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Germination time is a major determinant of plant fitness. Both the Abscisic acid (ABA) molecule and the protein Delay of Germination 1 (DOG1) are required to induce seed dormancy. While the ABA molecular pathway is well described, DOG1 encodes a protein lacking annotated domains with still enigmatic biochemical functions. The ABA and DOG1 molecular pathways function mostly independently. However, they operate coherently to shape seed dormancy, implying the presence of a crosstalk between these two molecular frames. We reported that DOG1 physically interacts with the type 2 C Protein Phosphatase (PP2C) ABA-HYPERSENSITIVE GERMINATION 1 (AHG1) and 3 (AHG3) in seeds and requires their activities to control seed dormancy. AHG1 is a non-canonical clade A PP2C whose catalytic activity is irresponsive to ABA inhibition, but its functions are controlled by DOG1. Our results demonstrated the existence of a unique module operating aside of the canonical ABA pathway in seeds that we termed the DOG1-PP2C module. This new molecular trail described in Arabidopsis has been confirmed by an independent study and found its echoes in monocotyledon seeds. However, the exact molecular mechanisms by which the DOG1-PP2C module controls dormancy are still unknown. Using phosphoproteomics we identified candidates as putative downstream targets of this module and confirmed by molecular and genetic methods their functional relevance for the DOG1 seed dormancy pathways. The integration of our latest experimental results into the ABA signalling pathways further defines the contour of an unexplored molecular framework unique to seeds, in which DOG1’s function is to ensure the proper functioning of ABA responses during early inhibition of dormant seeds. The outcome of our research may contribute to breeding programs aiming to modify germination traits without impeding other ABA-related relevant plant fitness traits.