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抑制 SIZ1 介导的 HOOKLESS1 的 SUMO 化促进拟南芥中光诱导的顶端弯钩张开。

Inhibition of SIZ1-mediated SUMOylation of HOOKLESS1 promotes light-induced apical hook opening in Arabidopsis.

机构信息

Ministry of Education Key Laboratory for Bio-Resource and Eco-Environment, College of Life Science, State Key Laboratory of Hydraulics and Mountain River Engineering, Sichuan University, Chengdu 610064, P.R. China.

出版信息

Plant Cell. 2023 May 29;35(6):2027-2043. doi: 10.1093/plcell/koad072.

DOI:10.1093/plcell/koad072
PMID:36890719
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10226575/
Abstract

The apical hook protects cotyledons and the shoot apical meristem from mechanical injuries during seedling emergence from the soil. HOOKLESS1 (HLS1) is a central regulator of apical hook development, as a terminal signal onto which several pathways converge. However, how plants regulate the rapid opening of the apical hook in response to light by modulating HLS1 function remains unclear. In this study, we demonstrate that the small ubiquitin-like modifier (SUMO) E3 ligase SAP AND MIZ1 DOMAIN-CONTAINING LIGASE1 (SIZ1) interacts with HLS1 and mediates its SUMOylation in Arabidopsis thaliana. Mutating SUMO attachment sites of HLS1 results in impaired function of HLS1, indicating that HLS1 SUMOylation is essential for its function. SUMOylated HLS1 was more likely to assemble into oligomers, which are the active form of HLS1. During the dark-to-light transition, light induces rapid apical hook opening, concomitantly with a drop in SIZ1 transcript levels, resulting in lower HLS1 SUMOylation. Furthermore, ELONGATED HYPOCOTYL5 (HY5) directly binds to the SIZ1 promoter and suppresses its transcription. HY5-initiated rapid apical hook opening partially depended on HY5 inhibition of SIZ1 expression. Taken together, our study identifies a function for SIZ1 in apical hook development, providing a dynamic regulatory mechanism linking the post-translational modification of HLS1 during apical hook formation and light-induced apical hook opening.

摘要

顶端弯钩在幼苗从土壤中破土而出时,可保护子叶和茎尖分生组织免受机械损伤。HOOKLESS1(HLS1)是顶端弯钩发育的中央调控因子,是几个途径汇聚的终端信号。然而,植物如何通过调节 HLS1 功能来调控顶端弯钩对光的快速开启,目前尚不清楚。在这项研究中,我们证明了小泛素样修饰物(SUMO)E3 连接酶 SAP AND MIZ1 结构域包含连接酶 1(SIZ1)与 HLS1 相互作用,并介导拟南芥中 HLS1 的 SUMO 化。HLS1 的 SUMO 附着位点发生突变会导致 HLS1 功能受损,表明 HLS1 的 SUMO 化对于其功能是必不可少的。SUMO 化的 HLS1 更有可能组装成寡聚物,这是 HLS1 的活性形式。在暗到光的转变过程中,光诱导顶端弯钩快速打开,同时 SIZ1 转录本水平下降,导致 HLS1 的 SUMO 化降低。此外,伸长的 HY5(HY5)直接结合到 SIZ1 启动子上并抑制其转录。HY5 启动的快速顶端弯钩打开部分依赖于 HY5 对 SIZ1 表达的抑制。总之,我们的研究确定了 SIZ1 在顶端弯钩发育中的功能,提供了一个动态调节机制,将顶端弯钩形成过程中 HLS1 的翻译后修饰与光诱导的顶端弯钩打开联系起来。

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