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.

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

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.