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HOS1 激活 DNA 修复系统以增强植物的耐热性。

HOS1 activates DNA repair systems to enhance plant thermotolerance.

机构信息

Department of Chemistry, Seoul National University, Seoul, Korea.

Plant Genomics and Breeding Institute, Seoul National University, Seoul, Korea.

出版信息

Nat Plants. 2020 Dec;6(12):1439-1446. doi: 10.1038/s41477-020-00809-6. Epub 2020 Nov 16.

DOI:10.1038/s41477-020-00809-6
PMID:33199892
Abstract

Plants possess an astonishing capability of effectively adapting to a wide range of temperatures, ranging from freezing to near-boiling temperatures. Yet, heat is a critical obstacle to plant survival. The deleterious effects of heat shock on cell function include misfolding of cellular proteins, disruption of cytoskeletons and membranes, and disordering of RNA metabolism and genome integrity. Plants stimulate diverse heat shock response pathways in response to abrupt temperature increases. While it is known that stressful high temperatures disturb genome integrity by causing nucleotide modifications and strand breakages or impeding DNA repair, it is largely unexplored how plants cope with heat-induced DNA damages. Here, we demonstrated that high expression of osmotically reponsive genes 1 (HOS1) induces thermotolerance by activating DNA repair components. Thermotolerance and DNA repair capacity were substantially reduced in HOS1-deficient mutants, in which thermal induction of genes encoding DNA repair systems, such as the DNA helicase RECQ2, was markedly decreased. Notably, HOS1 proteins were thermostabilized in a heat shock factor A1/heat shock protein 90 (HSP90)-dependent manner. Our data indicate that the thermoresponsive HSP90-HOS1-RECQ2 module contributes to sustaining genome integrity during the acquisition of thermotolerance, providing a distinct molecular link between DNA repair and thermotolerance.

摘要

植物具有令人惊讶的适应广泛温度范围的能力,从冰点到接近沸点。然而,高温是植物生存的关键障碍。热休克对细胞功能的有害影响包括细胞蛋白的错误折叠、细胞骨架和膜的破坏以及 RNA 代谢和基因组完整性的紊乱。植物在应对突然的温度升高时,会刺激多种热休克反应途径。虽然已知高温胁迫通过引起核苷酸修饰和链断裂或阻碍 DNA 修复来破坏基因组完整性,但植物如何应对热诱导的 DNA 损伤在很大程度上仍未得到探索。在这里,我们证明高渗透压响应基因 1(HOS1)的高表达通过激活 DNA 修复组件诱导耐热性。在 HOS1 缺陷突变体中,耐热性和 DNA 修复能力显著降低,其中编码 DNA 修复系统的基因(如 DNA 解旋酶 RECQ2)的热诱导明显降低。值得注意的是,HOS1 蛋白以热休克因子 A1/热休克蛋白 90(HSP90)依赖性的方式热稳定化。我们的数据表明,热响应 HSP90-HOS1-RECQ2 模块有助于在获得耐热性的过程中维持基因组完整性,为 DNA 修复和耐热性之间提供了一个独特的分子联系。

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本文引用的文献

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The HOS1-PIF4/5 module controls callus formation in leaf explants.HOS1-PIF4/5 模块控制叶片外植体的愈伤组织形成。
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