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Peer-reviewedCC BYBiochemistry and biophysics reports

Med1 deletion reprograms dental epithelium into a hair-forming epidermal architecture associated with Trp63 induction.

  • Roman Thaler1,2
  • Yuta Chiba3
  • Zhiyun Lin4
  • Sun Hee Won Kim4
  • Satoshi Fukumoto3,5
  • Pamela Den Besten6
  • Daniel D Bikle4
  • Keigo Yoshizaki5
  • Yuko Oda4
6 affiliations
  1. 1Department of Orthopedic Surgery, Mayo Clinic, Rochester, MN, USA.
  2. 2Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, USA.
  3. 3Division of Pediatric Dentistry, Department of Community Social Dentistry, Tohoku University Graduate School of Dentistry, Sendai, Japan.
  4. 4Departments of Medicine and Endocrinology, University of California San Francisco and San Francisco Veterans Affairs Health Center, CA, USA.
  5. 5Section of Orthodontics and Dentofacial Orthopedics, Division of Oral Health, Growth and Development, Kyushu University Faculty of Dental Science, Fukuoka, Japan.
  6. 6Department of Dentistry, University of California San Francisco, CA, USA.
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Abstract

Ectodermal fate decisions between tooth enamel and skin hair are governed by transcriptional regulation and tissue architecture. Deletion of the Mediator subunit Med1, which links enhancer activity to transcriptional output, induces a striking lineage conversion characterized by ectopic hair formation in mouse incisors. Here, we investigated the cellular and transcriptional mechanisms underlying this process. Single-cell and spatial transcriptomic analyses revealed extensive remodeling of the incisor epithelium following Med1 deletion, whereby dental cells are converted into hair germ-like populations while retaining dental identity. Epidermal fate is associated with induction of the master regulator Trp63. Mechanistically, Med1 deletion leads to chromatin opening where TRP63 enriches at alternative MED12 containing enhancers that associate with the transcription of epidermal genes. Together, these findings suggest that Med1 loss promotes hair formation through unusual reprogramming of the dental lineage to an epidermal state rather than direct trans-differentiation to skin epithelium, providing new insights in ectodermal plasticity.

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Cite

BibTeXRIS
BibTeX
@article{thaler2026med1,
  title = {{Med1 deletion reprograms dental epithelium into a hair-forming epidermal architecture associated with Trp63 induction.}},
  author = {Roman Thaler and Yuta Chiba and Zhiyun Lin and Sun Hee Won Kim and Satoshi Fukumoto and Pamela Den Besten and Daniel D Bikle and Keigo Yoshizaki and Yuko Oda},
  journal = {Biochemistry and biophysics reports},
  year = {2026},
  month = oct,
  doi = {10.1016/j.bbrep.2026.102828},
  url = {https://europepmc.org/article/MED/42904106},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Med1 deletion reprograms dental epithelium into a hair-forming epidermal architecture associated with Trp63 induction.
AU  - Roman Thaler
AU  - Yuta Chiba
AU  - Zhiyun Lin
AU  - Sun Hee Won Kim
AU  - Satoshi Fukumoto
AU  - Pamela Den Besten
AU  - Daniel D Bikle
AU  - Keigo Yoshizaki
AU  - Yuko Oda
PY  - 2026
DA  - 2026/10/12
JO  - Biochemistry and biophysics reports
DO  - 10.1016/j.bbrep.2026.102828
UR  - https://europepmc.org/article/MED/42904106
AB  - Ectodermal fate decisions between tooth enamel and skin hair are governed by transcriptional regulation and tissue architecture. Deletion of the Mediator subunit Med1, which links enhancer activity to transcriptional output, induces a striking lineage conversion characterized by ectopic hair formation in mouse incisors. Here, we investigated the cellular and transcriptional mechanisms underlying this process. Single-cell and spatial transcriptomic analyses revealed extensive remodeling of the incisor epithelium following Med1 deletion, whereby dental cells are converted into hair germ-like populations while retaining dental identity. Epidermal fate is associated with induction of the master regulator Trp63. Mechanistically, Med1 deletion leads to chromatin opening where TRP63 enriches at alternative MED12 containing enhancers that associate with the transcription of epidermal genes. Together, these findings suggest that Med1 loss promotes hair formation through unusual reprogramming of the dental lineage to an epidermal state rather than direct trans-differentiation to skin epithelium, providing new insights in ectodermal plasticity.
SN  - 2405-5808
ER  -