2020
In vivo analysis of FANCD2 recruitment at meiotic DNA breaks in Caenorhabditis elegans
GERMOGLIO, M., A. VALENTI, I. GALLO, C. FORENZA, P. SANTONICOLA et. al.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
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
Odkazy
Impakt faktor
Impact factor: 4.379
Kód RIV
RIV/00216224:14110/20:00115984
Organizační jednotka
Lékařská fakulta
UT WoS
000517989900054
Klíčová slova anglicky
DOUBLE-STRAND BREAK; FANCONI-ANEMIA PROTEINS; INTERSTRAND CROSS-LINKS; C-ELEGANS; REPAIR PATHWAY; RECOMBINATION; CHROMOSOME; MONOUBIQUITINATION; COMPLEX; CANCER
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 15. 7. 2020 09:51, Mgr. Tereza Miškechová
Anotace
V originále
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.