Light is a crucial environmental signal that promotes photomorphogenesis,the developmental process with a series of light-dependent alterations for plants to adapt various exteal challenges.Chromatin modification has been proposed to be involved in such light-mediated growth,but the underlying mechanism is still elusive.In this study,we identified fourArabidopsis thaliana Nuclear Factor-YC homologs,NF-YC1,NF-YC3,NF-YC4,and NF-YC9 (NF-YCs),which function redundantly as repressors of light-controlled hypocotyl elongation via histone deacetylation.Obvious etiolation phenotypes are observed in NF-YCs loss-of-function mutant seedlings grown under light conditions,including significant elongated hypocotyls and fewer opened cotyledons.We found that NF-YCs interact with histone deacetylase HDA15 in the light,co-target the promoters of a set of hypocotyl elongation-related genes,and modulate the levels of histone H4 acetylation on the associated chromatins,thus repressing gene expression.In contrast,NF-YC-HDA15 complex is dismissed from the target genes in the dark,resulting in increased level of H4 acetylation and consequent etiolated growth.Further analyses revealed that transcriptional repression activity of NF-YCs on the light-controlled hypocotyl elongation partially depends on the deacetylation activity of H DA15,and loss of HDA 15 function could rescue the short-hypocotyl phenotype of NF-YCs overexpression plants.Taken together,our results indicate that NF-YC1,NF-YC3,NF-YC4,and NF-YC9 function as transcriptional co-repressors by interacting with HDA15 to inhibit hypocotyl elongation in photomorphogenesis during the early seedling stage.Our findings highlight that NF-YCs can modulate plant development in response to environmental cues via epigenetic regulation.