ETHYLENE RESPONSE FACTOR11 (MaERF11) and HDA1 interact to repress the expression of ACO1 and expansins via histone deacetylation.

Light is a major external factor in regulating seed germination. Photoreceptor phytochrome B (PHYB) plays a predominant role in promoting seed germination in the initial phase after imbibition, partially by repressing phytochrome-interacting factor1 (PIF1). However, the mechanism underlying the PHYB-PIF1-mediated transcription regulation remains largely unclear. Here, we identified that histone deacetylase15 (HDA15) is a negative component of PHYB-dependent seed germination. Overexpression of HDA15 in Arabidopsis inhibits PHYB-dependent seed germination, whereas loss of function of HDA15 increases PHYB-dependent seed germination. Genetic evidence indicated that HDA15 acts downstream of PHYB and represses seed germination dependent on PIF1. Furthermore, HDA15 interacts with PIF1 both in vitro and in vivo. Genome-wide transcriptome analysis revealed that HDA15 and PIF1 co-regulate the transcription of the light-responsive genes involved in multiple hormonal signaling pathways and cellular processes in germinating seeds in the dark. In addition, PIF1 recruits HDA15 to the promoter regions of target genes and represses their expression by decreasing the histone H3 acetylation levels in the dark. Taken together, our analysis uncovered the role of histone deacetylation in the light-regulated seed germination process and identified that HDA15-PIF1 acts as a key repression module directing the transcription network of seed germination.

Photomorphogenesis is a critical plant developmental process that involves light-mediated transcriptome and histone modification changes. The transcription factor ELONGATED HYPOCOTYL5 (HY5) acts downstream of multiple families of photoreceptors to promote photomorphogenesis by regulating the expression of light-responsive genes. However, the molecular mechanism for HY5-mediated transcriptional regulation remains largely unclear. Here, we demonstrated that HY5 directly interacts with a Reduced Potassium Dependence3/Histone Deacetylase1 (HDA1)-type histone deacetylase, HDA15, both in vitro and in vivo. Phenotypic analysis revealed that HDA15 is a negative regulator of hypocotyl cell elongation under both red and far-red light conditions in Arabidopsis (Arabidopsis thaliana) seedlings. The enzymatic activity of HDA15 is required for inhibition of hypocotyl elongation. Furthermore, HDA15 and HY5 act interdependently in the repression of hypocotyl cell elongation in photomorphogenesis. Genome-wide transcriptome analysis revealed that HDA15 and HY5 corepress the transcription of a subset of cell wall organization and auxin signaling-related genes. In addition, HDA15 is required for the function of HY5 in the repression of genes related to hypocotyl cell elongation in Arabidopsis seedlings. Moreover, HY5 recruits HDA15 to the promoters of target genes and represses gene expression by decreasing the levels of histone H4 acetylation in a light-dependent manner. Our study revealed a key transcription regulatory node in which HY5 interacts with HDA15 involved in repressing hypocotyl cell elongation to promote photomorphogenesis.

Seed dormancy controls germination and plays a critical role in regulating the beginning of the life cycle of plants. Seed dormancy is established and maintained during seed maturation and is gradually broken during dry storage (after-ripening). The plant hormone abscisic acid (ABA) and DELAY OF GERMINATION1 (DOG1) protein are essential regulators of seed dormancy. Recent studies revealed that chromatin modifications are also involved in the transcription regulation of seed dormancy. Here, we showed that two Arabidopsis histone demethylases, LYSINESPECIFIC DEMETHYLASE LIKE 1 and 2 (LDL1 and LDL2) act redundantly in repressing of seed dormancy. LDL1 and LDL2 are highly expressed in the early silique developing stage. The ldl1 ldl2 double mutant displays increased seed dormancy, whereas overexpression of LDL1 or LDL2 in Arabidopsis causes reduced dormancy. Furthermore, we showed that LDL1 and LDL2 repress the expression of seed dormancy-related genes, including DOG1, ABA2 and ABI3 during seed dormancy establishment. Furthermore, genetic analysis revealed that the repression of seed dormancy by LDL1 and LDL2 requires DOG1, ABA2 and ABI3. Taken together, our findings revealed that LDL1 and LDL2 play an essential role in seed dormancy.

BREVIPEDICELLUS (BP or KNAT1), a class-I KNOTTED1-like homeobox (KNOX) transcription factor in Arabidopsis thaliana, contributes to shaping the normal inflorescence architecture through negatively regulating other two class-I KNOX genes, KNAT2 and KNAT6. However, the molecular mechanism of BP-mediated transcription regulation remains unclear. In this study, we showed that BP directly interacts with the SWI2/SNF2 chromatin remodeling ATPase BRAHMA (BRM) both in vitro and in vivo. Loss-of-function BRM mutants displayed inflorescence architecture defects, with clustered inflorescences, horizontally orientated pedicels, and short pedicels and internodes, a phenotype similar to the bp mutants. Furthermore, the transcript levels of KNAT2 and KNAT6 were elevated in brm-3, bp-9 and brm-3 bp-9 double mutants. Increased histone H3 lysine 4 tri-methylation (H3K4me3) levels were detected in brm-3, bp-9 and brm-3 bp-9 double mutants. Moreover, BRM and BP co-target to KNAT2 and KNAT6 genes, and BP is required for the binding of BRM to KNAT2 and KNAT6. Taken together, our results indicate that BP interacts with the chromatin remodeling factor BRM to regulate the expression of KNAT2 and KNAT6 in control of inflorescence architecture. BP is a class-I KNOX transcription factor that controls normal inflorescence architecture development by repressing the expression of two KNOX genes, KNAT2 and KNAT6. In this study, we showed that Arabidopsis BP directly interacts with the SWI2/SNF2 chromatin remodeling ATPase BRM. brm and bp mutants displayed similar inflorescence architecture defects, with clustered inflorescences, horizontally orientated pedicels, and short pedicels and internodes. Furthermore, BP and BRM co-target to KNAT2 and KNAT6 genes and repress their expression. This work reveals a new regulatory mechanism that BP associates with BRM in control of inflorescence architecture development.