Heat stress (HS), causing impairment in several physiological processes, is one of the most damaging environmental cues for plants. To counteract the harmful effects of high temperatures, plants activate complex signalling networks, indicated as HS response (HSR). Expression of heat shock proteins (HSPs) and adjustment of redox homeostasis are crucial events of HSR, required for thermotolerance. By pharmacological approaches, the involvement of cAMP in triggering plant HSR has been recently proposed. In this study, to investigate the role of cAMP in HSR signalling, tobacco BY‐2 cells overexpressing the ‘cAMP‐sponge’, a genetic tool that reduces intracellular cAMP levels, have been used. in vivo cAMP dampening increased HS susceptibility in a HSPs‐independent way. The failure in cAMP elevation during HS caused a high accumulation of reactive oxygen species, due to increased levels of respiratory burst oxidase homolog D, decreased activities of catalase and ascorbate peroxidase, as well as down‐accumulation of proteins involved in the control of redox homeostasis. In addition, cAMP deficiency impaired proteasome activity and prevented the accumulation of many proteins of ubiquitin‐proteasome system (UPS). By a large‐scale proteomic approach together with in silico analyses, these UPS proteins were identified in a specific cAMP‐dependent network of HSR.

中文翻译：

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循环AMP通过控制氧化还原稳态和泛素-蛋白酶体系统介导热应激反应。

在几个生理过程中造成损害的热应激（HS）是植物危害最大的环境线索之一。为了抵消高温的有害影响，植物激活了复杂的信号网络，表示为HS响应（HSR）。热休克蛋白（HSP）的表达和氧化还原稳态的调节是耐热性所需的HSR的关键事件。通过药理学方法，最近已经提出了cAMP参与触发植物HSR。在这项研究中，为了研究cAMP在高铁信号中的作用，使用了烟草BY-2细胞过表达'cAMP-sponge'（一种降低细胞内cAMP水平的遗传工具）的方法。体内cAMP抑制以不依赖HSP的方式增加了HS易感性。HS期间cAMP升高的失败导致了活性氧的大量积累，这是由于呼吸爆发氧化酶同系物D的水平增加，过氧化氢酶和抗坏血酸过氧化物酶的活性降低以及控制氧化还原稳态所涉及的蛋白质的积累不足所致。 。此外，cAMP缺乏会损害蛋白酶体活性，并阻止泛素-蛋白酶体系统（UPS）的许多蛋白质积聚。通过大规模蛋白质组学方法以及计算机分析，可以在特定的cAMP依赖的HSR网络中识别出这些UPS蛋白。cAMP缺乏会损害蛋白酶体活性，并阻止泛素-蛋白酶体系统（UPS）的许多蛋白质积聚。通过大规模蛋白质组学方法以及计算机分析，可以在特定的cAMP依赖的HSR网络中识别出这些UPS蛋白。cAMP缺乏会损害蛋白酶体活性，并阻止泛素-蛋白酶体系统（UPS）的许多蛋白质积聚。通过大规模蛋白质组学方法以及计算机分析，可以在特定的cAMP依赖的HSR网络中识别出这些UPS蛋白。