THO complex deficiency impairs DNA double-strand break repair via the RNA surveillance kinase SMG-1

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

THO complex deficiency impairs DNA double-strand break repair via the RNA surveillance kinase SMG-1. / Kamp, Juliette A; Lemmens, Bennie B L G; Romeijn, Ron J; González-Prieto, Román; Olsen, Jesper V.; Vertegaal, Alfred C O; van Schendel, Robin; Tijsterman, Marcel.

In: Nucleic Acids Research, Vol. 50, No. 11, 2022, p. 6235-6250.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Kamp, JA, Lemmens, BBLG, Romeijn, RJ, González-Prieto, R, Olsen, JV, Vertegaal, ACO, van Schendel, R & Tijsterman, M 2022, 'THO complex deficiency impairs DNA double-strand break repair via the RNA surveillance kinase SMG-1', Nucleic Acids Research, vol. 50, no. 11, pp. 6235-6250. https://doi.org/10.1093/nar/gkac472

APA

Kamp, J. A., Lemmens, B. B. L. G., Romeijn, R. J., González-Prieto, R., Olsen, J. V., Vertegaal, A. C. O., van Schendel, R., & Tijsterman, M. (2022). THO complex deficiency impairs DNA double-strand break repair via the RNA surveillance kinase SMG-1. Nucleic Acids Research, 50(11), 6235-6250. https://doi.org/10.1093/nar/gkac472

Vancouver

Kamp JA, Lemmens BBLG, Romeijn RJ, González-Prieto R, Olsen JV, Vertegaal ACO et al. THO complex deficiency impairs DNA double-strand break repair via the RNA surveillance kinase SMG-1. Nucleic Acids Research. 2022;50(11):6235-6250. https://doi.org/10.1093/nar/gkac472

Author

Kamp, Juliette A ; Lemmens, Bennie B L G ; Romeijn, Ron J ; González-Prieto, Román ; Olsen, Jesper V. ; Vertegaal, Alfred C O ; van Schendel, Robin ; Tijsterman, Marcel. / THO complex deficiency impairs DNA double-strand break repair via the RNA surveillance kinase SMG-1. In: Nucleic Acids Research. 2022 ; Vol. 50, No. 11. pp. 6235-6250.

Bibtex

@article{37d70c8a65ab47a8bab8e1c03527f3c1,
title = "THO complex deficiency impairs DNA double-strand break repair via the RNA surveillance kinase SMG-1",
abstract = "The integrity and proper expression of genomes are safeguarded by DNA and RNA surveillance pathways. While many RNA surveillance factors have additional functions in the nucleus, little is known about the incidence and physiological impact of converging RNA and DNA signals. Here, using genetic screens and genome-wide analyses, we identified unforeseen SMG-1-dependent crosstalk between RNA surveillance and DNA repair in living animals. Defects in RNA processing, due to viable THO complex or PNN-1 mutations, induce a shift in DNA repair in dividing and non-dividing tissues. Loss of SMG-1, an ATM/ATR-like kinase central to RNA surveillance by nonsense-mediated decay (NMD), restores DNA repair and radio-resistance in THO-deficient animals. Mechanistically, we find SMG-1 and its downstream target SMG-2/UPF1, but not NMD per se, to suppress DNA repair by non-homologous end-joining in favour of single strand annealing. We postulate that moonlighting proteins create short-circuits in vivo, allowing aberrant RNA to redirect DNA repair.",
author = "Kamp, {Juliette A} and Lemmens, {Bennie B L G} and Romeijn, {Ron J} and Rom{\'a}n Gonz{\'a}lez-Prieto and Olsen, {Jesper V.} and Vertegaal, {Alfred C O} and {van Schendel}, Robin and Marcel Tijsterman",
note = "{\textcopyright} The Author(s) 2022. Published by Oxford University Press on behalf of Nucleic Acids Research.",
year = "2022",
doi = "10.1093/nar/gkac472",
language = "English",
volume = "50",
pages = "6235--6250",
journal = "Nucleic Acids Research",
issn = "0305-1048",
publisher = "Oxford University Press",
number = "11",

}

RIS

TY - JOUR

T1 - THO complex deficiency impairs DNA double-strand break repair via the RNA surveillance kinase SMG-1

AU - Kamp, Juliette A

AU - Lemmens, Bennie B L G

AU - Romeijn, Ron J

AU - González-Prieto, Román

AU - Olsen, Jesper V.

AU - Vertegaal, Alfred C O

AU - van Schendel, Robin

AU - Tijsterman, Marcel

N1 - © The Author(s) 2022. Published by Oxford University Press on behalf of Nucleic Acids Research.

PY - 2022

Y1 - 2022

N2 - The integrity and proper expression of genomes are safeguarded by DNA and RNA surveillance pathways. While many RNA surveillance factors have additional functions in the nucleus, little is known about the incidence and physiological impact of converging RNA and DNA signals. Here, using genetic screens and genome-wide analyses, we identified unforeseen SMG-1-dependent crosstalk between RNA surveillance and DNA repair in living animals. Defects in RNA processing, due to viable THO complex or PNN-1 mutations, induce a shift in DNA repair in dividing and non-dividing tissues. Loss of SMG-1, an ATM/ATR-like kinase central to RNA surveillance by nonsense-mediated decay (NMD), restores DNA repair and radio-resistance in THO-deficient animals. Mechanistically, we find SMG-1 and its downstream target SMG-2/UPF1, but not NMD per se, to suppress DNA repair by non-homologous end-joining in favour of single strand annealing. We postulate that moonlighting proteins create short-circuits in vivo, allowing aberrant RNA to redirect DNA repair.

AB - The integrity and proper expression of genomes are safeguarded by DNA and RNA surveillance pathways. While many RNA surveillance factors have additional functions in the nucleus, little is known about the incidence and physiological impact of converging RNA and DNA signals. Here, using genetic screens and genome-wide analyses, we identified unforeseen SMG-1-dependent crosstalk between RNA surveillance and DNA repair in living animals. Defects in RNA processing, due to viable THO complex or PNN-1 mutations, induce a shift in DNA repair in dividing and non-dividing tissues. Loss of SMG-1, an ATM/ATR-like kinase central to RNA surveillance by nonsense-mediated decay (NMD), restores DNA repair and radio-resistance in THO-deficient animals. Mechanistically, we find SMG-1 and its downstream target SMG-2/UPF1, but not NMD per se, to suppress DNA repair by non-homologous end-joining in favour of single strand annealing. We postulate that moonlighting proteins create short-circuits in vivo, allowing aberrant RNA to redirect DNA repair.

U2 - 10.1093/nar/gkac472

DO - 10.1093/nar/gkac472

M3 - Journal article

C2 - 35670662

VL - 50

SP - 6235

EP - 6250

JO - Nucleic Acids Research

JF - Nucleic Acids Research

SN - 0305-1048

IS - 11

ER -

ID: 310852975