The Evening Complex and the Chromatin-Remodeling Factor PICKLE Coordinately Control Seed Dormancy by Directly Repressing DOG1 in Arabidopsis

Abstract Primary seed dormancy is acquired during seed development and maturation and is important for plant fitness and survival. DELAY OF GERMINATION1 (DOG1) plays a critical role in inducing seed dormancy. DOG1 transcription increases rapidly during seed development, but the precise mechanism underlying this process remains elusive. In this study, we showed that mutants with a loss or reduced functioning of the chromatin-remodeling factor PICKLE (PKL) exhibit increased seed dormancy. PKL associates with DOG1 chromatin and inhibits its transcription. PKL physically interacts with LUX ARRYTHMO (LUX), a member of the evening complex (EC) of the circadian clock. Furthermore, LUX binds directly to a specific coding sequence of DOG1, and DOG1 acts genetically downstream of PKL and LUX. Mutations in LUX and EARLY FLOWERING3 (ELF3), another member of the EC, led to increased DOG1 expression and enhanced seed dormancy. Surprisingly, these phenotypes were abolished when the parent plants were grown under continuous light. Finally, the loss of function of PKL and LUX decreased H3K27me3 levels at the DOG1 locus. Our study reveals a regulatory mechanism in which EC proteins coordinate with PKL to transmit circadian signals that directly regulate DOG1 expression and seed dormancy during seed development.