Institute of Plant Biology, College of Life Sciences, National Taiwan University, Taipei, Taiwan; Center for Food & Bio Convergence, College of Agriculture & Life Sciences, Seoul National University, South Korea; Science Department, College of Natural Sciences & Mathematics, Mindanao State University-General Santos City, Philippines.
Institute of Plant Biology, College of Life Sciences, National Taiwan University, Taipei, Taiwan; Department of Life Sciences, College of Science, Pohang University of Science & Technology, Pohang, South Korea.
Biochem Biophys Res Commun. 2020 Dec 17;533(4):806-812. doi: 10.1016/j.bbrc.2020.09.089. Epub 2020 Sep 28.
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.
可逆的组蛋白乙酰化和去乙酰化在调节幼苗发育过程中的光调控基因表达中起着至关重要的作用。然而，组蛋白修饰酶如何介入光信号网络的分子框架仍然很大程度上未知。在这项研究中，我们表明 AtHDA15 通过直接与 COP1 结合正向调控光形态建成，COP1 是光形态建成抑制中的主要调控因子。hda15 T-DNA 敲除和 RNAi 系表现出光低敏感性，HY5 和 PIF3 蛋白水平降低，导致黑暗中长下胚轴表型，而过表达导致 HY5 浓度增加和短下胚轴表型。体内和体外结合实验表明，HDA15 在内核中直接与 COP1 相互作用，调节 COP1 的抑制活性。由于 COP1 被确定为在核内发挥作用，以调节 skotomorphogenesis 中与生长和发育相关的特定转录因子，因此预测在存在光的情况下，HDA15 的直接结合会消除 COP1 的活性，并调节其在黑暗中的抑制活性。我们的研究结果为 HDAC 在除了它们众所周知的组蛋白修饰功能之外的翻译后调节中的作用提供了越来越多的证据。
