J Integr Plant Biol. ›› 2021, Vol. 63 ›› Issue (6): 1161-1178.DOI: 10.1111/jipb.13096

• Plant-abiotic Interactions • Previous Articles    

TMK4 receptor kinase negatively modulates ABA signaling by phosphorylating ABI2 and enhancing its activity

Lan Li1†, Bin Li1†, Sirui Zhu1, Long Wang1, Limei Song1, Jia Chen1, Zhenhua Ming2, Xuanming Liu1*, Xiushan Li1* and Feng Yu1*   

  1. 1College of Biology, State Key Laboratory of Chemo/Biosensing and Chemometrics and Hunan Key Laboratory of Plant Functional Genomics and Developmental Regulation, Hunan University, Changsha 410082, China
    2State Key Laboratory for Conservation and Utilization of Subtropical Agro‐bioresources, College of Life Science and Technology, Guangxi University, Nanning 530004, China

    These authors contributed equally to this work.
    *Correspondences: Feng Yu (Feng_yu@hnu.edu.cn, Dr. Yu is responsible for the distribution of the materials associated with this article); Xiushan Li (lxs812_88@163.com); Xuanming Liu (xmL05@hnu.edu.cn)
  • Received:2021-03-16 Accepted:2021-03-31 Online:2021-04-03 Published:2021-06-01

Abstract: In plants, clade A type 2C protein phosphatases (PP2CAs) have emerged as major players in abscisic acid (ABA)-regulated stress responses by inhibiting protein kinase activity. However, how different internal and external environmental signals modulate the activity of PP2CAs are not well known. The transmembrane kinase (TMK) protein 4 (TMK4), one member of a previously identified receptor kinase subfamily on the plasma membrane that plays vital roles in plant cell growth, directly interacts with PP2CAs member (ABA-Insensitive 2, ABI2). tmk4 mutant is hypersensitive to ABA in both ABA-inhibited seed germination and primary root growth, indicating that TMK4 is a negative regulator in ABA signaling pathway. Further analyses indicate that TMK4 phosphorylates ABI2 at three conserved Ser residues, thus enhancing the activity of ABI2. The phosphorylation-mimic ABI2S139DS140DS266D can complement but non-phosphorylated form ABI2S139AS140AS266A cannot complement ABA hypersensitive phenotype of the loss-of-function mutant abi1-2abi2-2. This study provides a previously unidentified mechanism for positively regulating ABI2 by a plasma membrane protein kinase.

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