Abscisic acid (ABA) is known to suppress seed germination and post-germinative growth of Arabidopsis (Arabidopsis thaliana), and jasmonate (JA) enhances ABA function. However, the molecular mechanism underlying the crosstalk between the ABA and JA signaling pathways remains largely elusive. Here, we show that exogenous coronatine, a JA analog structurally similar to the active conjugate jasmonate-isoleucine, significantly enhances the delayed seed germination response to ABA. Disruption of the JA receptor CORONATINE INSENSITIVE1 or accumulation of the JA signaling repressor JASMONATE ZIM-DOMAIN (JAZ) reduced ABA signaling, while jaz mutants enhanced ABA responses. Mechanistic investigations revealed that several JAZ repressors of JA signaling physically interact with ABSCISIC ACID INSENSITIVE3 (ABI3), a critical transcription factor that positively modulates ABA signaling, and that JAZ proteins repress the transcription of ABI3 and ABI5. Further genetic analyses showed that JA activates ABA signaling and requires functional ABI3 and ABI5. Overexpression of ABI3 and ABI5 simultaneously suppressed the ABA-insensitive phenotypes of the coi1-2 mutant and JAZ-accumulating (JAZ-ΔJas) plants. Together, our results reveal a previously uncharacterized signaling module in which JAZ repressors of the JA pathway regulate the ABA-responsive ABI3 and ABI5 transcription factors to integrate JA and ABA signals during seed germination and post-germinative growth.
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