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Reactivation of the G1 enhancer landscape underlies core circuitry addiction to SWI/SNF

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F24%3A00580756" target="_blank" >RIV/61388963:_____/24:00580756 - isvavai.cz</a>

  • Result on the web

    <a href="https://doi.org/10.1093/nar/gkad1081" target="_blank" >https://doi.org/10.1093/nar/gkad1081</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1093/nar/gkad1081" target="_blank" >10.1093/nar/gkad1081</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Reactivation of the G1 enhancer landscape underlies core circuitry addiction to SWI/SNF

  • Original language description

    Several cancer core regulatory circuitries (CRCs) depend on the sustained generation of DNA accessibility by SWI/SNF chromatin remodelers. However, the window when SWI/SNF is acutely essential in these settings has not been identified. Here we used neuroblastoma (NB) cells to model and dissect the relationship between cell-cycle progression and SWI/SNF ATPase activity. We find that SWI/SNF inactivation impairs coordinated occupancy of non-pioneer CRC members at enhancers within 1 hour, rapidly breaking their autoregulation. By precisely timing inhibitor treatment following synchronization, we show that SWI/SNF is dispensable for survival in S and G2/M, but becomes acutely essential only during G1 phase. We furthermore developed a new approach to analyze the oscillating patterns of genome-wide DNA accessibility across the cell cycle, which revealed that SWI/SNF-dependent CRC binding sites are enriched at enhancers with peak accessibility during G1 phase, where they activate genes involved in cell-cycle progression. SWI/SNF inhibition strongly impairs G1-S transition and potentiates the ability of retinoids used clinically to induce cell-cycle exit. Similar cell-cycle effects in diverse SWI/SNF-addicted settings highlight G1-S transition as a common cause of SWI/SNF dependency. Our results illustrate that deeper knowledge of the temporal patterns of enhancer-related dependencies may aid the rational targeting of addicted cancers.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10401 - Organic chemistry

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2024

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Nucleic Acids Research

  • ISSN

    0305-1048

  • e-ISSN

    1362-4962

  • Volume of the periodical

    52

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    18

  • Pages from-to

    4-21

  • UT code for WoS article

    001106053000001

  • EID of the result in the Scopus database

    2-s2.0-85182500830