Abscisic Acid Signaling Inhibits Bmssinosteroid Signaling through Dampening the Dephosphorylation of BIN2 by ABI1 and ABI2  

作　　者：Haijiao Wang Jie Tang Jing Liu Jin Hu Jingjing Liu Yuxiao Chen Zhenying Cai Xuelu Wang 

机构地区：[1]Center of Integrative Biology, College of Life Science and Technology, Huazhong Agricultural University, Wuhan 430070, China [2]State Key Laboratory of Genetic Engineering, Department of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China

出　　处：《Molecular Plant》2018年第2期315-325,共11页分子植物（英文版）

基　　金：This work was supported by Grant 2015CB910200 from the National Key Basic Research Foundation of China （to X.W.）, Grants 31430046 （to X.W.） and 31401032 （to H,W.） of the National Natural Science Foundation of China, and the Fund 2014RC002 （to X.W.）, 2662015PY0202 （to X.W.）, and 2662014PY068 and 2662017PY122 （to H.W.） of Huazhong Agricultural University,

摘　　要：Abscisic acid （ABA） and brassinosteroid （BR） antagonistically regulate many aspects of plant growth and development. Previous physiological studies have revealed that the inhibition of BR signaling by ABA is largely dependent on ABI1 and ABI2. However, the genetic and molecular basis of how ABI1 and ABI2 are involved in inhibiting BR signaling remains unclear. Although it is known that in the BR signaling pathway the ABA-BR crosstalk occurs in the downstream of BR receptor complex but upstream of BIN2 kinase, a negative regulator of BR signaling, the component that acts as the hub to directly mediate their crosstalk remains a big mystery. Here, we found that ABI1 and ABI2 interact with and dephosphorylate BIN2 to regu- late its activity toward the phosphorylation of BESl. Byin vitro mimicking ABA signal transduction, we found that ABA can promote BIN2 phosphorylation by inhibiting ABI2 through ABA receptors. RNA-sequencing analysis further demonstrated that ABA inhibits BR signaling through the ABA primary signaling components, including its receptors and ABI2, and that ABA and GSK3s co-regulate a common set of stress- responsive genes. Because BIN2 can interact with and phosphorylate SnRK2s to activate its kinase activity, our study also reveals there is a module of PP2Cs--BIN2-SnRK2s in the ABA signaling pathway. Collectively, these findings provide significant insights into how plants balance growth and survival by coordinately regu- lating the growth-promoting signaling pathway and stress responses under abiotic stresses.Abscisic acid （ABA） and brassinosteroid （BR） antagonistically regulate many aspects of plant growth and development. Previous physiological studies have revealed that the inhibition of BR signaling by ABA is largely dependent on ABI1 and ABI2. However, the genetic and molecular basis of how ABI1 and ABI2 are involved in inhibiting BR signaling remains unclear. Although it is known that in the BR signaling pathway the ABA-BR crosstalk occurs in the downstream of BR receptor complex but upstream of BIN2 kinase, a negative regulator of BR signaling, the component that acts as the hub to directly mediate their crosstalk remains a big mystery. Here, we found that ABI1 and ABI2 interact with and dephosphorylate BIN2 to regu- late its activity toward the phosphorylation of BESl. Byin vitro mimicking ABA signal transduction, we found that ABA can promote BIN2 phosphorylation by inhibiting ABI2 through ABA receptors. RNA-sequencing analysis further demonstrated that ABA inhibits BR signaling through the ABA primary signaling components, including its receptors and ABI2, and that ABA and GSK3s co-regulate a common set of stress- responsive genes. Because BIN2 can interact with and phosphorylate SnRK2s to activate its kinase activity, our study also reveals there is a module of PP2Cs--BIN2-SnRK2s in the ABA signaling pathway. Collectively, these findings provide significant insights into how plants balance growth and survival by coordinately regu- lating the growth-promoting signaling pathway and stress responses under abiotic stresses.

关 键 词：BRASSINOSTEROIDS Abscisic acid GSK3 cross-talk PHOSPHATASE 

分 类 号：Q945.3[生物学—植物学] TN911.6[电子电信—通信与信息系统]