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Non-canonical reader modules of BAZ1A promote recovery from DNA damage

Author

Listed:
  • Mariano Oppikofer

    (Genentech, Inc.
    Pfizer Worldwide Research and Development)

  • Meredith Sagolla

    (Genentech, Inc.)

  • Benjamin Haley

    (Genentech, Inc.)

  • Hui-Min Zhang

    (Genentech, Inc.)

  • Sarah K. Kummerfeld

    (Genentech, Inc.)

  • Jawahar Sudhamsu

    (Genentech, Inc.)

  • E. Megan Flynn

    (Genentech, Inc.)

  • Tianyi Bai

    (Genentech, Inc.
    STEMCELL Technologies Inc.)

  • Jennifer Zhang

    (Genentech, Inc.)

  • Claudio Ciferri

    (Genentech, Inc.)

  • Andrea G. Cochran

    (Genentech, Inc.)

Abstract

Members of the ISWI family of chromatin remodelers mobilize nucleosomes to control DNA accessibility and, in some cases, are required for recovery from DNA damage. However, it remains poorly understood how the non-catalytic ISWI subunits BAZ1A and BAZ1B might contact chromatin to direct the ATPase SMARCA5. Here, we find that the plant homeodomain of BAZ1A, but not that of BAZ1B, has the unusual function of binding DNA. Furthermore, the BAZ1A bromodomain has a non-canonical gatekeeper residue and binds relatively weakly to acetylated histone peptides. Using CRISPR-Cas9-mediated genome editing we find that BAZ1A and BAZ1B each recruit SMARCA5 to sites of damaged chromatin and promote survival. Genetic engineering of structure-designed bromodomain and plant homeodomain mutants reveals that reader modules of BAZ1A and BAZ1B, even when non-standard, are critical for DNA damage recovery in part by regulating ISWI factors loading at DNA lesions and supporting transcriptional programs required for survival.

Suggested Citation

  • Mariano Oppikofer & Meredith Sagolla & Benjamin Haley & Hui-Min Zhang & Sarah K. Kummerfeld & Jawahar Sudhamsu & E. Megan Flynn & Tianyi Bai & Jennifer Zhang & Claudio Ciferri & Andrea G. Cochran, 2017. "Non-canonical reader modules of BAZ1A promote recovery from DNA damage," Nature Communications, Nature, vol. 8(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00866-0
    DOI: 10.1038/s41467-017-00866-0
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    Cited by:

    1. Yeongjae Kim & Na Young Ha & Mi-Sun Kang & Eunjin Ryu & Geunil Yi & Juyeong Yoo & Nalae Kang & Byung-Gyu Kim & Kyungjae Myung & Sukhyun Kang, 2024. "ATAD5-BAZ1B interaction modulates PCNA ubiquitination during DNA repair," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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