On the Interplay of the DNA Replication Program and the Intra-S Phase Checkpoint Pathway.
ATR
Chk1
DNA replication
MBT
initiation rate
intra-S phase checkpoint
numerical
replication checkpoint
theoretical models
Journal
Genes
ISSN: 2073-4425
Titre abrégé: Genes (Basel)
Pays: Switzerland
ID NLM: 101551097
Informations de publication
Date de publication:
29 01 2019
29 01 2019
Historique:
received:
09
01
2019
revised:
23
01
2019
accepted:
25
01
2019
entrez:
1
2
2019
pubmed:
1
2
2019
medline:
1
2
2019
Statut:
epublish
Résumé
DNA replication in eukaryotes is achieved by the activation of multiple replication origins which needs to be precisely coordinated in space and time. This spatio-temporal replication program is regulated by many factors to maintain genome stability, which is frequently threatened through stresses of exogenous or endogenous origin. Intra-S phase checkpoints monitor the integrity of DNA synthesis and are activated when replication forks are stalled. Their activation leads to the stabilization of forks, to the delay of the replication program by the inhibition of late firing origins, and the delay of G2/M phase entry. In some cell cycles during early development these mechanisms are less efficient in order to allow rapid cell divisions. In this article, we will review our current knowledge of how the intra-S phase checkpoint regulates the replication program in budding yeast and metazoan models, including early embryos with rapid S phases. We sum up current models on how the checkpoint can inhibit origin firing in some genomic regions, but allow dormant origin activation in other regions. Finally, we discuss how numerical and theoretical models can be used to connect the multiple different actors into a global process and to extract general rules.
Identifiants
pubmed: 30700024
pii: genes10020094
doi: 10.3390/genes10020094
pmc: PMC6410103
pii:
doi:
Substances chimiques
Cell Cycle Proteins
0
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
Topoisomerase II binding protein 1
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