Type XVII collagen interacts with the aPKC‐PAR complex and maintains epidermal cell polarity

Type XVII collagen (COL17) is a transmembrane protein expressed in the basal epidermis. COL17 serves as a niche for epidermal stem cells, and although its reduction has been implicated in altering cell polarity and ageing of the epidermis, it is unknown how COL17 affects epidermal cell polarity. Her...

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Bibliographic Details
Published in:Experimental dermatology 2021-01, Vol.30 (1), p.62-67
Main Authors: Watanabe, Mika, Kosumi, Hideyuki, Osada, Shin‐Ichi, Takashima, Shota, Wang, Yunan, Nishie, Wataru, Oikawa, Tsukasa, Hirose, Tomonori, Shimizu, Hiroshi, Natsuga, Ken
Format: Article
Language:English
Subjects:
Adaptor Proteins, Signal Transducing - metabolism
Aging
Animals
atypical PKC
Autoantigens - genetics
Autoantigens - metabolism
Cell Cycle Proteins - metabolism
Cell division
Cell Polarity
COL17
Collagen
Collagen Type XVII
epidermal stem cell
Epidermis
Epidermis - metabolism
HEK293 Cells
Humans
Immunoprecipitation
Keratinocytes
Mice
Mice, Knockout
Neonates
Non-Fibrillar Collagens - genetics
Non-Fibrillar Collagens - metabolism
PAR3
Polarity
Protein Isoforms - metabolism
Protein Kinase C - metabolism
Proteins
Stem cells
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Summary:Type XVII collagen (COL17) is a transmembrane protein expressed in the basal epidermis. COL17 serves as a niche for epidermal stem cells, and although its reduction has been implicated in altering cell polarity and ageing of the epidermis, it is unknown how COL17 affects epidermal cell polarity. Here, we uncovered COL17 as a binding partner of the aPKC‐PAR complex, which is a key regulating factor of cell polarity. Immunoprecipitation‐immunoblot assay and protein‐protein binding assay revealed that COL17 interacts with aPKC and PAR3. COL17 deficiency or epidermis‐specific aPKCλ deletion destabilized PAR3 distribution in the epidermis, while aPKCζ knockout did not. Asymmetrical cell division was pronounced in COL17‐null neonatal paw epidermis. These results show that COL17 is pivotal for maintaining epidermal cell polarity. Our study highlights the previously unrecognized role of COL17 in the basal keratinocytes.
ISSN:0906-6705
1600-0625
DOI:10.1111/exd.14196