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Abstract：
Reversible histone acetylation and deacetylation play crucial roles in modulating light-regulated gene expression during seedling development. However, it remains largely unknown how histone-modifying enzymes interpose within the molecular framework of light signaling network. In this study, we show that AtHDA15 positively regulates photomorphogenesis by directly binding to COP1, a master regulator in the repression of photomorphogenesis. hda15 T-DNA knock-out and RNAi lines exhibited light hyposensitivity with reduced HY5 and PIF3 protein levels leading to long hypocotyl phenotypes in the dark while its overexpression leads to increased HY5 concentrations and short hypocotyl phenotypes. In vivo and in vitro binding assays show that HDA15 directly interacts with COP1 inside the nucleus modulating COP1\'s repressive activities. As COP1 is established to act within the nucleus to regulate specific transcription factors associated with growth and development in skotomorphogenesis, the direct binding by HDA15 is predicted to abrogate activities of COP1 in the presence of light and modulate its repressive activities in the dark. Our results append the mounting evidence for the role of HDACs in post-translational regulation in addition to their well-known histone modifying functions.
摘要：
可逆组蛋白乙酰化和去乙酰化在调节幼苗发育过程中光调节基因表达中起着至关重要的作用。然而,组蛋白修饰酶是如何在光信号网络的分子框架内进行干预的，这在很大程度上仍然是未知的。在这项研究中,我们表明，AtHDA15通过直接结合COP1来积极调节光形态发生，COP1是光形态发生抑制中的主要调节因子。hda15T-DNA敲除和RNAi品系表现出光敏感性低，HY5和PIF3蛋白水平降低，导致黑暗中下胚轴表型长，而其过度表达导致HY5浓度增加和下胚轴表型短。体内和体外结合实验表明，HDA15直接与细胞核内的COP1相互作用，调节COP1的抑制活性。由于COP1在细胞核内发挥作用，以调节与形态发生中的生长和发育相关的特定转录因子，预测HDA15的直接结合会在光的存在下消除COP1的活性，并在黑暗中调节其抑制活性。除了众所周知的组蛋白修饰功能外，我们的结果还为HDAC在翻译后调控中的作用提供了越来越多的证据。
