Structure-Specific Endonucleases and the Resolution of Chromosome Underreplication.
DNA replication
Holliday junction resolvase
chromosome segregation
chromosome stability
genome stability
mitotic DNA synthesis
replication stress
structure-specific nuclease
ultrafine anaphase bridge
Journal
Genes
ISSN: 2073-4425
Titre abrégé: Genes (Basel)
Pays: Switzerland
ID NLM: 101551097
Informations de publication
Date de publication:
19 03 2019
19 03 2019
Historique:
received:
22
02
2019
revised:
11
03
2019
accepted:
13
03
2019
entrez:
22
3
2019
pubmed:
22
3
2019
medline:
22
3
2019
Statut:
epublish
Résumé
Complete genome duplication in every cell cycle is fundamental for genome stability and cell survival. However, chromosome replication is frequently challenged by obstacles that impede DNA replication fork (RF) progression, which subsequently causes replication stress (RS). Cells have evolved pathways of RF protection and restart that mitigate the consequences of RS and promote the completion of DNA synthesis prior to mitotic chromosome segregation. If there is entry into mitosis with underreplicated chromosomes, this results in sister-chromatid entanglements, chromosome breakage and rearrangements and aneuploidy in daughter cells. Here, we focus on the resolution of persistent replication intermediates by the structure-specific endonucleases (SSEs) MUS81, SLX1-SLX4 and GEN1. Their actions and a recently discovered pathway of mitotic DNA repair synthesis have emerged as important facilitators of replication completion and sister chromatid detachment in mitosis. As RS is induced by oncogene activation and is a common feature of cancer cells, any advances in our understanding of the molecular mechanisms related to chromosome underreplication have important biomedical implications.
Identifiants
pubmed: 30893921
pii: genes10030232
doi: 10.3390/genes10030232
pmc: PMC6470701
pii:
doi:
Substances chimiques
DNA-Binding Proteins
0
Recombinases
0
EME2 protein, human
EC 3.1.-
Endodeoxyribonucleases
EC 3.1.-
Endonucleases
EC 3.1.-
MUS81 protein, human
EC 3.1.-
SLX1 protein, human
EC 3.1.-
SLX4 protein, human
EC 3.1.-
GEN1 protein, human
EC 3.1.21.-
Holliday Junction Resolvases
EC 3.1.21.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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