Arabidopsis MYC2–ARF16–ABI5 complex functions as a transcriptional switch to regulate jasmonate, auxin, and abscisic acid signaling synergy

Seed germination and post-germination growth are strictly regulated by phytohormones. In Arabidopsis thaliana, jasmonate (JA) and auxin suppress these processes by boosting abscisic acid (ABA) signaling. However, whether there exists a transcriptional switch orchestrating the intricate interplay among these hormones and the underlying molecular mechanisms remain elusive. Herein, we demonstrated that endogenous JA signaling, involving the CORONATINE INSENSITIVE1 (COI1)-JASMONATE ZIM-DOMAIN (JAZ) module and the downstream MYC2, MYC3, and MYC4 transcription factors, potentiates auxin-induced ABA responses. MYC2, MYC3, and MYC4 interact with AUXIN RESPONSE FACTOR10 (ARF10) and ARF16. Consistently, MYC2 and ARF16 synergistically augment ABA signaling-delayed seed germination. Furthermore, MYC2 and MYC4 form a protein complex with ABSCISIC ACID INSENSITIVE5 (ABI5), a master activator of ABA signaling. Genetic analyses suggested that MYC2 positively facilitates ABA responses largely through ABI5. Notably, MYC2 collaborates with ARF16 to enhance the transcriptional activity and protein abundance of ABI5. Intriguingly, MYC2, ARF16, and ABI5 assemble into a ternary complex. Simultaneously disrupting MYC, ARF10/ARF16, and ABI5 renders the seed germination process insensitive to combined JA, auxin, and ABA. Collectively, our findings unveil the MYC-ARF10/ARF16-ABI5 module as a pivotal molecular switch that integrates JA, auxin, and ABA signaling pathways, thereby enabling plants to mount adaptive responses to challenging environmental conditions.