秀丽隐杆线虫的热休克恢复过程中起作用。在热休克后耗尽 miRNA Argonaute、Argonaute Like Gene 1 (ALG-1) 会导致存活能力降低和高 hsp-70 水平持续时间延长。我们提供的证据表明，hsp-70 的调节依赖于 miR-85 和 hsp-70 3'UTR 中的序列，这些序列包含该 miRNA 的靶位点。miRNA 途径对 hsp-70 的调节在 HS 恢复期间尤为重要，因为缺乏 miR-85 或其在 hsp-70 3'UTR 中的靶位点的动物过表达 HSP-70 并表现出降低的活力。总之，我们的发现表明，HS 后 miR-85 下调 hsp-70 可促进存活，突出了 miRNA 途径在应激恢复过程中的以前未被重视的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f50/8370650/5950f463ed32/pgen.1009734.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f50/8370650/ca427a810949/pgen.1009734.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f50/8370650/4e96b07e9204/pgen.1009734.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f50/8370650/288e281e0d90/pgen.1009734.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f50/8370650/5950f463ed32/pgen.1009734.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f50/8370650/ca427a810949/pgen.1009734.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f50/8370650/4e96b07e9204/pgen.1009734.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f50/8370650/288e281e0d90/pgen.1009734.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f50/8370650/5950f463ed32/pgen.1009734.g004.jpg

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