Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells

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Standard

Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells. / Wu, Wei; Barwacz, Szymon A.; Bhowmick, Rahul; Lundgaard, Katrine; Gonçalves Dinis, Marisa M.; Clausen, Malgorzata; Kanemaki, Masato T.; Liu, Ying.

I: Nature Communications, Bind 14, Nr. 1, 706, 2023.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Wu, W, Barwacz, SA, Bhowmick, R, Lundgaard, K, Gonçalves Dinis, MM, Clausen, M, Kanemaki, MT & Liu, Y 2023, 'Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells', Nature Communications, bind 14, nr. 1, 706. https://doi.org/10.1038/s41467-023-35992-5

APA

Wu, W., Barwacz, S. A., Bhowmick, R., Lundgaard, K., Gonçalves Dinis, M. M., Clausen, M., Kanemaki, M. T., & Liu, Y. (2023). Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells. Nature Communications, 14(1), [706]. https://doi.org/10.1038/s41467-023-35992-5

Vancouver

Wu W, Barwacz SA, Bhowmick R, Lundgaard K, Gonçalves Dinis MM, Clausen M o.a. Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells. Nature Communications. 2023;14(1). 706. https://doi.org/10.1038/s41467-023-35992-5

Author

Wu, Wei ; Barwacz, Szymon A. ; Bhowmick, Rahul ; Lundgaard, Katrine ; Gonçalves Dinis, Marisa M. ; Clausen, Malgorzata ; Kanemaki, Masato T. ; Liu, Ying. / Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells. I: Nature Communications. 2023 ; Bind 14, Nr. 1.

Bibtex

@article{f3908bfe615a4bf7a83cd5d28176b7a5,
title = "Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells",
abstract = "Oncogene activation creates DNA replication stress (RS) in cancer cells, which can generate under-replicated DNA regions (UDRs) that persist until cells enter mitosis. UDRs also have the potential to generate DNA bridges in anaphase cells or micronuclei in the daughter cells, which could promote genomic instability. To suppress such damaging changes to the genome, human cells have developed a strategy to conduct {\textquoteleft}unscheduled{\textquoteright} DNA synthesis in mitosis (termed MiDAS) that serves to rescue under-replicated loci. Previous studies have shown that MiDAS proceeds via a POLD3-dependent pathway that shows some features of break-induced replication. Here, we define how human cells utilize both DNA gap filling (REV1 and Pol ζ) and replicative (Pol δ) DNA polymerases to complete genome duplication following a perturbed S-phase. We present evidence for the existence of a polymerase-switch during MiDAS that is required for new DNA synthesis at UDRs. Moreover, we reveal that, upon oncogene activation, cancer cell survival is significantly compromised when REV1 is depleted, suggesting that REV1 inhibition might be a feasible approach for the treatment of some human cancers.",
author = "Wei Wu and Barwacz, {Szymon A.} and Rahul Bhowmick and Katrine Lundgaard and {Gon{\c c}alves Dinis}, {Marisa M.} and Malgorzata Clausen and Kanemaki, {Masato T.} and Ying Liu",
note = "Publisher Copyright: {\textcopyright} 2023, The Author(s).",
year = "2023",
doi = "10.1038/s41467-023-35992-5",
language = "English",
volume = "14",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells

AU - Wu, Wei

AU - Barwacz, Szymon A.

AU - Bhowmick, Rahul

AU - Lundgaard, Katrine

AU - Gonçalves Dinis, Marisa M.

AU - Clausen, Malgorzata

AU - Kanemaki, Masato T.

AU - Liu, Ying

N1 - Publisher Copyright: © 2023, The Author(s).

PY - 2023

Y1 - 2023

N2 - Oncogene activation creates DNA replication stress (RS) in cancer cells, which can generate under-replicated DNA regions (UDRs) that persist until cells enter mitosis. UDRs also have the potential to generate DNA bridges in anaphase cells or micronuclei in the daughter cells, which could promote genomic instability. To suppress such damaging changes to the genome, human cells have developed a strategy to conduct ‘unscheduled’ DNA synthesis in mitosis (termed MiDAS) that serves to rescue under-replicated loci. Previous studies have shown that MiDAS proceeds via a POLD3-dependent pathway that shows some features of break-induced replication. Here, we define how human cells utilize both DNA gap filling (REV1 and Pol ζ) and replicative (Pol δ) DNA polymerases to complete genome duplication following a perturbed S-phase. We present evidence for the existence of a polymerase-switch during MiDAS that is required for new DNA synthesis at UDRs. Moreover, we reveal that, upon oncogene activation, cancer cell survival is significantly compromised when REV1 is depleted, suggesting that REV1 inhibition might be a feasible approach for the treatment of some human cancers.

AB - Oncogene activation creates DNA replication stress (RS) in cancer cells, which can generate under-replicated DNA regions (UDRs) that persist until cells enter mitosis. UDRs also have the potential to generate DNA bridges in anaphase cells or micronuclei in the daughter cells, which could promote genomic instability. To suppress such damaging changes to the genome, human cells have developed a strategy to conduct ‘unscheduled’ DNA synthesis in mitosis (termed MiDAS) that serves to rescue under-replicated loci. Previous studies have shown that MiDAS proceeds via a POLD3-dependent pathway that shows some features of break-induced replication. Here, we define how human cells utilize both DNA gap filling (REV1 and Pol ζ) and replicative (Pol δ) DNA polymerases to complete genome duplication following a perturbed S-phase. We present evidence for the existence of a polymerase-switch during MiDAS that is required for new DNA synthesis at UDRs. Moreover, we reveal that, upon oncogene activation, cancer cell survival is significantly compromised when REV1 is depleted, suggesting that REV1 inhibition might be a feasible approach for the treatment of some human cancers.

U2 - 10.1038/s41467-023-35992-5

DO - 10.1038/s41467-023-35992-5

M3 - Journal article

C2 - 36759509

AN - SCOPUS:85147790732

VL - 14

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

IS - 1

M1 - 706

ER -

ID: 337595874