Seed germination and the establishment of young seedlings are critical phases in the plant’s life cycle. To control these processes, plants have evolved diverse hormonal signaling networks in which brassinosteroids (BRs) attenuate abscisic acid (ABA) responses; however, the underlying regulatory mechanism remains elusive. Here, we reveal that epigenetic silencing of the ABA signaling regulator ABI3 via the BR-related transcription factor BES1 is essential for the inhibitory effect of BRs on ABA signaling during early seedling development. BR-activated BES1 forms a transcriptional repressor complex with TPL via its EAR motif that recruits the histone deacetylase HDA19. This facilitates the histone H3-mediated deacetylation of ABI3 chromatin, leading to the suppression of ABI3 and its downstream target ABI5, which results in reduced ABA sensitivity. We propose that the BR-activated BES1-TPL-HDA19 repressor complex controls epigenetic silencing of ABI3 and thereby suppresses the ABA response during early seedling development.

Mitogen-activated protein kinase (MAPK) signaling cascades play critical roles in various cellular events including abiotic/biotic stress responses, innate immunity, hormone signaling and cell specificity in plants. The MAPK-mediated stress and ethylene signaling are recently known to be involved in nitogen-fixing symbiotic interactions; however, the biological role of MAPK for nodule development in legume plants is largely unknown. We here elucidated that MtMKK5-MtMPK3/6 cascade negatively regulate the nitrogen fixing nodule formation in Medicago truncatula. MtMKK5, an ortholog of SIMKK, overexpression significantly reduces the nodule formation in M. truncatula roots. MtMKK5 directly activates MtMPK3/6 by phosphorylation on the TEY motif within the activation loop in the cytoplasm, which might link to EFD as a negative regulator for nodule formation. EFD has a putative MAPK phosphorylation Thr residue and could be a target of the activated MtMPK3/6 in the nucleus. Consistently, a MAPK specific inhibitor U0126 enhances nodule formation and confers similar nodule phenotypes to the efd-1 mutant such as lower proliferation and differentiation to symbiotic tissues. Our works thus reveal a key negative signaling module mediated by MtMKK5-MtMPK3/6-EFD for symbiotic nitrogen fixing nodule organogenesis.