Template Activating Factor-I α Regulates Retroviral Silencing during Reprogramming

Phuong Linh Bui, Ken Nishimura, Gonzalo Seminario Mondejar, Arun Kumar, Shiho Aizawa, Kensaku Murano, Kyosuke Nagata, Yohei Hayashi, Aya Fukuda, Yasuko Onuma, Yuzuru Ito, Mahito Nakanishi, Koji Hisatake

研究成果: Article査読

3 被引用数 (Scopus)

抄録

Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) is accompanied by dramatic changes in epigenetic programs, including silencing of endogenous and exogenous retroviruses. Here, we utilized replication-defective and persistent Sendai virus (SeVdp)-based vectors to monitor retroviral silencing during reprogramming. We observed that retroviral silencing occurred at an early reprogramming stage without a requirement for KLF4 or the YY1-binding site in the retroviral genome. Insertional chromatin immunoprecipitation (iChIP) enabled us to isolate factors assembled on the silenced provirus, including components of inhibitor of histone acetyltransferase (INHAT), which includes the SET/TAF-I oncoprotein. Knockdown of SET/TAF-I in mouse embryonic fibroblasts (MEFs) diminished retroviral silencing during reprogramming, and overexpression of template activating factor-I α (TAF-Iα), a SET/TAF-I isoform predominant in embryonic stem cells (ESCs), reinforced retroviral silencing by an SeVdp-based vector that is otherwise defective in retroviral silencing. Our results indicate an important role for TAF-Iα in retroviral silencing during reprogramming.

本文言語English
ページ(範囲)1909-1922.e5
ジャーナルCell Reports
29
7
DOI
出版ステータスPublished - 2019 11 12

ASJC Scopus subject areas

  • 生化学、遺伝学、分子生物学(全般)

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