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Mammalian ISWI and SWI/SNF selectively mediate binding of distinct transcription factors

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  • Darko Barisic

    (Friedrich Miescher Institute for Biomedical Research
    University of Basel
    Weill Cornell Medicine)

  • Michael B. Stadler

    (Friedrich Miescher Institute for Biomedical Research
    Swiss Institute of Bioinformatics)

  • Mario Iurlaro

    (Friedrich Miescher Institute for Biomedical Research)

  • Dirk Schübeler

    (Friedrich Miescher Institute for Biomedical Research
    University of Basel)

Abstract

Chromatin remodelling complexes evict, slide, insert or replace nucleosomes, which represent an intrinsic barrier for access to DNA. These remodellers function in most aspects of genome utilization including transcription-factor binding, DNA replication and repair1,2. Although they are frequently mutated in cancer3, it remains largely unclear how the four mammalian remodeller families (SWI/SNF, ISWI, CHD and INO80) orchestrate the global organization of nucleosomes. Here we generated viable embryonic stem cells that lack SNF2H, the ATPase of ISWI complexes, enabling study of SNF2H cellular function, and contrast it to BRG1, the ATPase of SWI/SNF. Loss of SNF2H decreases nucleosomal phasing and increases linker lengths, providing in vivo evidence for an ISWI function in ruling nucleosomal spacing in mammals. Systematic analysis of transcription-factor binding reveals that these remodelling activities have specific effects on binding of different transcription factors. One group critically depends on BRG1 and contains the transcriptional repressor REST, whereas a non-overlapping set of transcription factors, including the insulator protein CTCF, relies on SNF2H. This selectivity readily explains why chromosomal folding and insulation of topologically associated domains requires SNF2H, but not BRG1. Collectively, this study shows that mammalian ISWI is critical for nucleosomal periodicity and nuclear organization and that transcription factors rely on specific remodelling pathways for correct genomic binding.

Suggested Citation

  • Darko Barisic & Michael B. Stadler & Mario Iurlaro & Dirk Schübeler, 2019. "Mammalian ISWI and SWI/SNF selectively mediate binding of distinct transcription factors," Nature, Nature, vol. 569(7754), pages 136-140, May.
  • Handle: RePEc:nat:nature:v:569:y:2019:i:7754:d:10.1038_s41586-019-1115-5
    DOI: 10.1038/s41586-019-1115-5
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    Cited by:

    1. Yan Jiang & Siqi Sun & Yuan Quan & Xin Wang & Yuling You & Xiao Zhang & Yue Zhang & Yin Liu & Bingjing Wang & Henan Xu & Xuetao Cao, 2023. "Nuclear RPSA senses viral nucleic acids to promote the innate inflammatory response," Nature Communications, Nature, vol. 14(1), pages 1-14, December.
    2. Dhurjhoti Saha & Solomon Hailu & Arjan Hada & Junwoo Lee & Jie Luo & Jeff A. Ranish & Yuan-chi Lin & Kyle Feola & Jim Persinger & Abhinav Jain & Bin Liu & Yue Lu & Payel Sen & Blaine Bartholomew, 2023. "The AT-hook is an evolutionarily conserved auto-regulatory domain of SWI/SNF required for cell lineage priming," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
    3. Marko Dunjić & Felix Jonas & Gilad Yaakov & Roye More & Yoav Mayshar & Yoach Rais & Ayelet-Hashahar Orenbuch & Saifeng Cheng & Naama Barkai & Yonatan Stelzer, 2023. "Histone exchange sensors reveal variant specific dynamics in mouse embryonic stem cells," Nature Communications, Nature, vol. 14(1), pages 1-19, December.
    4. Gang Ren & Wai Lim Ku & Guangzhe Ge & Jackson A. Hoffman & Jee Youn Kang & Qingsong Tang & Kairong Cui & Yong He & Yukun Guan & Bin Gao & Chengyu Liu & Trevor K. Archer & Keji Zhao, 2024. "Acute depletion of BRG1 reveals its primary function as an activator of transcription," Nature Communications, Nature, vol. 15(1), pages 1-16, December.

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