DOG1 prevents AFPs activation by AHG1 to control dormancy separately from ABA core signaling

Abstract

AbstractSeed dormancy determines germination timing and thereby critically influences seed plant adaptation and overall fitness. DELAY OF GERMINATION1 (DOG1) is a conserved central regulator of dormancy acting in concert with the phytohormone abscisic acid (ABA) through negative regulation of ABA HYPERSENSITIVE GERMINATION (AHG) 1 and AHG3 phosphatases. The current molecular mechanism of DOG1 signaling proposes that it regulates the activation state of central ABA-related SnRK2 kinases. Here, we unveil DOG1’s functional autonomy from the regulation of ABA core signaling components and unravel its pivotal control over the activation of ABSCISIC ACID INSENSITIVE FIVE BINDING PROTEINs (AFPs). Our data revealed a DOG1-AHG1-AFP relay in which AFPs’ genuine activation by AHG1 is contained by DOG1 to prevent the breakdown of maturation-imposed ABA responses independently of ABA-related kinase activation status. This work offers a molecular understanding of how plants fine-tune germination timing, while preserving seed responsiveness to adverse environmental cues, and thus represents a milestone in the realm of conservation and breeding programs.One-Sentence SummaryAutonomous control of maturation-imposed ABA responses by DOG1 enables seeds to regulate dormancy and stress-reactivity traits independently.