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

Abstract

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 of ARABIDOPSIS RESPONSE REGULATOR 1 (ARR1), PLETHORA 3 (PLT3), and WOUND-INDUCED DEDIFFERENTIATION 3 (WIND3) and promotes wound-induced callus formation. Expression of ASHR3 was rapidly induced by wounding, and the ASHR3 protein possibly catalyzed H3K36me3 deposition at the ARR1, PLT3, and WIND3 loci to activate gene expression. In support, loss-of-function mutants of ASHR3 displayed 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.