Wounding activates HSFA1 to promote cellular reprogramming in Arabidopsis

In this study we identify the HEAT SHOCK FACTOR A1 (HSFA1) class of transcription factors, key regulators of the heat stress response, as a central player in wound-induced callus formation and shoot regeneration in Arabidopsis. Loss of HSFA1 function in the hsfa1abd triple mutants severely impairs cellular reprogramming, reducing callus formation from wounded hypocotyls and shoot regeneration from explants.

Conversely, overexpression of a gain-of-function HSFA1d variant markedly enhances regeneration. Time-series RNA-seq and ChIP-seq analyses revealed that HSFA1 directly activates key reprogramming regulators, WOUND-INDUCED DEDIFFERENTIATION 1 (WIND1), PLETHORA 3 (PLT3) and ZINC FINGER OF ARABIDOPSIS THALIANA 6 (ZAT6). Furthermore, we demonstrate that the HSFA1d activity is attenuated by SIZ1-mediated SUMOylation, linking post-translational modification to the regulation of wound responses.