Stress effects on the reactive oxygen species-dependent regulation of plant growth and development

被引:38
|
作者
Considine, Michael J. [1 ]
Foyer, Christine H. [2 ]
机构
[1] Univ Western Australia, Sch Mol Sci, Perth, WA 6009, Australia
[2] Univ Birmingham, Sch Biosci, Coll Life & Environm Sci, Edgbaston B15 2TT, England
基金
澳大利亚研究理事会; 英国生物技术与生命科学研究理事会;
关键词
Abiotic stress; cell cycle; oxygen signalling; reactive oxygen species; root apical meristem; stem cell niche; shoot apical meristem; AXILLARY BUD OUTGROWTH; CELL-DEATH; TRANSCRIPTION FACTORS; ROOT ARCHITECTURE; REDOX REGULATION; APICAL MERISTEM; AUXIN; ABA; OXIDASE; SHOOT;
D O I
10.1093/jxb/erab265
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Plant growth is mediated by cell proliferation and expansion. Both processes are controlled by a network of endogenous factors such as phytohormones, reactive oxygen species (ROS), sugars, and other signals, which influence gene expression and post-translational regulation of proteins. Stress resilience requires rapid and appropriate responses in plant growth and development as well as defence. Regulation of ROS accumulation in different cellular compartments influences growth responses to abiotic and biotic stresses. While ROS are essential for growth, they are also implicated in the stress-induced cessation of growth and, in some cases, programmed cell death. It is widely accepted that redox post-translational modifications of key proteins determine the growth changes and cell fate responses to stress, but the molecular pathways and factors involved remain poorly characterized. Here we discuss ROS as a signalling molecule, the mechanisms of ROS-dependent regulation that influence protein-protein interactions, protein function, and turnover, together with the relocation of key proteins to different intracellular compartments in a manner that can alter cell fate. Understanding how the redox interactome responds to stress-induced increases in ROS may provide a road map to tailoring the dynamic ROS interactions that determine growth and cell fate in order to enhance stress resilience.
引用
收藏
页码:5795 / 5806
页数:12
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