Upon injury, both mammalian and plant cells activate a survival mechanism by sensing endogenous damage-associated molecular patterns (DAMPs). Plant elicitor peptides (Peps), a representative DAMP, are released from their precursors (PROPEPs; Precursors of Peps) through cleavage by metacaspases (MCs), but the control of Pep generation remains unclear. Here, we discovered that several PROPEPs in Arabidopsis thaliana are substrates for SUMOylation and that Ca²⁺ upregulates PROPEP1 SUMOylation, facilitated by the SUMO E3 ligase SAP and MIZ1 domain-containing ligase1 (SIZ1). Mutations at the SUMOylation site on PROPEP1, or at the SUMO-interacting motifs (SIMs) on its protease MC4, reduced the PROPEP1-MC4 association and PROPEP1 cleavage. Overexpression of the wild-type form, but not the SUMOylation-defective variant of PROPEP1, enhanced plant tolerance to cell wall damage. Consistently, SIZ1 contributes to PROPEP1 processing and cell wall damage responses. These findings support the idea that SUMOylation promotes PROPEP1 cleavage via MC4 and provide insights into how DAMP generation is controlled in eukaryotic cells.

中文翻译：

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SUMOylation 控制肽加工以在拟南芥中产生损伤相关的分子模式


损伤后，哺乳动物和植物细胞都通过感应内源性损伤相关分子模式 （DAMP） 来激活生存机制。植物引出肽 （Peps） 是一种具有代表性的 DAMP，从其前体 （PROPEPs;Peps 的前体），但 Pep 生成的控制仍不清楚。在这里，我们发现拟南芥中的几种 PROPEP 是 SUMOylation 的底物，并且 Ca²⁺ 在 SUMO E3 连接酶 SAP 和 MIZ1 结构域包含连接酶 1 （SIZ1） 的促进下PROPEP1 SUMOylation 上调。PROPEP1 上 SUMOylation 位点或其蛋白酶 MC4 上 SUMO 相互作用基序 （SIM） 的突变减少了 PROPEP1-MC4 结合并PROPEP1切割。野生型形式的过表达，而不是 PROPEP1 的 SUMO 化缺陷变体的过表达，增强了植物对细胞壁损伤的耐受性。SIZ1 始终有助于PROPEP1加工和细胞壁损伤反应。这些发现支持 SUMOylation 通过 MC4 促进 PROPEP1 切割的观点，并为真核细胞中如何控制 DAMP 的产生提供了见解。