RRC ID 59495
著者 Germoglio M, Valenti A, Gallo I, Forenza C, Santonicola P, Silva N, Adamo A.
タイトル In vivo analysis of FANCD2 recruitment at meiotic DNA breaks in Caenorhabditis elegans.
ジャーナル Sci Rep
Abstract Fanconi Anemia is a rare genetic disease associated with DNA repair defects, congenital abnormalities and infertility. Most of FA pathway is evolutionary conserved, allowing dissection and mechanistic studies in simpler model systems such as Caenorhabditis elegans. In the present study, we employed C. elegans to better understand the role of FA group D2 (FANCD2) protein in vivo, a key player in promoting genome stability. We report that localization of FCD-2/FANCD2 is dynamic during meiotic prophase I and requires its heterodimeric partner FNCI-1/FANCI. Strikingly, we found that FCD-2 recruitment depends on SPO-11-induced double-strand breaks (DSBs) but not RAD-51-mediated strand invasion. Furthermore, exposure to DNA damage-inducing agents boosts FCD-2 recruitment on the chromatin. Finally, analysis of genetic interaction between FCD-2 and BRC-1 (the C. elegans orthologue of mammalian BRCA1) supports a role for these proteins in different DSB repair pathways. Collectively, we showed a direct involvement of FCD-2 at DSBs and speculate on its function in driving meiotic DNA repair.
巻・号 10(1)
ページ 103
公開日 2020-1-9
DOI 10.1038/s41598-019-57096-1
PII 10.1038/s41598-019-57096-1
PMID 31919410
PMC PMC6952437
MeSH Animals Caenorhabditis elegans / genetics* Caenorhabditis elegans / growth & development Caenorhabditis elegans / metabolism Caenorhabditis elegans Proteins / genetics Caenorhabditis elegans Proteins / metabolism* DNA Breaks, Double-Stranded* DNA Repair* Fanconi Anemia Complementation Group D2 Protein / genetics Fanconi Anemia Complementation Group D2 Protein / metabolism* Meiosis* Recombination, Genetic*
IF 4.011
引用数 0
リソース情報
線虫 tm1298 tm1145 tm3081