Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
Nat Cell Biol. 2011 Jun;13(6):668-75. doi: 10.1038/ncb2228. Epub 2011 May 1.
Reversible histone methylation and demethylation are highly regulated processes that are crucial for chromatin reorganization and regulation of gene transcription in response to extracellular conditions. However, the mechanisms that regulate histone-modifying enzymes are largely unknown. Here, we characterized a protein kinase A (PKA)-dependent histone lysine demethylase complex, PHF2-ARID5B. PHF2, a jmjC demethylase, is enzymatically inactive by itself, but becomes an active H3K9Me2 demethylase through PKA-mediated phosphorylation. We found that phosphorylated PHF2 then associates with ARID5B, a DNA-binding protein, and induce demethylation of methylated ARID5B. This modification leads to targeting of the PHF2-ARID5B complex to its target promoters, where it removes the repressive H3K9Me2 mark. These findings suggest that the PHF2-ARID5B complex is a signal-sensing modulator of histone methylation and gene transcription, in which phosphorylation of PHF2 enables subsequent formation of a competent and specific histone demethylase complex.
可逆的组蛋白甲基化和去甲基化是高度调控的过程,对于染色质重排和基因转录的调节至关重要,以响应细胞外条件。然而,调节组蛋白修饰酶的机制在很大程度上是未知的。在这里,我们描述了一个蛋白激酶 A(PKA)依赖性组蛋白赖氨酸去甲基酶复合物,PHF2-ARID5B。PHF2 是一个 jmjC 去甲基酶,本身没有酶活性,但通过 PKA 介导的磷酸化成为活性 H3K9Me2 去甲基酶。我们发现,磷酸化的 PHF2 然后与 ARID5B 结合,ARID5B 是一种 DNA 结合蛋白,并诱导甲基化的 ARID5B 去甲基化。这种修饰导致 PHF2-ARID5B 复合物靶向其靶启动子,在那里它去除抑制性 H3K9Me2 标记。这些发现表明,PHF2-ARID5B 复合物是组蛋白甲基化和基因转录的信号感应调节剂,其中 PHF2 的磷酸化使随后形成有能力的和特异性的组蛋白去甲基酶复合物成为可能。