Reactive oxygen species and temperature stresses: A delicate balance between signaling and destruction

Temperature stress can have a devastating effect on plant metabolism, disrupting cellular homeostasis, and uncoupling major physiological processes. A direct result of stress‐induced cellular changes is the enhanced accumulation of toxic compounds in cells that include reactive oxygen species (ROS)....

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Bibliographic Details
Published inPhysiologia plantarum Vol. 126; no. 1; pp. 45 - 51
Main Authors Suzuki, Nobuhiro, Mittler, Ron
Format Journal Article
LanguageEnglish
Published Oxford, UK; Malden, USA Munksgaard International Publishers 01.01.2006
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Summary:Temperature stress can have a devastating effect on plant metabolism, disrupting cellular homeostasis, and uncoupling major physiological processes. A direct result of stress‐induced cellular changes is the enhanced accumulation of toxic compounds in cells that include reactive oxygen species (ROS). Although a considerable amount of work has shown a direct link between ROS scavenging and plant tolerance to temperature stress, recent studies have shown that ROS could also play a key role in mediating important signal transduction events. Thus, ROS, such as superoxide (O2–), are produced by NADPH oxidases during abiotic stress to activate stress‐response pathways and induce defense mechanisms. The rates and cellular sites of ROS production during temperature stress could play a central role in stress perception and protection. ROS levels, as well as ROS signals, are thought to be controlled by the ROS gene network of plants. It is likely that in plants this network is interlinked with the different networks that control temperature stress acclimation and tolerance. In this review paper, we attempt to summarize some of the recent studies linking ROS and temperature stress in plants and propose a model for the involvement of ROS in temperature stress sensing and defense.
Bibliography:istex:C97F08604C096A171655578C608ACABA693A136D
ark:/67375/WNG-0XPLCV7R-F
ArticleID:PPL582
Edited by C. Guy
ObjectType-Article-2
SourceType-Scholarly Journals-1
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ObjectType-Review-1
ISSN:0031-9317
1399-3054
DOI:10.1111/j.0031-9317.2005.00582.x