Hypoxic reprograming of H3K27me3 and H3K4me3 at the INK4A locus

被引：13

作者：

Chang, Soojeong ^{[1
]}

Park, Bongju ^{[1
]}

Choi, Kang ^{[1
]}

Moon, Yunwon ^{[1
]}

Lee, Ho-Youl ^{[1
,2
]}

Park, Hyunsung ^{[1
]}

机构：

[1] Univ Seoul, Dept Life Sci, Siripdae Gil 13, Seoul 130743, South Korea

[2] CJ Healthcare, Deokpyeong Ro 811, Icheon Si 467812, Gyeonggi Do, South Korea

来源：

FEBS LETTERS | 2016年 / 590卷 / 19期

基金：

新加坡国家研究基金会;

关键词：

Hypoxia; INK4A locus; JMJD3; DEMETHYLASE JMJD3 CONTRIBUTES; HISTONE DEMETHYLASES; STEM-CELLS; LIFE-SPAN; TRANSCRIPTIONAL REGULATION; CELLULAR SENESCENCE; EXPRESSION; POLYCOMB; PROTEIN; OXYGEN;

D O I：

10.1002/1873-3468.12375

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Activation of Raf reduces the repressive histone mark H3K27me3 at the INK4a locus by inducing the H3K27me3 demethylase JMJD3. During hypoxia, the catalyitc activity of JMJD3 is reduced due to the limited availability of O-2 as a substrate. In our study, we found that hypoxia prevented Raf-induced JMJD3 from demethylating H3K27me3 at the INK4a locus. Nonetheless, hypoxia did not prevent Raf signaling from inducing INK4a mRNA. Interestingly, we found that hypoxia strongly enhanced the active histone mark H3K4me3 at the INK4a locus by inhibiting the H3K4me3 demethylases JARID1A and JARID1B. Therefore, this study demonstrates that the O-2 concentration in the microenvironment differentially affects the repressive methylation on K27 and the activating methylation on K4 at the INK4a locus by inhibiting the H3K27me3 and H3K4me3 demethylases.

引用

收藏

页码：3407 / 3415

页数：9

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