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Regulatory mechanism of abscisic acid signaling.


ABSTRACT: Abscisic acid (ABA) is a major phytohormone that mediates the adaptation of plants to environmental stresses such as drought and regulates developmental signals such as seed maturation. Studies on ABA signaling have progressed rapidly since the recent discovery of PYR/PYL receptor proteins as soluble ABA receptors. In plant cells, the receptor receives ABA to inhibit the phosphatase activity of type 2C protein phosphatase (PP2C), which is the major negative regulator in ABA signaling. SNF1-related protein kinase 2 (SnRK2) is then released from negative regulation by PP2C, turning on ABA signals by the phosphorylation of downstream factors. Insights into the regulation of PYR/PYL receptor proteins is therefore required in order to control drought-stress tolerance in plants. This article reviews the regulatory mechanism of the ABA receptor by ABA and its selective agonist. Structural analyses of PYR/PYL receptors have clearly elucidated the mechanism of ABA perception of the receptor or the mechanism of interaction with PP2C that leads to inhibition of its phosphatase activity. Moreover, the structures of PYR/PYL receptors complexed with pyrabactin, a selective ABA agonist, have provided the structural basis of ABA agonism and antagonism.

SUBMITTER: Miyakawa T 

PROVIDER: S-EPMC5036775 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature

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Regulatory mechanism of abscisic acid signaling.

Miyakawa Takuya T   Tanokura Masaru M  

Biophysics (Nagoya-shi, Japan) 20111123


Abscisic acid (ABA) is a major phytohormone that mediates the adaptation of plants to environmental stresses such as drought and regulates developmental signals such as seed maturation. Studies on ABA signaling have progressed rapidly since the recent discovery of PYR/PYL receptor proteins as soluble ABA receptors. In plant cells, the receptor receives ABA to inhibit the phosphatase activity of type 2C protein phosphatase (PP2C), which is the major negative regulator in ABA signaling. SNF1-relat  ...[more]

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