UVH6 regulates osmotic and heat stress tolerance by modulating transcription.

Abstract

Nucleotide excision repair (NER) is a critical mechanism for repairing DNA damage, including UV-induced lesions and chemically induced adducts. The <i>UVH6</i> gene encodes a subunit of the transcription factor IIH complex and is essential for both NER and transcription initiation. In <i>Arabidopsis thaliana</i>, <i>UVH6</i> mutations impair DNA repair, enhance UV sensitivity, and decrease heat stress tolerance. We here isolated <i>acquired osmotolerance-defective12</i> (<i>aod12</i>) 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 <i>UVH6</i> underlies these phenotypes of <i>aod12</i>. RNA sequencing demonstrated that <i>UVH6</i> is necessary for appropriate transcriptional responses under osmotic stress, as expression of some stress-response genes was altered in <i>aod12</i>. 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 (<i>xpf</i>, <i>xpg</i>, <i>ercc1</i>) were not osmosensitive. Signaling pathways involving UVR8 and SOG1 were not implicated in <i>UVH6</i> 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.