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

نویسندگان

  • Masayasu Hayashi
  • Kazumitsu Maehara
  • Akihito Harada
  • Yuichiro Semba
  • Kensuke Kudo
  • Hidehisa Takahashi
  • Shinya Oki
  • Chikara Meno
  • Kenji Ichiyanagi
  • Koichi Akashi
  • Yasuyuki Ohkawa
چکیده

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.

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عنوان ژورنال:
  • Journal of cellular biochemistry

دوره 117 3  شماره 

صفحات  -

تاریخ انتشار 2016