GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE232nnn/GSE232157/primaryOK200GenomicsArabidopsis thalianaGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE232157GEOGSEfalseWounding activates HSFA1 to promote cellular reprogramming in ArabidopsisMechanical injury is a primary trigger for cellular reprogramming during organ regeneration, yet the transcriptional mechanisms that link wounding to reprogramming remain poorly understood. 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. Our findings establish HSFA1 as an early transcriptional hub that integrates wound signals to activate a broad gene network that drives cellular reprogramming, thereby providing a mechanistic framework for understanding how stress-responsive transcription factors control regeneration.2026/04/22GSE232157GSM7316587GSM7316598GSM7316599GSM7316588GSM7316596GSM7316597GSM7316602GSM7316603GSM7316600GSM7316589GSM7316601GSM7316606GSM7316604GSM7316605GSM7316590GSM7316591GSM7316594GSM7316595GSM7316592GSM731659319580232157Arabidopsis thaliana