FIRRM/C1orf112 is synthetic lethal with PICH and mediates RAD51 dynamics.
C1orf112
CP: Molecular biology
FIRRM
PICH
UFBs
cell cycle
genetic screen
mitosis
rad51
replication
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
25 07 2023
25 07 2023
Historique:
received:
11
11
2022
revised:
21
04
2023
accepted:
05
06
2023
medline:
31
7
2023
pubmed:
22
6
2023
entrez:
22
6
2023
Statut:
ppublish
Résumé
Joint DNA molecules are natural byproducts of DNA replication and repair. Persistent joint molecules give rise to ultrafine DNA bridges (UFBs) in mitosis, compromising sister chromatid separation. The DNA translocase PICH (ERCC6L) has a central role in UFB resolution. A genome-wide loss-of-function screen is performed to identify the genetic context of PICH dependency. In addition to genes involved in DNA condensation, centromere stability, and DNA-damage repair, we identify FIGNL1-interacting regulator of recombination and mitosis (FIRRM), formerly known as C1orf112. We find that FIRRM interacts with and stabilizes the AAA
Identifiants
pubmed: 37347663
pii: S2211-1247(23)00679-4
doi: 10.1016/j.celrep.2023.112668
pii:
doi:
Substances chimiques
Proteins
0
Adenosine Triphosphatases
EC 3.6.1.-
DNA
9007-49-2
Rad51 Recombinase
EC 2.7.7.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
112668Informations de copyright
Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests The authors declare no competing interests.