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ABA perception and signalling

脱落酸 生物 信号 磷酸酶 脱落 非生物胁迫 第二信使系统 细胞生物学 生物化学 信号转导 植物 基因 磷酸化
作者
Agepati S. Raghavendra,Vijay K. Gonugunta,Alexander Christmann,Erwin Grill
出处
期刊:Trends in Plant Science [Elsevier]
卷期号:15 (7): 395-401 被引量:1137
标识
DOI:10.1016/j.tplants.2010.04.006
摘要

Plant productivity is continuously challenged by pathogen attack and abiotic stress such as drought and salt stress. The phytohormone abscisic acid (ABA) is a key endogenous messenger in plants’ responses to such stresses and understanding ABA signalling is essential for improving plant performance in the future. Since the discovery of ABA as a leaf abscission- and seed dormancy-promoting sesquiterpenoid in the 1960s, our understanding of the action of the phytohormone ABA has come a long way. Recent breakthroughs in the field of ABA signalling now unfold a unique hormone perception mechanism where binding of ABA to the ABA receptors RCARs/PYR1/PYLs leads to inactivation of type 2C protein phosphatases such as ABI1 and ABI2. The protein phosphatases seem to function as coreceptors and their inactivation launches SNF1-type kinase action which targets ABA-dependent gene expression and ion channels. Plant productivity is continuously challenged by pathogen attack and abiotic stress such as drought and salt stress. The phytohormone abscisic acid (ABA) is a key endogenous messenger in plants’ responses to such stresses and understanding ABA signalling is essential for improving plant performance in the future. Since the discovery of ABA as a leaf abscission- and seed dormancy-promoting sesquiterpenoid in the 1960s, our understanding of the action of the phytohormone ABA has come a long way. Recent breakthroughs in the field of ABA signalling now unfold a unique hormone perception mechanism where binding of ABA to the ABA receptors RCARs/PYR1/PYLs leads to inactivation of type 2C protein phosphatases such as ABI1 and ABI2. The protein phosphatases seem to function as coreceptors and their inactivation launches SNF1-type kinase action which targets ABA-dependent gene expression and ion channels. ABA responsive element (ABRE) binding factors, a subfamily of bZIP transcription factor proteins, interact with the ABRE and promotes ABA-induced gene expression. Also named ABF (see below). ABA responsive promoter element, a conserved cis-element (c/tACGTggc), that allows the binding of AREB/ABF while promoting ABA-induced gene expression. ABA-responsive element binding protein, binds to ABRE and modulates gene expression. Also named ABF (see above). birch pollen allergen, coded by a member of a large family of genes, similar to those of RCAR/PYR1/PYLs. Calcineurin B-like Protein (CBL) Interacting Protein Kinases, a group of protein kinases that regulate ABA responses. Calcium-dependent Protein Kinases, positive regulators of ABA responses. inwardly-rectifying (transporting) K+ channel, essential for K+ uptake during stomatal opening. an ABA-activated protein kinase, homologue of SnRK2.2/SnRK2.3, that are positive regulators of ABA responses. The name is due to the physiological phenotype of OPEN STOMATA that is produced on the suppression of OST1 expression. protein phosphatases which fall under the category of type 2C, some members are negative regulators of ABA-induced responses. Regulatory Components of ABA Receptor/Pyrabactin Resistance Protein1/PYR-Like proteins; a family of START domain proteins; demonstrated to inhibit clade A PP2Cs, which are known to be negative regulators of ABA responses. These bind to ABA and facilitate the formation of a trimeric RCAR–ABA–PP2C complex which releases the negative regulation of ABA responses exerted by the PP2C.
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