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, which is important for plant fitness and survival. DELAY OF GERMINATION1 (DOG1) plays a critical role in inducing seed dormancy. <i>DOG1</i> expression 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 function of the chromatin-remodeling factor PICKLE (PKL) exhibit increased seed dormancy. PKL associates with <i>DOG1</i> chromatin and inhibits its transcription. We found that PKL physically interacts with LUX ARRHYTHMO (LUX), a member of the evening complex (EC) of the circadian clock. Furthermore, LUX directly binds to a specific coding sequence of <i>DOG1</i>, and DOG1 acts genetically downstream of PKL and LUX. Mutations in either <i>LUX</i> or <i>EARLY FLOWERING3</i> (<i>ELF3</i>) encoding another member of the EC led to increased <i>DOG1</i> expression and enhanced seed dormancy. Surprisingly, these phenotypes were abolished when the parent plants were grown under continuous light. In addition, we observed that loss of function of either <i>PKL</i> or <i>LUX</i> decreased H3K27me3 levels at the <i>DOG1</i> locus. Taken together, our study reveals a regulatory mechanism in which EC proteins coordinate with PKL to transmit circadian signals for directly regulating <i>DOG1</i> expression and seed dormancy during seed development.