Heat Shock Signaling in Land Plants: From Plasma Membrane Sensing to the Transcription of Small Heat Shock Proteins.

Heat Shock Signaling in Land Plants: From Plasma Membrane Sensing to the Transcription of Small Heat Shock Proteins.
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陆地植物的热休克信号:从质膜感应到小热休克蛋白的转录。

DOI:
10.3389/fpls.2021.710801
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发表时间:
2021
影响因子:
5.6
通讯作者:
Guihur A
Guihur A
中科院分区:
生物学2区
文献类型:
--
作者:
Bourgine B;Guihur A

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热应激事件是限制作物生产力的主要因素。在夏季,陆地植物必须及时预测即将到来的温和和严酷的气温。它们通过积累保护性热休克蛋白(HSP)来做出反应,从而赋予获得的耐热性。所有生物体都会合成热休克蛋白;其中许多是受保护的监护人家庭的成员。这篇综述描述了植物温度传感、信号传导和响应方面的最新进展。我们重点介绍了从质膜通过钙通道(例如环核苷酸门控通道)感知热到热休克转录因子(HSF)激活的途径。不清楚的细胞信号会激活 HSF,而 HSF 充当重要的调节因子。特别是,HSFA 亚家族可以结合 HSP 启动子中的热激元件,并可以介导结合组蛋白的解离,从而导致 HSP 转录。尽管植物可以调节转录组、蛋白质组和代谢组来保护细胞机制,但 HSP 伴侣可以防止、使用和恢复错误折叠蛋白质的形成,从而避免热诱导的细胞死亡。值得注意的是,HSP20 家族在低温下大多受到紧密抑制,这表明昂贵的机制在不必要的条件下可能会变得有害。在此,讨论了 HSP20 在 HS 响应中的作用以及它们在非 HS 温度下可能的有害表达。
Heat stress events are major factors limiting crop productivity. During summer days, land plants must anticipate in a timely manner upcoming mild and severe temperature. They respond by accumulating protective heat-shock proteins (HSPs), conferring acquired thermotolerance. All organisms synthetize HSPs; many of which are members of the conserved chaperones families. This review describes recent advances in plant temperature sensing, signaling, and response. We highlight the pathway from heat perception by the plasma membrane through calcium channels, such as cyclic nucleotide-gated channels, to the activation of the heat-shock transcription factors (HSFs). An unclear cellular signal activates HSFs, which act as essential regulators. In particular, the HSFA subfamily can bind heat shock elements in HSP promoters and could mediate the dissociation of bound histones, leading to HSPs transcription. Although plants can modulate their transcriptome, proteome, and metabolome to protect the cellular machinery, HSP chaperones prevent, use, and revert the formation of misfolded proteins, thereby avoiding heat-induced cell death. Remarkably, the HSP20 family is mostly tightly repressed at low temperature, suggesting that a costly mechanism can become detrimental under unnecessary conditions. Here, the role of HSP20s in response to HS and their possible deleterious expression at non-HS temperatures is discussed.
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