Detailed Information on Publication Record
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.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
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
10601 Cell biology
Country of publisher
United Kingdom of Great Britain and Northern Ireland
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 4.379
RIV identification code
RIV/00216224:14110/20:00115984
Organization unit
Faculty of Medicine
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
International impact, Reviewed
Změněno: 15/7/2020 09:51, Mgr. Tereza Miškechová
Abstract
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.