Nature Communications (Oct 2020)
The ALPK1/TIFA/NF-κB axis links a bacterial carcinogen to R-loop-induced replication stress
- Michael Bauer,
- Zuzana Nascakova,
- Anca-Irina Mihai,
- Phil F. Cheng,
- Mitchell P. Levesque,
- Simon Lampart,
- Robert Hurwitz,
- Lennart Pfannkuch,
- Jana Dobrovolna,
- Melanie Jacobs,
- Sina Bartfeld,
- Anders Dohlman,
- Xiling Shen,
- Alevtina A. Gall,
- Nina R. Salama,
- Antonia Töpfer,
- Achim Weber,
- Thomas F. Meyer,
- Pavel Janscak,
- Anne Müller
Affiliations
- Michael Bauer
- Institute of Molecular Cancer Research, University of Zurich
- Zuzana Nascakova
- Institute of Molecular Genetics, Academy of Sciences of the Czech Republic
- Anca-Irina Mihai
- Institute of Molecular Cancer Research, University of Zurich
- Phil F. Cheng
- Department of Dermatology, University Hospital Zurich
- Mitchell P. Levesque
- Department of Dermatology, University Hospital Zurich
- Simon Lampart
- Institute of Molecular Cancer Research, University of Zurich
- Robert Hurwitz
- Max Planck Institute for Infection Biology, Department of Molecular Biology
- Lennart Pfannkuch
- Max Planck Institute for Infection Biology, Department of Molecular Biology
- Jana Dobrovolna
- Institute of Molecular Genetics, Academy of Sciences of the Czech Republic
- Melanie Jacobs
- Research Center for Infectious Diseases, Institute for Molecular Infection Biology, University of Würzburg
- Sina Bartfeld
- Research Center for Infectious Diseases, Institute for Molecular Infection Biology, University of Würzburg
- Anders Dohlman
- Biomedical Engineering, Duke University
- Xiling Shen
- Biomedical Engineering, Duke University
- Alevtina A. Gall
- Division of Human Biology, Fred Hutchinson Cancer Research Center
- Nina R. Salama
- Division of Human Biology, Fred Hutchinson Cancer Research Center
- Antonia Töpfer
- Department of Pathology and Molecular Pathology, University Hospital Zurich and University of Zurich
- Achim Weber
- Institute of Molecular Cancer Research, University of Zurich
- Thomas F. Meyer
- Max Planck Institute for Infection Biology, Department of Molecular Biology
- Pavel Janscak
- Institute of Molecular Cancer Research, University of Zurich
- Anne Müller
- Institute of Molecular Cancer Research, University of Zurich
- DOI
- https://doi.org/10.1038/s41467-020-18857-z
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 16
Abstract
The bacterial pathogen Helicobacter pylori is known for its ability to induce DNA double-strand breaks in the genome of its target cells. Here, we show that H. pylori-induced DNA damage and replication stress occurs in S-phase cells as a result of R-loop-mediated transcription/replication conflicts that are triggered by activation of the ALPK1/TIFA/NF-κB signaling axis.
