Journal
PLANT PHYSIOLOGY
Volume 170, Issue 3, Pages 1714-1731Publisher
OXFORD UNIV PRESS INC
DOI: 10.1104/pp.15.00744
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Funding
- Program for Changjiang Scholars and Innovative Research Team in University [IRT0829]
- Key Program of NSFC-Guangdong Joint Funds of China [U0931005]
- National High Technology Research and Development Program of China (863 Program) [2007AA10Z204]
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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.
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