-UVH6 regulates osmotic and heat stress tolerance by modulating transcription

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.