The OPEN STOMATA1–SPIRAL1 module regulates microtubule stability during abscisic acid-induced stomatal closure in Arabidopsis

Author:

Wang Pan1ORCID,Qi Sijia1ORCID,Wang Xiaohong1ORCID,Dou Liru1ORCID,Jia Meng-ao2ORCID,Mao Tonglin1ORCID,Guo Yushuang2ORCID,Wang Xiangfeng1ORCID

Affiliation:

1. State Key Laboratory of Plant Physiology and Biochemistry, Department of Plant Sciences, College of Biological Sciences, China Agricultural University , Beijing 100193, China

2. Key Laboratory of Molecular Genetics, Guizhou Academy of Tobacco Science , Guiyang 550081, China

Abstract

Abstract Drought stress triggers abscisic acid (ABA) signaling in guard cells and induces stomatal closure to prevent water loss in land plants. Stomatal movement is accompanied by reorganization of the cytoskeleton. Cortical microtubules disassemble in response to ABA, which is required for stomatal closure. However, how ABA signaling regulates microtubule disassembly is unclear, and the microtubule-associated proteins (MAPs) involved in this process remain to be identified. In this study, we show that OPEN STOMATA 1 (OST1), a central component in ABA signaling, mediates microtubule disassembly during ABA-induced stomatal closure in Arabidopsis thaliana. We identified the MAP SPIRAL1 (SPR1) as the substrate of OST1. OST1 interacts with and phosphorylates SPR1 at Ser6, which promotes the disassociation of SPR1 from microtubules and facilitates microtubule disassembly. Compared with the wild type, the spr1 mutant exhibited significantly greater water loss and reduced ABA responses, including stomatal closure and microtubule disassembly in guard cells. These phenotypes were restored by introducing the phosphorylated active form of SPR1. Our findings demonstrate that SPR1 positively regulates microtubule disassembly during ABA-induced stomatal closure, which depends on OST1-mediated phosphorylation. These findings reveal a specific connection between a core component of ABA signaling and MAPs.

Funder

Natural Science Foundation of China

Key Special Program of China National Tobacco Corporation

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,Plant Science

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