Type XVII collagen interacts with the aPKC‐PAR complex and maintains epidermal cell polarity
Type XVII collagen interacts with the aPKC‐PAR complex and maintains epidermal cell polarity
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DOI：
10.1111/exd.14196
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发表时间：
2020-09
影响因子：
3.6
通讯作者：
M. