TaZAT11-B interacts with corepressor TaTPL-A to regulate dark-induced leaf senescence by modulating H2O2 homeostasis in wheat

Leaf senescence represents the final developmental program characterized by the catabolism of macromolecules and nutrient recycling, significantly influencing the crop’s yield potential and nutritional value. However, the molecular mechanism underlying leaf senescence regulation in wheat remains to be elucidated. In this study, we identified of a C2H2-type zinc finger protein TaZAT11-B using transcriptomics and demonstrated its role as a key regulator of leaf senescence. Silencing TaZAT11-B via virus-induced gene silencing retarded dark-induced leaf senescence, whereas overexpressing TaZAT11-B promoted dark-induced leaf senescence in wheat. TaZAT11-B localized to the nucleus and exerted transcriptional repression through its C-terminal EAR motif. TaZAT11-B was physically associated with transcriptional corepressor TaTPL-A through the EAR motif. In addition, TaZAT11-B was induced by abscisic acid (ABA) treatment and functioned as a mediator of ABA-induced leaf senescence. Furthermore, TaZAT11-B bound to the promoters of reactive oxygen species homeostasis genes TaNOX8 and TaCAT2 , thereby inhibiting their expression. Collectively, our results revealed a potential link between the ABA-mediated transcriptional induction of TaZAT11-B and the oxidant-mediated modulation of leaf senescence. • Zinc finger protein TaZAT11-B positively regulates leaf senescence in wheat. • TaZAT11-B interacts with TaTPL to repress transcription via its EAR motif. • TaZAT11-B binds TaNOX8 and TaCAT2 promoters to regulate H 2 ​O 2 ​ accumulation.