ROS stress resets circadian clocks to coordinate pro-survival signals
Dysfunction of circadian clocks exacerbates various diseases, in part likely due to impaired stress resistance. It is unclear how circadian clock system responds toward critical stresses, to evoke life-protective adaptation. We identified a reactive oxygen species (ROS), H2O2 -responsive circadian p...
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creator | Tamaru, Teruya Hattori, Mitsuru Ninomiya, Yasuharu Kawamura, Genki Varès, Guillaume Honda, Kousuke Mishra, Durga Prasad Wang, Bing Benjamin, Ivor Sassone-Corsi, Paolo Ozawa, Takeaki Takamatsu, Ken |
description | Dysfunction of circadian clocks exacerbates various diseases, in part likely due to impaired stress resistance. It is unclear how circadian clock system responds toward critical stresses, to evoke life-protective adaptation. We identified a reactive oxygen species (ROS), H2O2 -responsive circadian pathway in mammals. Near-lethal doses of ROS-induced critical oxidative stress (cOS) at the branch point of life and death resets circadian clocks, synergistically evoking protective responses for cell survival. The cOS-triggered clock resetting and pro-survival responses are mediated by transcription factor, central clock-regulatory BMAL1 and heat shock stress-responsive (HSR) HSF1. Casein kinase II (CK2) -mediated phosphorylation regulates dimerization and function of BMAL1 and HSF1 to control the cOS-evoked responses. The core cOS-responsive transcriptome includes CK2-regulated crosstalk between the circadian, HSR, NF-kappa-B-mediated anti-apoptotic, and Nrf2-mediated anti-oxidant pathways. This novel circadian-adaptive signaling system likely plays fundamental protective roles in various ROS-inducible disorders, diseases, and death. |
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It is unclear how circadian clock system responds toward critical stresses, to evoke life-protective adaptation. We identified a reactive oxygen species (ROS), H2O2 -responsive circadian pathway in mammals. Near-lethal doses of ROS-induced critical oxidative stress (cOS) at the branch point of life and death resets circadian clocks, synergistically evoking protective responses for cell survival. The cOS-triggered clock resetting and pro-survival responses are mediated by transcription factor, central clock-regulatory BMAL1 and heat shock stress-responsive (HSR) HSF1. Casein kinase II (CK2) -mediated phosphorylation regulates dimerization and function of BMAL1 and HSF1 to control the cOS-evoked responses. The core cOS-responsive transcriptome includes CK2-regulated crosstalk between the circadian, HSR, NF-kappa-B-mediated anti-apoptotic, and Nrf2-mediated anti-oxidant pathways. This novel circadian-adaptive signaling system likely plays fundamental protective roles in various ROS-inducible disorders, diseases, and death.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0082006</identifier><identifier>PMID: 24312621</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adaptive systems ; Animals ; Apoptosis ; Biological clocks ; BMAL1 protein ; Casein ; Casein kinase II ; Casein Kinase II - metabolism ; Cell cycle ; Cell Survival ; Circadian Clocks ; Circadian rhythm ; Circadian rhythms ; Cosmic rays ; Crosstalk ; Dimerization ; Feedback ; Gene expression ; Heat shock ; Heat-Shock Response ; HSF1 protein ; Hydrogen peroxide ; Kinases ; Medicine ; Metabolism ; Mice ; NIH 3T3 Cells ; Oxidative Stress ; Oxidizing agents ; Oxygen ; Phosphorylation ; Physiological aspects ; Physiology ; Proteins ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Science ; Signal Transduction ; Signaling ; Survival ; Transcriptome</subject><ispartof>PloS one, 2013-12, Vol.8 (12), p.e82006-e82006</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Tamaru et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/3.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Tamaru et al 2013 Tamaru et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c802t-4328b77fc3a5fb52d801454ee936a6dc47f502bdec87e637e45c13035dc63d1b3</citedby><cites>FETCH-LOGICAL-c802t-4328b77fc3a5fb52d801454ee936a6dc47f502bdec87e637e45c13035dc63d1b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3846904/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3846904/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24312621$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Foulkes, Nicholas S</contributor><creatorcontrib>Tamaru, Teruya</creatorcontrib><creatorcontrib>Hattori, Mitsuru</creatorcontrib><creatorcontrib>Ninomiya, Yasuharu</creatorcontrib><creatorcontrib>Kawamura, Genki</creatorcontrib><creatorcontrib>Varès, Guillaume</creatorcontrib><creatorcontrib>Honda, Kousuke</creatorcontrib><creatorcontrib>Mishra, Durga