Completing genome replication outside of S phase

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Completing genome replication outside of S phase. / Bhowmick, Rahul; Hickson, Ian D.; Liu, Ying.

In: Molecular Cell, Vol. 83, No. 20, 2023, p. 3596-3607.

Research output: Contribution to journal › Review › Research › peer-review

Harvard

Bhowmick, R, Hickson, ID & Liu, Y 2023, 'Completing genome replication outside of S phase', Molecular Cell, vol. 83, no. 20, pp. 3596-3607. https://doi.org/10.1016/j.molcel.2023.08.023

APA

Bhowmick, R., Hickson, I. D., & Liu, Y. (2023). Completing genome replication outside of S phase. Molecular Cell, 83(20), 3596-3607. https://doi.org/10.1016/j.molcel.2023.08.023

Vancouver

Bhowmick R, Hickson ID, Liu Y. Completing genome replication outside of S phase. Molecular Cell. 2023;83(20):3596-3607. https://doi.org/10.1016/j.molcel.2023.08.023

Author

Bhowmick, Rahul ; Hickson, Ian D. ; Liu, Ying. / Completing genome replication outside of S phase. In: Molecular Cell. 2023 ; Vol. 83, No. 20. pp. 3596-3607.

Bibtex

@article{1d3efc0657834c06be4aaa6da82f0459,
title = "Completing genome replication outside of S phase",
abstract = "Mitotic DNA synthesis (MiDAS) is an unusual form of DNA replication that occurs during mitosis. Initially, MiDAS was characterized as a process associated with intrinsically unstable loci known as common fragile sites that occurs after cells experience DNA replication stress (RS). However, it is now believed to be a more widespread “salvage” mechanism that is called upon to complete the duplication of any under-replicated genomic region. Emerging data suggest that MiDAS is a DNA repair process potentially involving two or more pathways working in parallel or sequentially. In this review, we introduce the causes of RS, regions of the human genome known to be especially vulnerable to RS, and the strategies used to complete DNA replication outside of S phase. Additionally, because MiDAS is a prominent feature of aneuploid cancer cells, we will discuss how targeting MiDAS might potentially lead to improvements in cancer therapy.",
keywords = "BIR, break-induced replication, fragile sites, homologous recombination, MiDAS, MiDAS-seq, mitotic DNA synthesis, replication stress",
author = "Rahul Bhowmick and Hickson, {Ian D.} and Ying Liu",
note = "Publisher Copyright: {\textcopyright} 2023 The Authors",
year = "2023",
doi = "10.1016/j.molcel.2023.08.023",
language = "English",
volume = "83",
pages = "3596--3607",
journal = "Molecular Cell",
issn = "1097-2765",
publisher = "Cell Press",
number = "20",

}

RIS

TY - JOUR

T1 - Completing genome replication outside of S phase

AU - Bhowmick, Rahul

AU - Hickson, Ian D.

AU - Liu, Ying

N1 - Publisher Copyright: © 2023 The Authors

PY - 2023

Y1 - 2023

N2 - Mitotic DNA synthesis (MiDAS) is an unusual form of DNA replication that occurs during mitosis. Initially, MiDAS was characterized as a process associated with intrinsically unstable loci known as common fragile sites that occurs after cells experience DNA replication stress (RS). However, it is now believed to be a more widespread “salvage” mechanism that is called upon to complete the duplication of any under-replicated genomic region. Emerging data suggest that MiDAS is a DNA repair process potentially involving two or more pathways working in parallel or sequentially. In this review, we introduce the causes of RS, regions of the human genome known to be especially vulnerable to RS, and the strategies used to complete DNA replication outside of S phase. Additionally, because MiDAS is a prominent feature of aneuploid cancer cells, we will discuss how targeting MiDAS might potentially lead to improvements in cancer therapy.

AB - Mitotic DNA synthesis (MiDAS) is an unusual form of DNA replication that occurs during mitosis. Initially, MiDAS was characterized as a process associated with intrinsically unstable loci known as common fragile sites that occurs after cells experience DNA replication stress (RS). However, it is now believed to be a more widespread “salvage” mechanism that is called upon to complete the duplication of any under-replicated genomic region. Emerging data suggest that MiDAS is a DNA repair process potentially involving two or more pathways working in parallel or sequentially. In this review, we introduce the causes of RS, regions of the human genome known to be especially vulnerable to RS, and the strategies used to complete DNA replication outside of S phase. Additionally, because MiDAS is a prominent feature of aneuploid cancer cells, we will discuss how targeting MiDAS might potentially lead to improvements in cancer therapy.

KW - BIR

KW - break-induced replication

KW - fragile sites

KW - homologous recombination

KW - MiDAS

KW - MiDAS-seq

KW - mitotic DNA synthesis

KW - replication stress

U2 - 10.1016/j.molcel.2023.08.023

DO - 10.1016/j.molcel.2023.08.023

M3 - Review

C2 - 37716351

AN - SCOPUS:85172923568

VL - 83

SP - 3596

EP - 3607

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

IS - 20

ER -

ID: 371277118