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  • Title: Arabidopsis NF-YCs Mediate the Light-Controlled Hypocotyl Elongation via Modulating Histone Acetylation.
    Author: Tang Y, Liu X, Liu X, Li Y, Wu K, Hou X.
    Journal: Mol Plant; 2017 Feb 13; 10(2):260-273. PubMed ID: 27876642.
    Abstract:
    Light is a crucial environmental signal that promotes photomorphogenesis, the developmental process with a series of light-dependent alterations for plants to adapt various external 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 four Arabidopsis 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 HDA15, and loss of HDA15 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.
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