E‐cadherin controls adherens junctions in the epidermis and the renewal of hair follicles
Open accessAbstract
E-cadherin is thought to mediate intercellular adhesion in the mammalian epidermis and in hair follicles as the adhesive component of adherens junctions. We have tested this role of E-cadherin directly by conditional gene ablation in the mouse. We show that postnatal loss of E-cadherin in keratinocytes leads to a loss of adherens junctions and altered epidermal differentiation without accompanying signs of inflammation. Overall tissue integrity and desmosomal structures were maintained, but skin hair follicles were progressively lost. Tumors were not observed and beta-catenin levels were not strongly altered in the mutant skin. We conclude that E-cadherin is required for maintaining the adhesive properties of adherens junctions in keratinocytes and proper skin differentiation. Furthermore, continuous hair follicle cycling is dependent on E-cadherin.
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No difference in localization of desmosomal markers plakoglobin, desmocollin 2 and desmoglein 1/2 was observed between control and E-cadherin mutant mice.
“As described previously (Young et al, 2003;Tinkle et al, 2004), no difference in localization of desmosomal markers like plakoglobin, desmocollin 2 and desmoglein 1/2 was observed (Figure 3A).”
From E‐cadherin is essential for in vivo epidermal barrier function by regulating tight junctions (2005) · cites this paper as Young et al, 2003
The ‘Ablation of E-cadherin alters epidermal differentiation’ section (page not provided) says desmoglein expression was comparable in mutant and control tissue, and the Figure 6 caption reports similar localization of desmoplakin. The copy also reports preserved desmosomes, but it does not establish unchanged localization for plakoglobin or desmocollin 2, or specify desmoglein 1/2. (LLM, conf=0.86)
Experimental — accuracy not yet measuredBoth blistering and overgrowth phenotypes are not observed in K14-Cre/Ecad Fl/À mice.
“Both phenotypes are not observed in K14-Cre/Ecad Fl/À mice (Young et al, 2003;Tinkle et al, 2004;this paper).”
From E‐cadherin is essential for in vivo epidermal barrier function by regulating tight junctions (2005) · cites this paper as Young et al, 2003
The “Generation of conditional E-cadherin-deficient mice” section identifies the mutants as Krox20-Cre; E-cadherin ±/lox, not K14-Cre/Ecad Fl/−. The “Reduced proliferation in hair follicles” section reports no detected increase in epidermal proliferation in those mutants, but the paper does not establish the absence of both blistering and overgrowth in the K14-Cre genotype. (LLM, conf=0.76)
Experimental — accuracy not yet measuredThis paper, and another study, in which E-cadherin was inactivated in the epidermis after birth, showed a gradual loss of hair in the E-cadherin mutant mice.
“This paper, and another study, in which E-cadherin was inactivated in the epidermis after birth, showed a gradual loss of hair in the E-cadherin mutant mice (Young et al, 2003;Tinkle et al, 2004).”
From E‐cadherin is essential for in vivo epidermal barrier function by regulating tight junctions (2005) · cites this paper as Young et al, 2003
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- Authors
- Young, P., Boussadia, O., Halfter, H., Grose, R., Berger, P., Leone, D. P., Robenek, H., Charnay, P., Kemler, R., & Suter, U.
- Affiliations
- University of Münster (DE)
- Cancer Research UK (GB)
- ETH Zurich (CH)
- Inserm (FR)
- Max Planck Institute of Immunobiology and Epigenetics (DE)
- Corresponding author
- Suter, Ueli
- Venue
- The EMBO Journal
- Published
- 2003-11-03
- Volume
- 22
- Issue
- 21
- Pages
- 5723-5733
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC275417
- OpenAlex
- W2097736136
- Cited by
- 156
- References
- 50
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 8 · 2023: 8 · 2022: 2 · 2021: 9 · 2020: 7 · 2019: 5 · 2018: 2 · 2017: 6 · 2016: 5 · 2015: 5 · 2014: 10 · 2013: 10 · 2012: 8
- FWCI
- 6.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Digital Library (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- National Science Foundation
- Deutsche Forschungsgemeinschaft
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Topics
- Health Sciences › Medicine › Urology › Hair Growth and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Skin and Cellular Biology Research
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Keywords
- E-cadherin, adherens junctions, epidermis, keratinocytes, epidermal differentiation, conditional gene deletion, β-catenin, desmosomes, hair cycle, cell-cell adhesion
- MeSH terms
- Epidermal Cells, Animals, Cell Differentiation, DNA-Binding Proteins, Epidermis, Mice, Inbred C57BL, Transcription Factors, Keratinocytes, Cadherins, Mice, Knockout, Gene Expression Regulation, Developmental, Hair Follicle, Adherens Junctions, Mice, Early Growth Response Protein 2
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