BRI1-EMS-SUPPRESSOR1 (BES1), a core transcription factor in the brassinosteroid (BR) signaling pathway, primarily regulates plant growth and development by influencing BR-regulated gene expression. Several E3 ubiquitin (Ub) ligases regulate BES1 stability, but little is known about BES1 deubiquitination, which antagonizes E3 ligase-mediated ubiquitination to maintain BES1 homeostasis. Here, we report that two Arabidopsis thaliana deubiquitinating enzymes, Ub-SPECIFIC PROTEASE (UBP) 12 and UBP13, interact with BES1. UBP12 and UBP13 removed Ub from polyubiquitinated BES1 to stabilize both phosphorylated and dephosphorylated forms of BES1. A double mutant, ubp12-2w ubp13-3, lacking UBP12 and UBP13 function showed both BR-deficient and BR-insensitive phenotypes, whereas transgenic plants overexpressing UBP12 or UBP13 exhibited an increased BR response. Expression of UBP12 and UPB13 was induced during recovery after carbon starvation, which led to BES1 accumulation and quick recovery of stressed plants. Our work thus establishes a mechanism by which UBP12 and UBP13 regulate BES1 protein abundance to enhance BR-regulated growth during recovery after carbon starvation.

中文翻译：

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去泛素化酶 UBP12 和 UBP13 通过调节拟南芥中 BES1 的稳定性来正向调节碳饥饿后的恢复。

BRI1-EMS-SUPPRESSOR1 (BES1) 是油菜素类固醇 (BR) 信号通路中的核心转录因子，主要通过影响 BR 调节的基因表达来调节植物生长和发育。几种 E3 泛素 (Ub) 连接酶调节 BES1 稳定性，但对 BES1 去泛素化知之甚少，BES1 去泛素化会拮抗 E3 连接酶介导的泛素化以维持 BES1 稳态。在这里，我们报道了两种拟南芥去泛素化酶 Ub 特异性蛋白酶 (UBP) 12 和 UBP13 与 BES1 相互作用。UBP12 和 UBP13 从多聚泛素化 BES1 中去除 Ub，以稳定 BES1 的磷酸化和去磷酸化形式。缺乏UBP12和UBP13功能的双突变体ubp12-2w ubp13-3表现出BR缺陷和BR不敏感表型，而过表达UBP12或UBP13的转基因植物则表现出增强的BR反应。UBP12和UPB13的表达在碳饥饿后的恢复过程中被诱导，从而导致BES1的积累和胁迫植物的快速恢复。因此，我们的工作建立了一种机制，UBP12和UBP13通过该机制调节BES1蛋白丰度，以增强碳饥饿后恢复期间BR调节的生长。