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 a-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.

Pre-harvest sprouting (PHS), which reduces grain yield and quality, is controlled by seed dormancy genes. Because few dormancy-related genes have been cloned, the genetic basis of seed dormancy in rice (Oryza sativa L.) remains unclear. Here, we performed a genome-wide association study and linkage mapping to dissect the genetic basis of seed dormancy in rice. Our findings suggest that Seed Dormancy4 (Sdr4), a central modulator of seed dormancy, integrates the abscisic acid and gibberellic acid signaling pathways at the transcriptional level. Haplotype analysis revealed that three Sdr4 alleles in rice cultivars already existed in ancestral Oryza rufipogon accessions. Furthermore, like the semi-dwarf 1 (SD1) and Rc loci, Sdr4 underwent selection during the domestication and improvement of Asian cultivated rice. The distribution frequency of the Sdr4-n allele in different locations in Asia is negatively associated with local annual temperature and precipitation. Finally, we developed functional molecular markers for Sdr4, SD1, and Rc for use in molecular breeding. Our results provide clues about the molecular basis of Sdr4-regulated seed dormancy. Moreover, these findings provide guidance for utilizing the favorable alleles of Sdr4 and Rc to synergistically boost PHS resistance, yield, and quality in modern rice varieties.

Seed development, dormancy, and germination are key physiological events that are not only important for seed generation, survival, and dispersal, but also contribute to agricultural production. RNA-binding proteins (RBPs) directly interact with target mRNAs and fine-tune mRNA metabolism by governing post-transcriptional regulation, including RNA processing, intron splicing, nuclear export, trafficking, stability/decay, and translational control. Recent studies have functionally characterized increasing numbers of diverse RBPs and shown that they participate in seed development and performance, providing significant insight into the role of RBP–mRNA interactions in seed processes. In this review, we discuss recent research progress on newly defined RBPs that have crucial roles in RNA metabolism and affect seed development, dormancy, and germination.

ODR1 negatively controls seed dormancy by interacting with the transcription factor bHLH57 and preventing its induction of NCED6 and NCED9 expression and ABA biosynthesis. The control of seed dormancy by abscisic acid (ABA) has been extensively studied, but the underlying mechanism is not fully understood. Here, we report the characterization of two ABA-related seed dormancy regulators in Arabidopsis (Arabidopsis thaliana): ODR1 (for reversal of rdo5), an ortholog of the rice (Oryza sativa) Seed dormancy4 (Sdr4), and the basic helix-loop-helix transcription factor bHLH57. ODR1, whose transcript levels are directly suppressed by the transcription factor ABA INSENSITIVE3 (ABI3), negatively regulates seed dormancy by affecting ABA biosynthesis and ABA signaling. By contrast, bHLH57 positively regulates seed dormancy by inducing the expression of the genes 9-CIS-EPOXYCAROTENOID DIOXYGENASE6 (NCED6) and NCED9, which encode ABA biosynthetic enzymes, and thus leads to higher ABA levels. ODR1 interacts with bHLH57 and inhibits bHLH57-modulated NCED6 and NCED9 expression in the nucleus. bhlh57 loss-of-function alleles can partially counteract the enhanced NCED6 and NCED9 expression seen in odr1 mutants and can therefore rescue their associated hyper-dormancy phenotype. Thus, we identified a novel ABI3-ODR1-bHLH57-NCED6/9 network that provides insights into the regulation of seed dormancy by ABA biosynthesis and signaling.