Prasad</creatorcontrib><creatorcontrib>Wang, Bing</creatorcontrib><creatorcontrib>Benjamin, Ivor</creatorcontrib><creatorcontrib>Sassone-Corsi, Paolo</creatorcontrib><creatorcontrib>Ozawa, Takeaki</creatorcontrib><creatorcontrib>Takamatsu, Ken</creatorcontrib><title>ROS stress resets circadian clocks to coordinate pro-survival signals</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Dysfunction of circadian clocks exacerbates various diseases, in part likely due to impaired stress resistance. It is unclear how circadian clock system responds toward critical stresses, to evoke life-protective adaptation. We identified a reactive oxygen species (ROS), H2O2 -responsive circadian pathway in mammals. Near-lethal doses of ROS-induced critical oxidative stress (cOS) at the branch point of life and death resets circadian clocks, synergistically evoking protective responses for cell survival. The cOS-triggered clock resetting and pro-survival responses are mediated by transcription factor, central clock-regulatory BMAL1 and heat shock stress-responsive (HSR) HSF1. Casein kinase II (CK2) -mediated phosphorylation regulates dimerization and function of BMAL1 and HSF1 to control the cOS-evoked responses. The core cOS-responsive transcriptome includes CK2-regulated crosstalk between the circadian, HSR, NF-kappa-B-mediated anti-apoptotic, and Nrf2-mediated anti-oxidant pathways. This novel circadian-adaptive signaling system likely plays fundamental protective roles in various ROS-inducible disorders, diseases, and death.</description><subject>Adaptive systems</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological clocks</subject><subject>BMAL1 protein</subject><subject>Casein</subject><subject>Casein kinase II</subject><subject>Casein Kinase II - metabolism</subject><subject>Cell cycle</subject><subject>Cell Survival</subject><subject>Circadian Clocks</subject><subject>Circadian rhythm</subject><subject>Circadian rhythms</subject><subject>Cosmic rays</subject><subject>Crosstalk</subject><subject>Dimerization</subject><subject>Feedback</subject><subject>Gene expression</subject><subject>Heat shock</subject><subject>Heat-Shock Response</subject><subject>HSF1 protein</subject><subject>Hydrogen peroxide</subject><subject>Kinases</subject><subject>Medicine</subject><subject>Metabolism</subject><subject>Mice</subject><subject>NIH 3T3 Cells</subject><subject>Oxidative Stress</subject><subject>Oxidizing agents</subject><subject>Oxygen</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - 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It is unclear how circadian clock system responds toward critical stresses, to evoke life-protective adaptation. We identified a reactive oxygen species (ROS), H2O2 -responsive circadian pathway in mammals. Near-lethal doses of ROS-induced critical oxidative stress (cOS) at the branch point of life and death resets circadian clocks, synergistically evoking protective responses for cell survival. The cOS-triggered clock resetting and pro-survival responses are mediated by transcription factor, central clock-regulatory BMAL1 and heat shock stress-responsive (HSR) HSF1. Casein kinase II (CK2) -mediated phosphorylation regulates dimerization and function of BMAL1 and HSF1 to control the cOS-evoked responses. The core cOS-responsive transcriptome includes CK2-regulated crosstalk between the circadian, HSR, NF-kappa-B-mediated anti-apoptotic, and Nrf2-mediated anti-oxidant pathways. This novel circadian-adaptive signaling system likely plays fundamental protective roles in various ROS-inducible disorders, diseases, and death.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24312621</pmid><doi>10.1371/journal.pone.0082006</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adaptive systems Animals Apoptosis Biological clocks BMAL1 protein Casein Casein kinase II Casein Kinase II - metabolism Cell cycle Cell Survival Circadian Clocks Circadian rhythm Circadian rhythms Cosmic rays Crosstalk Dimerization Feedback Gene expression Heat shock Heat-Shock Response HSF1 protein Hydrogen peroxide Kinases Medicine Metabolism Mice NIH 3T3 Cells Oxidative Stress Oxidizing agents Oxygen Phosphorylation Physiological aspects Physiology Proteins Reactive oxygen species Reactive Oxygen Species - metabolism Science Signal Transduction Signaling Survival Transcriptome |
title | ROS stress resets circadian clocks to coordinate pro-survival signals |
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