An unrecognized host response to microbial exposure resets circadian timing
or nascent transcription. A targeted inhibitor screen and biochemical assays implicate p38 MAPK as a modulator of this response. Taken together, this positions bacterial exposure as a previously unrecognized circadian clock input, revealing a new axis of host-microbe interaction that modulates biological timing at the cellular level.
Authors
- John S. O’Neill (ORCID: https://orcid.org/0000-0003-2204-6096)
- Antony N. Dodd (ORCID: https://orcid.org/0000-0001-6859-0105)
- Carrie L. Partch (ORCID: https://orcid.org/0000-0002-4677-2861)
- Jacqueline M. Kimmey (ORCID: https://orcid.org/0000-0003-1330-8525)
- Devons Mo
- Gerben van Ooijen (ORCID: https://orcid.org/0000-0001-7967-0637)
- Priya Crosby (ORCID: https://orcid.org/0000-0002-7532-7708)
- Jack Dorling (ORCID: https://orcid.org/0000-0002-2012-3054)
- Ti Lam
- Ella Baker
- Olivia P Fraser
Institutions
- John Innes Centre (GB)
- Howard Hughes Medical Institute (US)
- MRC Laboratory of Molecular Biology (GB)
- University of California, Santa Cruz (US)
- Norwich Research Park (GB)
- University of California San Diego (US)
- University of Edinburgh (GB)
Publication Details
- Journal
- bioRxiv (Cold Spring Harbor Laboratory)
- Published
- 2026-04-14
- DOI
- https://doi.org/10.64898/2026.04.11.717924
- Primary Topic
- Circadian rhythm and melatonin
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Howard Hughes Medical Institute
- Alfred P. Sloan Foundation
- University of California, Santa Cruz
- Wellcome Trust
- Boehringer Ingelheim Fonds
- National Institutes of Health
- Medical Research Council
- Biotechnology and Biological Sciences Research Council
- National Institute of General Medical Sciences