Cellular reprogramming in vivo initiated by SOX4 pioneer factor activity
Open accessAbstract
Tissue damage elicits cell fate switching through a process called metaplasia, but how the starting cell fate is silenced and the new cell fate is activated has not been investigated in animals. In cell culture, pioneer transcription factors mediate “reprogramming” by opening new chromatin sites for expression that can attract transcription factors from the starting cell’s enhancers. Here we report that SOX4 is sufficient to initiate hepatobiliary metaplasia in the adult mouse liver, closely mimicking metaplasia initiated by toxic damage to the liver. In lineage-traced cells, we assessed the timing of SOX4-mediated opening of enhancer chromatin versus enhancer decommissioning. Initially, SOX4 directly binds to and closes hepatocyte regulatory sequences via an overlapping motif with HNF4A, a hepatocyte master regulatory transcription factor. Subsequently, SOX4 exerts pioneer factor activity to open biliary regulatory sequences. The results delineate a hierarchy by which gene networks become reprogrammed under physiological conditions, providing deeper insight into the basis for cell fate transitions in animals.
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Lineage-tracing studies in animal models have confirmed that hepatocytes contribute to bile duct remodeling following cholangiocyte injury.
“Lineage-tracing studies in animal models have confirmed that hepatocytes contribute to bile duct remodeling following cholangiocyte injury10,43–48”
From HBO1 functions as an epigenetic barrier to hepatocyte plasticity and reprogramming during liver injury (2025) · cites this paper as [48]
The Introduction (page unavailable) says hepatocytes can become biliary epithelial cells after liver injury and that the model permits tracing cells during this change. The Results section on Sox4 and Sox9 (page unavailable) documents hepatocyte reprogramming after DDC-induced cholestatic injury, but does not establish bile duct remodeling specifically following cholangiocyte injury. (LLM, conf=0.85)
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SOX4: A potential therapeutic target for liver disease
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- Authors
- Katsuda, T., Sussman, J. H., Ito, K., Katznelson, A., Yuan, S., Takenaka, N., Li, J., Merrell, A. J., Cure, H., Li, Q., Rasool, R. U., Asangani, I. A., Zaret, K. S., & Stanger, B. Z.
- Affiliations
- Abramson Cancer Center (US)
- University of Pennsylvania (US)
- Corresponding author
- Zaret, Kenneth S.
- Stanger, Ben Z.
- ORCID
- Venue
- Nature Communications
- Published
- 2024-02-26
- Volume
- 15
- Issue
- 1
- Pages
- 1761-1761
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC10897393
- OpenAlex
- W4392169818
- Cited by
- 33
- References
- 65
- Citations by year
- 2026: 9 · 2025: 18 · 2024: 5 · 2023: 1
- FWCI
- 8.38
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- U.S. Department of Health & Human Services | National Institutes of Health (R01DK083355, R01DK125387, P30DK050306, R01CA249210)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- SOX4, pioneer transcription factors, cellular reprogramming, liver injury, cell fate transitions, HNF4α, lineage tracing, gene regulatory networks
- MeSH terms
- Animals, Cell Differentiation, Chromatin, Metaplasia, Transcription Factors, Mice, SOXC Transcription Factors, Cellular Reprogramming
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