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FANCD 2 protects genome stability by recruiting RNA processing enzymes to resolve R‐loops during mild replication stress
Author(s) -
Okamoto Yusuke,
Abe Masako,
Itaya Akiko,
Tomida Junya,
Ishiai Masamichi,
TakaoriKondo Akifumi,
Taoka Masato,
Isobe Toshiaki,
Takata Minoru
Publication year - 2019
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.14700
Subject(s) - rna , chromatin , transcription (linguistics) , biology , dna replication , dna , rna polymerase ii , genetics , gene , microbiology and biotechnology , gene expression , promoter , linguistics , philosophy
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, FANCD 2, accumulates on large fragile genes during mild replication stress in a manner depending on R‐loops. In this study, we found that FANCD 2 suppresses R‐loop levels. Furthermore, we identified FANCD 2 interactions with RNA processing factors, including hn RNP U and DDX 47. Our data suggest that FANCD 2, 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.