Early Events in Plant Abiotic Stress Signaling: Interplay Between Calcium, Reactive Oxygen Species and Phytohormones

NADPH氧化酶 活性氧 细胞生物学 第二信使系统 胞浆 钙信号传导 非生物胁迫 MAPK/ERK通路 蛋白激酶A 细胞信号 质外体 生物化学 激酶 化学 生物 信号转导 细胞壁 基因 有机化学
作者
Tapan Kumar Mohanta,Tufail Bashir,Abeer Hashem,Elsayed Fathi Abd Allah,Abdul Latif Khan,Ahmed Sulaiman Al-Harrasi
出处
期刊:Journal of Plant Growth Regulation [Springer Science+Business Media]
卷期号:37 (4): 1033-1049 被引量:96
标识
DOI:10.1007/s00344-018-9833-8
摘要

Upon exposure to abiotic stresses, plants activate early stress-signaling mechanisms within a few seconds to a few hours to counter the stress responses and bring tolerance. The most versatile signaling molecules involved during the early events of abiotic stress signaling are Ca2+ (calcium ion) and reactive oxygen species (ROS), 1O2, O2−, and H2O2. Initially, apoplastic Ca2+ activates plasma membrane-bound NADPH oxidase and generates H2O2, which acts as a second messenger and further leads to the activation of downstream signaling processes. Subsequently, H2O2 activates calcium-dependent protein kinase (CDPK) and mitogen activated protein kinase (MAPK) pathways, leading to stress tolerance through downstream signaling cascades. In addition, fast influx of Ca2+ from the apoplast to the cytosol further activates cytosolic CDPKs and respiratory burst oxidase D and regulates Ca2+ and ROS signaling. Sub-cellular organelles further produce ROS and Ca2+ to bring stress tolerance. Excessive ROS produced during these processes are quenched by ROS scavenging enzymes, whereas excessive Ca2+ is neutralized by the action of the calcium binding proteins CDPKs, CaMs, CMLs, and CBLs. The phytohormone ABA further regulates the production of H2O2, thus maintaining the positive feedback system for ROS production and stress tolerance. Additionally, CBL proteins modulate H2O2 production in the presence of NADPH oxidase via interaction with CIPK, thus maintaining a positive feedback mechanism in stress tolerance. Similarly, CaM proteins bind with MAPK and regulate stress tolerance by activating the MAPK cascade.
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