The SUMO E3 Ligase SIZ1 Negatively Regulates Shoot Regeneration
The SUMO E3 Ligase SIZ1 Negatively Regulates Shoot Regeneration
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DOI：
10.1104/pp.20.00626
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发表时间：
2020-09-01
期刊：
影响因子：
7.4
通讯作者：
Sugimoto, Keiko
中科院分区：
文献类型：
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作者：
Coleman, Duncan;Kawamura, Ayako;Sugimoto, Keiko
当植物在含有植物激素的培养基上培养时，会形成愈伤组织并再生新的器官。虽然越来越多的证据表明这些再生过程是由协调伤口反应和发育转变的转录网络控制的，但翻译后调节机制是否参与这一过程仍不清楚。在这项研究中，我们证明了含有SAP和MIZ1结构域的LIGASE1 (SIZ1)，一种E3连接酶，催化小泛素样修饰物（SUMO）附着到蛋白质上，调节拟南芥（拟南芥）伤口诱导的信号转导和器官再生。我们发现，在体外组织培养条件下，SIZ1的功能缺失突变体表现出茎分生组织的过剩，而在表达pSIZ1::SIZ1的互补系中，这种缺陷得到了恢复。RNA测序分析显示，siz1-2突变体对伤口应激表现出增强的转录反应，导致超过400个基因在受伤后立即被超诱导。其中，我们发现，在siz1突变体中，伤口诱导的去分化1 （WIND1）和WIND2水平的升高有助于增强茎再生，因为在siz1-3突变体中，显性负嵌合蛋白WIND1- srdx （SUPERMAN抑制结构域）的表达部分地挽救了这种表型。虽然SIZ1功能受损不会改变生长素诱导的愈伤组织形成和/或多能性获得相关基因的转录，但它确实会导致细胞分裂素诱导的茎部分生组织调节因子如WUSCHEL的诱导增强，促进外植体中表达WUSCHEL的灶的形成。本研究表明，SIZ1通过抑制创伤诱导的发育重编程，在一定程度上负调控茎再生。
Plants form calluses and regenerate new organs when incubated on phytohormone-containing media. While accumulating evidence suggests that these regenerative processes are governed by transcriptional networks orchestrating wound response and developmental transitions, it remains unknown if posttranslational regulatory mechanisms are involved in this process. In this study, we demonstrate that SAP AND MIZ1 DOMAIN- CONTAINING LIGASE1 (SIZ1), an E3 ligase-catalyzing attachment of the SMALL UBIQUITIN-LIKE MODIFIER (SUMO) to proteins, regulates wound-induced signal transduction and organ regeneration in Arabidopsis (Arabidopsis thaliana). We show that loss-of-function mutants for SIZ1 exhibit overproduction of shoot meristems under in vitro tissue culture conditions, while this defect is rescued in a complementation line expressing pSIZ1::SIZ1. RNA sequencing analysis revealed that siz1-2 mutants exhibit enhanced transcriptional responses to wound stress, resulting in the hyper-induction of over 400 genes immediately after wounding. Among them, we show that elevated levels of WOUND INDUCED DEDIFFERENTIATION1 (WIND1) and WIND2 contribute to the enhanced shoot regeneration observed in siz1 mutants, as expression of the dominant-negative chimeric protein WIND1-SRDX (SUPERMAN repression domain) in siz1-3 mutants partly rescues this phenotype. Although compromised SIZ1 function does not modify the transcription of genes implicated in auxin-induced callus formation and/or pluripotency acquisition, it does lead to enhanced induction of cytokinin-induced shoot meristem regulators such as WUSCHEL, promoting the formation of WUSCHEL-expressing foci in explants. This study thus suggests that SIZ1 negatively regulates shoot regeneration in part by repressing wound-induced developmental reprogramming.