Table 1_-UVH6 regulates osmotic and heat stress tolerance by modulating transcription.xlsx

Nucleotide excision repair (NER) is a critical mechanism for repairing DNA damage, including UV-induced lesions and chemically induced adducts. The UVH6 gene encodes a subunit of the transcription factor IIH complex and is essential for both NER and transcription initiation. In Arabidopsis thaliana, UVH6 mutations impair DNA repair, enhance UV sensitivity, and decrease heat stress tolerance. We here isolated acquired osmotolerance–defective12 (aod12) mutant derived from osmotolerant Bu-5 accession; this mutant had pale green leaves and was osmosensitive and heat sensitive. Genetic and molecular analyses revealed that a mutation in UVH6 underlies these phenotypes of aod12. RNA sequencing demonstrated that UVH6 is necessary for appropriate transcriptional responses under osmotic stress, as expression of some stress-response genes was altered in aod12. Expression of pathogenesis-related genes and cell death were increased, indicating that immune responses detrimental to osmotolerance were activated. Interestingly, UVH6-mediated osmotolerance was independent of its canonical DNA repair function, as other NER-related mutants (xpf, xpg, ercc1) were not osmosensitive. Signaling pathways involving UVR8 and SOG1 were not implicated in UVH6 mutation–induced immune responses, suggesting a novel regulatory mechanism linking transcriptional control and stress tolerance. This study highlights UVH6 as a key integrator of genome stability, transcription, and stress resilience in plants.

核苷酸切除修复（Nucleotide excision repair，NER）是修复DNA损伤的关键机制，可修复紫外线诱导的损伤与化学诱导的加合物。UVH6基因编码转录因子IIH复合物（transcription factor IIH complex）的一个亚基，对核苷酸切除修复与转录起始均至关重要。在拟南芥（Arabidopsis thaliana）中，UVH6基因突变会损伤DNA修复能力、增强紫外线敏感性并降低热胁迫耐受性。本研究从耐渗透胁迫的Bu-5种质系中分离得到获得性耐渗透缺陷12（acquired osmotolerance–defective12，aod12）突变体；该突变体叶片呈淡绿色，且对渗透胁迫与热胁迫敏感。遗传与分子分析表明，UVH6基因突变是aod12突变体上述表型的成因。RNA测序结果显示，UVH6对于渗透胁迫下的正常转录响应必不可少，因为aod12突变体中部分胁迫响应基因的表达发生了改变。病程相关基因的表达与细胞死亡水平均有所升高，表明对耐渗透胁迫不利的免疫反应被激活。有趣的是，UVH6介导的耐渗透胁迫能力与其经典的DNA修复功能相互独立，因为其他核苷酸切除修复相关突变体（xpf、xpg、ercc1）并未表现出渗透敏感性。涉及UVR8与SOG1的信号通路并未参与UVH6基因突变引发的免疫反应，这表明存在一种全新的调控机制，将转录调控与胁迫耐受性联系起来。本研究揭示UVH6是植物基因组稳定性、转录调控与胁迫抗性的关键整合因子。