<scp>FANCD</scp>2 protects genome stability by recruiting <scp>RNA</scp> processing enzymes to resolve R‐loops during mild replication stress

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  • 板谷, 亜希子
    Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University･Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University
  • 石合, 正道
    Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University
  • 高折, 晃史
    Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University
  • 髙田, 穣
    Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University･Department of Biological Sciences, University of North Carolina at Charlotte, 9201 University City Blvd
  • Ishiai, Masamichi
    Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University･National Cancer Center Research Institute, Tokyo
  • Takaori‐Kondo, Akifumi
    Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University
  • Taoka, Masato
    Department of Chemistry, Graduate School of Science, Tokyo Metropolitan University
  • Isobe, Toshiaki
    Department of Chemistry, Graduate School of Science, Tokyo Metropolitan University
  • Takata, Minoru
    Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University

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  • FANCD2 protects genome stability by recruiting RNA processing enzymes to resolve R-loops during mild replication stress

抄録

R‐loops, which consist of DNA : RNA hybrids and displaced single‐strand DNA, are a major threat to genome stability. We have previously reported that a key Fanconi anemia protein, FANCD2, accumulates on large fragile genes during mild replication stress in a manner depending on R‐loops. In this study, we found that FANCD2 suppresses R‐loop levels. Furthermore, we identified FANCD2 interactions with RNA processing factors, including hnRNP U and DDX47. Our data suggest that FANCD2, which accumulates with R‐loops in chromatin, recruits these factors and thereby promotes efficient processing of long RNA transcripts. This may lead to a reduction in transcription–replication collisions, as detected by PLA between PCNA and RNA Polymerase II, and hence, lowered R‐loop levels. We propose that this mechanism might contribute to maintenance of genome stability during mild replication stress.

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