Shin-Hee Han ¹, Young-Joon Park¹ and Chung-Mo Park ^1,2 ,*

¹Department of Chemistry, Seoul National University, Seoul, Korea.
²Plant Genomics and Breeding Institute, Seoul National University, Seoul, Korea.

^*Corresponding author

Plants possess an astonishing capability of effectively adapting to a wide range of temperatures, ranging from freezing to near-boiling temperatures1,2. 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 integrity3,4,5. 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 repair6, 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.