Plants employ multiple mechanisms to cope with a constantly changing and challenging environment, including using the ubiquitin proteasome system (UPS) to alter their proteome to assist in initiating, modulating and terminating responses to stress. We previously reported that the ubiquitin ligase XBAT35.2 mediates the proteasome‐dependent degradation of Accelerated Cell Death 11 (ACD11) to promote pathogen defense. Here, we demonstrate roles for XBAT35.2 and ACD11 in abiotic stress tolerance. As seen in response to pathogen infection, abiotic stress stabilizes XBAT35.2 and the abundance of ACD11 rose consistently with increasing concentrations of abscisic acid (ABA) and salt. Surprisingly, exposure to ABA and salt increased the stability of ACD11, and the overexpression of ACD11 improves plant survival of salt and drought stress, suggesting a role for ACD11 in promoting tolerance. Prolonged exposure to high concentrations of ABA or salt resulted in ubiquitination and the proteasome‐dependent degradation of ACD11, however. The stress‐induced turnover of ACD11 requires XBAT35.2, as degradation is slowed in the absence of the E3 ubiquitin ligase. Consistent with XBAT35.2 mediating the proteasome‐dependent degradation of ACD11, the loss of E3 ubiquitin ligase function enhances the tolerance of salt and drought stress, whereas overexpression increases sensitivity. A model is presented where, upon the perception of abiotic stress, ACD11 abundance increases to promote tolerance. Meanwhile, XBAT35.2 accumulates and in turn promotes the degradation of ACD11 to attenuate the stress response. The results characterize XBAT35.2 as an E3 ubiquitin ligase with opposing roles in abiotic and biotic stress.

中文翻译：

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拟南芥RING型E3泛素连接酶XBAT35.2促进蛋白酶体依赖性ACD11降解以减弱非生物胁迫耐受性

植物采用多种机制来应对不断变化和具有挑战性的环境，包括使用泛素蛋白酶体系统（UPS）来改变其蛋白质组，以协助启动，调节和终止对胁迫的反应。我们以前曾报道过，泛素连接酶XBAT35.2介导了蛋白酶体依赖的加速细胞死亡11（ACD11）降解，以促进病原体防御。在这里，我们展示了XBAT35.2和ACD11在非生物胁迫耐受性中的作用。如对病原体感染的反应所示，非生物胁迫使XBAT35.2稳定下来，随着脱落酸（ABA）和盐浓度的增加，ACD11的丰度不断增加。令人惊讶的是，暴露于ABA和盐下可提高ACD11的稳定性，而ACD11的过表达可提高盐和干旱胁迫下的植物存活率，提示ACD11在促进耐受性中的作用。然而，长时间暴露于高浓度的ABA或盐会导致泛素化和蛋白酶体依赖性的ACD11降解。应力诱导的ACD11转换需要XBAT35.2，因为在没有E3泛素连接酶的情况下降解会减慢。与XBAT35.2介导的蛋白酶体依赖性ACD11降解相一致，E3泛素连接酶功能的丧失增强了盐和干旱胁迫的耐受性，而过表达则提高了敏感性。提出了一个模型，其中基于非生物胁迫的感知，ACD11的丰度增加以促进耐受。同时，XBAT35.2积累并进而促进ACD11的降解，从而减弱了应力响应。结果表征了XBAT35。