The MKK3-MPK7 cascade phosphorylates ERF4 and promotes its rapid degradation to release seed dormancy in Arabidopsis.

Seeds establish dormancy to delay germination until the arrival of a favorable growing season. In this study, we identify a fate switch comprised of the MKK3-MPK7 kinase cascade and the ethylene response factor ERF4 that is responsible for the seed state transition from dormancy to germination. We show that dormancy-breaking factors activate the MKK3-MPK7 module, which affects the expression of some α-EXPANSIN (EXPA) genes to control seed dormancy. Furthermore, we identify a direct downstream substrate of this module, ERF4, which suppresses the expression of these EXPAs by directly binding to the GCC boxes in their exon regions. The activated MKK3-MPK7 module phosphorylates ERF4, leading to its rapid degradation and thereby releasing its inhibitory effect on the expression of these EXPAs. Collectively, our work identifies a signaling chain consisting of protein phosphorylation, degradation, and gene transcription , by which the germination promoters within the embryo sense and are activated by germination signals from ambient conditions.

DELAY OF GERMINATION 1, the Master Regulator of Seed Dormancy, Integrates the Regulatory Network of Phytohormones at the Transcriptional Level to Control Seed Dormancy.

Seed dormancy, an important adaptive trait that governs germination timing, is endogenously controlled by phytohormones and genetic factors. DELAY OF GERMINATION 1 (DOG1) is the vital genetic regulator of dormancy, significantly affecting the expression of numerous ABA and GA metabolic genes. However, whether DOG1 could influence the expression of other phytohormone-related genes is still unknown. Here, we comprehensively investigated all well-documented hormone-related genes which might be affected in dog1-2 dry or imbibed seeds by using whole-transcriptome sequencing (RNA-seq). We found that DOG1 could systematically control the expression of phytohormone-related genes. An evident decrease was observed in the endogenous signal intensity of abscisic acid (ABA) and indole-3-acetic acid (IAA), while a dramatic increase appeared in that of gibberellins (GA), brassinosteroids (BR), and cytokinin (CK) in the dog1-2 background, which may contribute considerably to its dormancy-deficient phenotype. Collectively, our data highlight the role of DOG1 in balancing the expression of phytohormone-related genes and provide inspirational evidence that DOG1 may integrate the phytohormones network to control seed dormancy.