Seed dormancy is an adaptive trait in plants. Breaking seed dormancy determines the timing of germination and is, thereby essential for ensuring plant survival and agricultural production. Seed dormancy and the subsequent germination are controlled by both internal cues (mainly hormones) and environmental signals. In the past few years, the roles of plant hormones in regulating seed dormancy and germination have been uncovered. However, we are only beginning to understand how light signaling pathways modulate seed dormancy and interaction with endogenous hormones. In this review, we summarize current views of the molecular mechanisms by which light controls the induction, maintenance and release of seed dormancy, as well as seed germination, by regulating hormone metabolism and signaling pathways.
Environmental light signal and GAs synergistically regulate seed dormancy and germination. The phytochrome B (phyB) photoreceptor regulates expression of the REVEILLE1 (RVE1) transcription factor, which directly inhibits GIBBERELLIN 3-OXIDASE2 transcription, suppressing GA biosynthesis. However, whether phyB-RVE1 coordinates with GA signaling in controlling seed dormancy and germination remains unknown.Here, we demonstrate that RVE1 regulation of seed dormancy and germination requires a DELLA repressor, REPRESSOR OF GA-LIKE2 (RGL2), in Arabidopsis thaliana.RVE1 interacts with both RGL2 and its E3 ubiquitin ligase SLEEPY1 (SLY1) and promotes RGL2 stability by restraining the RGL2-SLY1 interaction. Furthermore, RVE1 and RGL2 synergistically regulate global transcriptome changes; RGL2 enhances the DNA-binding capacity and transcriptional activity of RVE1 in regulating downstream gene expression. Moreover, RGL2 expression is repressed by phyB.Our study reveals a novel regulatory mechanism in which the RVE1-RGL2 module coordinately controls seed dormancy and germination by integrating light perception, GA metabolism and GA signaling pathways.
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