磷脂酰肌醇3激酶促进激活和液泡酸化，并延缓茉莉酸甲酯诱导的叶片衰老。
Phosphatidylinositol 3-Kinase Promotes Activation and Vacuolar Acidification and Delays Methyl Jasmonate-Induced Leaf Senescence.
作者信息
Liu Jian, Ji Yingbin, Zhou Jun, Xing Da
机构信息
MOE Key Laboratory of Laser Life Science, and Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China (J.L., Y.J., J.Z., D. X.).
出版信息
Plant Physiol. 2016 Mar;170(3):1714-31. doi: 10.1104/pp.15.00744. Epub 2016 Jan 6.
PI3K and its product PI3P are both involved in plant development and stress responses. In this study, the down-regulation of PI3K activity accelerated leaf senescence induced by methyl jasmonate (MeJA) and suppressed the activation of vacuolar H(+)-ATPase (V-ATPase). Yeast two-hybrid analyses indicated that PI3K bound to the V-ATPase B subunit (VHA-B). Analysis of bimolecular fluorescence complementation in tobacco guard cells showed that PI3K interacted with VHA-B2 in the tonoplasts. Through the use of pharmacological and genetic tools, we found that PI3K and V-ATPase promoted vacuolar acidification and stomatal closure during leaf senescence. Vacuolar acidification was suppressed by the PIKfyve inhibitor in 35S:AtVPS34-YFP Arabidopsis during MeJA-induced leaf senescence, but the decrease was lower than that in YFP-labeled Arabidopsis. These results suggest that PI3K promotes V-ATPase activation and consequently induces vacuolar acidification and stomatal closure, thereby delaying MeJA-induced leaf senescence.
磷脂酰肌醇-3激酶（PI3K）及其产物磷脂酰肌醇-3磷酸（PI3P）均参与植物发育和胁迫响应。在本研究中，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。酵母双杂交分析表明，PI3K与V-ATPase B亚基（VHA-B）结合。烟草保卫细胞中的双分子荧光互补分析表明，PI3K与液泡膜上的VHA-B2相互作用。通过药理学和遗传学手段，我们发现PI3K和V-ATPase在叶片衰老过程中促进液泡酸化和气孔关闭。在MeJA诱导的叶片衰老过程中，PIKfyve抑制剂抑制了35S:AtVPS34-YFP拟南芥中的液泡酸化，但下降幅度低于YFP标记的拟南芥。这些结果表明，PI3K促进V-ATPase激活，从而诱导液泡酸化和气孔关闭，进而延缓MeJA诱导的叶片衰老。
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