The ASHR3 SET-Domain Protein is a Pivotal Upstream Coordinator for Wound-Induced Callus Formation in Arabidopsis

Plants can induce callus formation at damaged tissue to replenish cellular damages and facilitate tissue regeneration. Physical wounding triggers a transcriptional signaling cascade to induce cell division for callus formation. Several transcriptional regulators involved in wound-induced callus formation have been identified, but how they are coordinated remains elusive. Here, we report that a SET-domain-containing protein, ASH1-RELATED 3 (ASHR3), acts as an upstream regulator ofARABIDOPSIS RESPONSE REGULATOR 1(ARR1),PLETHORA 3(PLT3), andWOUND-INDUCED DEDIFFERENTIATION 3(WIND3) and promotes wound-induced callus formation. Expression ofASHR3was rapidly induced by wounding, and the ASHR3 protein possibly catalyzed H3K36me3 deposition at theARR1,PLT3, andWIND3loci to activate gene expression. In support, loss-of-function mutants ofASHR3displayed reduced callus formation after wounding on hormone-free medium. Collectively, our study indicates that wounding activates a chromatin modifier, which establishes chromatin landscapes optimizing cell proliferation and reprogramming.