A direct link between BR and SA signaling: Negative regulation of TGA4 by BIN2
A direct link between BR and SA signaling: Negative regulation of TGA4 by BIN2
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BR 和 SA 信号传导之间的直接联系：BIN2 对 TGA4 的负调控
DOI：
10.1016/j.molp.2022.06.006
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发表时间：
2022
期刊：
影响因子：
27.5
通讯作者：
Mou, Zhonglin
中科院分区：
文献类型：
--
作者：
Liu, Cheng;Liu, Qingcai;Mou, Zhonglin
众所周知，植物的生长、发育和对环境胁迫的反应是通过一系列生长和防御信号分子的作用来协调的。油菜素内酯（BR）是一种调节植物生长发育的类固醇激素。BR结合并激活细胞表面BR不敏感1 (BRI1)/BRI1相关激酶1受体激酶复合体，使细胞内受体样细胞质激酶BR信号激酶1和组成型差异生长1磷酸化，进而使磷酸酶BRI1抑制因子1磷酸化。BRI1 SUPPRESSOR 1随后去磷酸化并抑制糖原合成酶激酶3样激酶BR-INSENSITIVE 2 (BIN2)， BIN2组成性地磷酸化并抑制br应答转录因子BRASSINAZOLE-RESISTANT 1和BRI1- ems -SUPPRESSOR 1，导致br介导的转录重编程（Wang et al., 2014）。在过去的几年里，BR信号通路的多个组分，包括BRI1-ASSOCIATED KINASE 1、BR signaling KINASE 1、BRASSINAZOLE-RESISTANT 1和BRI1-EMS-SUPPRESSOR 1，都与病原体相关的分子模式触发的免疫或茉莉酸介导的免疫反应有关（Chinchilla et al., 2007; Miyaji et al., 2014; Zhao et al., 2019; Liao et al., 2020）。此外，BR已被证明可诱导致病相关基因1 （PR1）基因的表达，该基因是水杨酸（SA）信号通路的标志（Divi等，2010）。最近，Kim等人（2022）发现BIN2磷酸化并抑制TGACG MOTIFBINDING FACTOR 1 （TGA1）和TGA4，这两种基本的亮氨酸拉链转录因子参与SA信号传导。这一结果揭示了BR和SA信号之间的直接联系（图1）。SA是基础免疫和全身获得性抵抗所必需的关键免疫信号分子。SA是由PR基因的非表达者（NPR）蛋白感知的（Fu and Dong, 2013）。NPR1是SA信号的关键正调控因子，作为共激活因子，通过与TGAs相互作用激活转录（Fu and Dong, 2013）。在拟南芥中，TGA家族有10个成员，分为5个支系（支系I: TGA1和TGA4，支系II: TGA2、TGA5和TGA6，支系III: TGA3和TGA7，支系IV: TGA9和TGA10，支系V: TGA8）。虽然分支I、II和III的成员都与NPR1相互作用，但它们通过不同的机制在植物免疫应答中起作用。TGA2、TGA5和TGA6转导sa诱导的信号，是系统性获得性耐药所必需的（Zhang et al., 2003）。TGA3连接细胞分裂素促进的免疫反应，并在基础免疫中发挥作用（Kesarwani et al., 2007; Choi et al., 2010）。TGA1和TGA4已被证明通过调节系统性ACQUIRED的表达来调节SA的生物合成
It is well known that plant growth, development, and response to environmental stresses are harmonized through the action of a suite of growth and defense signaling molecules. Brassinosteroid (BR) is a steroid hormone that regulates plant growth and development. BR binds to and activates the BR-INSENSITIVE 1 (BRI1)/BRI1-ASSOCIATED KINASE 1 receptor kinase complex on the cell surface to phosphorylate the intracellular receptor-like cytoplasmic kinases BR SIGNALING KINASE 1 and CONSTITUTIVE DIFFERENTIAL GROWTH 1, which in turn phosphorylate the phosphatase BRI1 SUPPRESSOR 1. BRI1 SUPPRESSOR 1 then dephosphorylates and inhibits the glycogen synthase kinase 3-like kinase BR-INSENSITIVE 2 (BIN2) that constitutively phosphorylates and suppresses the BR-responsive transcription factors BRASSINAZOLE-RESISTANT 1 and BRI1-EMS-SUPPRESSOR 1, leading to BR-mediated transcriptional reprogramming (Wang et al., 2014). In the past several years, multiple components of the BR signaling pathway, including BRI1-ASSOCIATED KINASE 1, BR SIGNALING KINASE 1, BRASSINAZOLE-RESISTANT 1, and BRI1-EMS-SUPPRESSOR 1, have been implicated in pathogen-associated molecular pattern-triggered immunity or jasmonic-acid-mediated immune responses (Chinchilla et al., 2007; Miyaji et al., 2014; Zhao et al., 2019; Liao et al., 2020). Moreover, BR has been shown to induce the expression of the PATHOGENESIS-RELATED GENE 1 (PR1) gene, a hallmark of the salicylic acid (SA) signaling pathway (Divi et al., 2010). Recently, Kim et al.(2022) showed that BIN2 phosphorylates and impedes TGACG MOTIFBINDING FACTOR 1 (TGA1) and TGA4, two basic leucine zipper transcription factors involved in SA signaling. This result unveiled a direct link between BR and SA signaling (Figure 1).SA is a key immune signaling molecule required for both basal immunity and systemic acquired resistance. SA is perceived by NONEXPRESSOR OF PR GENES (NPR) proteins (Fu and Dong, 2013). NPR1 is a key positive regulator of SA signaling, which functions as a co-activator and activates transcription through interaction with TGAs (Fu and Dong, 2013). In Arabidopsis thaliana, the TGA family has 10 members that are divided into five clades (clade I: TGA1 and TGA4; clade II: TGA2, TGA5, and TGA6; clad III: TGA3 and TGA7; clade IV: TGA9 and TGA10; and clade V: TGA8). Although members of clades I, II, and III all interact with NPR1, they function in plant immune responses through distinct mechanisms. TGA2, TGA5, and TGA6 transduce SA-induced signaling and are required for systemic acquired resistance (Zhang et al., 2003). TGA3 bridges cytokinin-promoted immune responses and plays a role in basal immunity (Kesarwani et al., 2007; Choi et al., 2010). TGA1 and TGA4 have been shown to modulate SA biosynthesis by regulating the expression of SYSTEMIC ACQUIRED