Abstract: In canonical jasmonate (JA) signaling, MYC2 activity is restrained by JA-inducible JAZ repressors that are rapidly degraded upon JA perception. However, it remains unclear how MYC2 is attenuated during prolonged developmental processes such as leaf senescence, where sustained repression is required independently of acute JA fluctuations. Here, we identify C-type cyclin 1;1 (CycC1;1) as a negative regulator of JA-induced leaf senescence in Arabidopsis. CycC1;1 physically interacts with MYC2 in the nucleus to inhibit MYC2-mediated transcriptional activation of senescence-associated genes (SAGs) by interfering with RNA polymerase II recruitment. Additionally, CycC1;1 interacts with the Mediator subunit MED25 to disrupt its association with MYC2. Disruption of CycC1;1 accelerates JA-dependent leaf yellowing, whereas loss of MYC2 or MED25 fully suppresses this premature-senescence phenotype. Unlike JAZ repressors, CycC1;1 expression and protein stability are uncoupled from JA signaling. Phylogenetic analyses suggest that the CycC1;1–MYC2 interaction may predate the emergence of JAZ repressors in aquatic ancestors, and CycC1;1 shows evolutionarily conserved ability to interact with and inhibit MYC2 across different plant species. Collectively, our findings uncover a CycC1;1–MED25–MYC2-regulatory module wherein CycC1;1 suppresses MYC2 activity by inhibiting MED25 binding to MYC2 and RNA polymerase II recruitment, downregulating SAG expression and thus delaying leaf senescence in plants.

Key words: CycC1, 1, JA, MED25, MYC2, SAG, senescence