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磷脂酰肌醇3-激酶在延缓茉莉酸甲酯诱导的叶片衰老中起关键作用。

A pivotal role of phosphatidylinositol 3-kinase in delaying of methyl jasmonate-induced leaf senescence.

作者信息

Liu Jian, Zhou Jun, Xing Da

机构信息

a MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University , Guangzhou , China.

出版信息

Plant Signal Behav. 2016 Jun 2;11(6):e1147642. doi: 10.1080/15592324.2016.1147642.

Abstract

Phosphatidylinositol 3-kinase (PI3K) and its product PI3P are involved in plant development and stress responses. Our recent report has suggested that down-regulation of PI3K activity accelerated leaf senescence induced by methyl jasmonate (MeJA) and suppressed the activation of vacuolar H(+)-ATPase (V-ATPase). In vitro and in vivo experiment revealed that PI3K interact with VHA-B2. The inhibition of V-ATPase activity suppressed the vacuolar acidification and enhanced the stomatal opening, thereby accelerating MeJA-induced leaf senescence. It was shown that there is close relationship between PI3K and V-ATPase. However, the factor which initiates the PI3K-V-ATPase pathway needs further improvement, and the domain of VHA-B that binds to PI3K is still not clear enough. By using the Arabidopsis and MeJA as the research model, studies have been performed to investigate the upstream regulation of PI3K and downstream function of PI3K-V-ATPase pathway in the plant senescence.

摘要

磷脂酰肌醇3激酶(PI3K)及其产物PI3P参与植物发育和胁迫反应。我们最近的报告表明,PI3K活性的下调加速了茉莉酸甲酯(MeJA)诱导的叶片衰老,并抑制了液泡H(+) -ATP酶(V-ATPase)的激活。体外和体内实验表明,PI3K与VHA-B2相互作用。V-ATPase活性的抑制抑制了液泡酸化并增强了气孔开放,从而加速了MeJA诱导的叶片衰老。结果表明,PI3K与V-ATPase之间存在密切关系。然而,启动PI3K-V-ATPase途径的因素仍需进一步研究,并且与PI3K结合的VHA-B结构域仍不够明确。以拟南芥和MeJA为研究模型,开展了研究以探究植物衰老过程中PI3K的上游调控和PI3K-V-ATPase途径的下游功能。

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