A repressor complex silencing ABA signaling in seeds?

Seed dormancy is induced primarily by abscisic acid (ABA) and maintained through elevated levels of ABA sensitivity in seeds. The core mechanisms of ABA-imposed seed dormancy are emerging, but it is still unclear how these blockages in seeds are eliminated during after-ripening, or what molecular events in imbibed seeds are responsible for the initial stages of germination induction. Some pieces of evidence suggest that a repressor complex, which potentially triggers seed germination through the suppression of ABA signaling components, might be present in seeds. The usual suspect, protein phosphatase 2C, which inactivates kinases and shuts down ABA signaling in the major dormancy pathway, is possibly associated with this complex. Other members, such as WD40 proteins and histone deacetylase subunits, homologs of which are found in the flowering repressor complex, perhaps constitute this complex in seeds. The repressor activity could counteract the dormancy mechanisms in an overwhelming manner, through well-coordinated inactivation and turnover of germination-suppressing transcription factors, which is probably accompanied by chromatin silencing and transcriptional repression of the transcription factor target genes. This review provides a perspective on a putative seed germination-inducing repressor complex, including its possible modes of action and upstream regulators.