SYP22 and VAMP727 regulate BRI1 plasma membrane targeting to control plant growth in Arabidopsis

SYP22 and VAMP727 regulate BRI1 plasma membrane targeting to control plant growth in Arabidopsis
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SYP22和VAMP727调节BRI1质膜靶向控制拟南芥植物生长

DOI:
10.1111/nph.15759
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发表时间:
2019
期刊:
影响因子:
9.4
通讯作者:
Xuan Yuan Hu
Xuan Yuan Hu
中科院分区:
生物学1区
文献类型:
--
作者:
Zhang Liang;Liu Yang;Zhu Xiao Feng;Jung Jin Hee;Sun Qian;Li Tian Ya;Chen Li Jie;Duan Yu Xi;Xuan Yuan Hu

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类甾醇(BRs)是一类具有生物活性的甾体分子,可作为植物激素发挥作用. BR信号传导由质膜(PM)结合受体BRASSINOSTEROPHYSITIVE 1(BRI 1)监测,BRI 1是一种富含亮氨酸重复序列(LRR)受体样激酶(RLK)(Belkhadir & Jaillais,2015)。BR与BRI 1胞外结构域的结合启动了细胞内信号级联反应,该反应迅速传递到细胞核,最终导致BR应答基因的转录(Jaillais & Vert,2016)。BR应答基因最终有助于控制植物生长和发育的各个方面,包括根发育、细胞分裂、维管模式、器官边界发育、胁迫应答和病原体防御(Nakashita et al. 2003; Yamamoto等人,2007; Gonzalez-Garcia等人,2011年; Gendron等人,2012; Bekh-Ochir等人,2013). BR的信号传导起始于PM,BRI 1的表达对于控制许多过程至关重要。先前,已经证明BRI 1以配体非依赖性方式经历组成性内吞作用并在PM和反式高尔基体网络/早期内体(TGN/EE)之间循环(Geldner et al.,2007年)。网格蛋白衔接蛋白复合物-2(AP-2)功能的破坏导致荧光标记配体的摄取减少,BRI 1的内体库减少,并因此增强BR应答,表明网格蛋白介导的内吞作用(CME)对于BRI 1内化是必需的(Irani et al.,2012; Di Rubbo等人,2013年)。此外,植物特异性TPLATE衔接子复合物(TPC),TML蛋白,介导BRI 1内吞作用(Gadeyne et al.,2014年)。此外,高分辨率成像已经证明,富flotillin 1(Flot 1)的膜微结构域介导非组织蛋白依赖性内吞作用(CIE),并作为BRI 1从PM易位的额外调节剂(Wang et al.,2015年)。然而,CME和CIE协调调节BRI 1的机制需要进一步阐明。内吞的BRI 1通过由泛素化或ESCRT分选机制调节进入晚期内体/多泡体(LE/MVB)的管腔内囊泡(ILV)的过程易位到液泡中进行降解(Cardona-Lopez et al. 2015; Zhou等人,2018年)。最近,它被证明
Brassinosteroids (BRs) are a group of bioactive steroid molecules that act as plant hormones. BR signaling is monitored by the plasma membrane (PM)-bound receptor BRASSINOSTEROID INSENSITIVE1 (BRI1), a leucine-rich repeat (LRR) receptor-like kinase (RLK)(Belkhadir & Jaillais, 2015). Binding of BRs to the extracellular domain of BRI1 initiates an intracellular signal cascade response which is rapidly transmitted to the nucleus ultimately resulting in transcription of BR-responsive genes (Jaillais & Vert, 2016). BR responsive genes ultimately help to control various aspects of plant growth and development, including root development, cell division, vascular patterning, organ boundary development, stress response and pathogen defense (Nakashita et al., 2003; Yamamoto et al., 2007; Gonzalez-Garcia et al., 2011; Gendron et al., 2012; Bekh-Ochir et al., 2013).Signaling of BR is initiated at the PM and expression of BRI1 is critical to controlling a number of processes. Previously, it has been demonstrated that BRI1 undergoes constitutive endocytosis and cycles between the PM and trans-Golgi network/early endosome (TGN/EE) in a ligand-independent manner (Geldner et al., 2007). Disruption of clathrin adaptor protein complex-2 (AP-2) function results in decreased uptake of a fluorescently labeled ligand, decreased endosomal pool of BRI1, and consequently enhanced the BR responses, indicating that clathrin-mediated endocytosis (CME) is essential for BRI1 internalization (Irani et al., 2012; Di Rubbo et al., 2013). In addition, the plant-specific TPLATE adaptor complex (TPC), TML protein, mediates BRI1 endocytosis (Gadeyne et al., 2014). Furthermore, high-resolution imaging has demonstrated that flotillin1 (Flot1)-enriched membrane microdomains mediate cathrin-independent endocytosis (CIE) and act as an additional regulator of BRI1 translocation from the PM (Wang et al., 2015). However, the mechanism of coordinated regulation of BRI1 by CME and CIE requires further elucidation. Endocytosed BRI1 is translocated to vacuoles for degradation through a process which is regulated by ubiquitination or ESCRT sorting machinery into intraluminal vesicles (ILVs) of late endosome/multivesicular body (LE/MVB)(Cardona-Lopez et al., 2015; Zhou et al., 2018). Recently, it has been demonstrated