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 a A. ADAMO. In vivo analysis of FANCD2 recruitment at meiotic DNA breaks in Caenorhabditis elegans. Scientific reports. LONDON: NATURE PUBLISHING GROUP, 2020, roč. 10, č. 1, s. 1-14. ISSN 2045-2322. Dostupné z: https://dx.doi.org/10.1038/s41598-019-57096-1.

Základní údaje

• Originální název: In vivo analysis of FANCD2 recruitment at meiotic DNA breaks in Caenorhabditis elegans
• Autoři: GERMOGLIO, M. (380 Itálie), A. VALENTI (380 Itálie), I. GALLO (380 Itálie), C. FORENZA (380 Itálie), P. SANTONICOLA (380 Itálie), Nicola SILVA (380 Itálie, domácí) a A. ADAMO (380 Itálie, garant).
• Vydání: Scientific reports, LONDON, NATURE PUBLISHING GROUP, 2020, 2045-2322.

Další údaje

• Originální jazyk: angličtina
• Typ výsledku: Článek v odborném periodiku
• Obor: 10601 Cell biology
• Stát vydavatele: Velká Británie a Severní Irsko
• Utajení: není předmětem státního či obchodního tajemství
• WWW: URL
• Impakt faktor: Impact factor: 4.379
• Kód RIV: RIV/00216224:14110/20:00115984
• Organizační jednotka: Lékařská fakulta
• Doi: http://dx.doi.org/10.1038/s41598-019-57096-1
• UT WoS: 000517989900054
• Klíčová slova anglicky: DOUBLE-STRAND BREAK; FANCONI-ANEMIA PROTEINS; INTERSTRAND CROSS-LINKS; C-ELEGANS; REPAIR PATHWAY; RECOMBINATION; CHROMOSOME; MONOUBIQUITINATION; COMPLEX; CANCER
• Štítky: 14110513, rivok
• Příznaky: Mezinárodní význam, Recenzováno

Anotace

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.