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RAD18 directs DNA double-strand break repair by homologous recombination to post-replicative chromatin

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F24%3A00588028" target="_blank" >RIV/68378050:_____/24:00588028 - isvavai.cz</a>

  • Alternative codes found

    RIV/00209805:_____/24:00080129 RIV/00216208:11110/24:10483982 RIV/00216208:11310/24:10483982 RIV/00064165:_____/24:10483982

  • Result on the web

    <a href="https://academic.oup.com/nar/article/52/13/7687/7694281?login=false" target="_blank" >https://academic.oup.com/nar/article/52/13/7687/7694281?login=false</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1093/nar/gkae499" target="_blank" >10.1093/nar/gkae499</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    RAD18 directs DNA double-strand break repair by homologous recombination to post-replicative chromatin

  • Original language description

    RAD18 is an E3 ubiquitin ligase that prevents replication fork collapse by promoting DNA translesion synthesis and template switching. Besides this classical role, RAD18 has been implicated in homologous recombination. however, this function is incompletely understood. Here, we show that RAD18 is recruited to DNA lesions by monoubiquitination of histone H2A at K15 and counteracts accumulation of 53BP1. Super-resolution microscopy revealed that RAD18 localizes to the proximity of DNA double strand breaks and limits the distribution of 53BP1 to the peripheral chromatin nanodomains. Whereas auto-ubiquitination of RAD18 mediated by RAD6 inhibits its recruitment to DNA breaks, interaction with SLF1 promotes RAD18 accumulation at DNA breaks in the post-replicative chromatin by recognition of histone H4K20me0. Surprisingly, suppression of 53BP1 function by RAD18 is not involved in homologous recombination and rather leads to reduction of non-homologous end joining. Instead, we provide evidence that RAD18 promotes HR repair by recruiting the SMC5/6 complex to DNA breaks. Finally, we identified several new loss-of-function mutations in RAD18 in cancer patients suggesting that RAD18 could be involved in cancer development.

  • 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

    10608 - Biochemistry and molecular biology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

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

    13

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    17

  • Pages from-to

    7687-7703

  • UT code for WoS article

    001247647900001

  • EID of the result in the Scopus database

    2-s2.0-85199398767