J 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

Štítky

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.