Format

Send to

Choose Destination
J Cell Biochem. 2016 Mar;117(3):780-92. doi: 10.1002/jcb.25368. Epub 2015 Sep 29.

Chd5 Regulates MuERV-L/MERVL Expression in Mouse Embryonic Stem Cells Via H3K27me3 Modification and Histone H3.1/H3.2.

Author information

1
Department of Advanced Medical Initiatives, Faculty of Medicine, Kyushu University, Fukuoka 812-8582, Japan.
2
Department of Medicine and Biosystemic Science, Faculty of Medicine, Kyushu University, Fukuoka 812-8582, Japan.
3
Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
4
Department of Biochemistry, Hokkaido University Graduate School of Medicine, Hokkaido 060-8638, Japan.
5
Department of Developmental Biology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
6
Division of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan.

Abstract

Chd5 is an essential factor for neuronal differentiation and spermatogenesis and is a known tumor suppressor. H3K27me3 and H3K4un are modifications recognized by Chd5; however, it remains unclear how Chd5 remodels chromatin structure. We completely disrupted the Chd5 locus using the CRISPR-Cas9 system to generate a 52 kbp long deletion and analyzed Chd5 function in mouse embryonic stem cells. Our findings show that Chd5 represses murine endogenous retrovirus-L (MuERV-L/MERVL), an endogenous retrovirus-derived retrotransposon, by regulating H3K27me3 and H3.1/H3.2 function.

KEYWORDS:

CHROMATIN REMODELING ENZYME; Chd5; RETROTRANSPOSON; STEM CELL BIOLOGY

PMID:
26359639
DOI:
10.1002/jcb.25368
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center