In vivo analysis of FANCD2 recruitment at meiotic DNA breaks in Caenorhabditis elegans

GERMOGLIO, M., A. VALENTI, I. GALLO, C. FORENZA, P. SANTONICOLA, Nicola SILVA and A. ADAMO. In vivo analysis of FANCD2 recruitment at meiotic DNA breaks in Caenorhabditis elegans. Scientific reports. LONDON: NATURE PUBLISHING GROUP, 2020, vol. 10, No 1, p. 1-14. ISSN 2045-2322. Available from: https://dx.doi.org/10.1038/s41598-019-57096-1.

Basic information

• Original name: In vivo analysis of FANCD2 recruitment at meiotic DNA breaks in Caenorhabditis elegans
• Authors: GERMOGLIO, M. (380 Italy), A. VALENTI (380 Italy), I. GALLO (380 Italy), C. FORENZA (380 Italy), P. SANTONICOLA (380 Italy), Nicola SILVA (380 Italy, belonging to the institution) and A. ADAMO (380 Italy, guarantor).
• Edition: Scientific reports, LONDON, NATURE PUBLISHING GROUP, 2020, 2045-2322.

Other information

• Original language: English
• Type of outcome: Article in a journal
• Field of Study: 10601 Cell biology
• Country of publisher: United Kingdom of Great Britain and Northern Ireland
• Confidentiality degree: is not subject to a state or trade secret
• WWW: URL
• Impact factor: Impact factor: 4.379
• RIV identification code: RIV/00216224:14110/20:00115984
• Organization unit: Faculty of Medicine
• Doi: http://dx.doi.org/10.1038/s41598-019-57096-1
• UT WoS: 000517989900054
• Keywords in English: DOUBLE-STRAND BREAK; FANCONI-ANEMIA PROTEINS; INTERSTRAND CROSS-LINKS; C-ELEGANS; REPAIR PATHWAY; RECOMBINATION; CHROMOSOME; MONOUBIQUITINATION; COMPLEX; CANCER
• Tags: 14110513, rivok
• Tags: International impact, Reviewed

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.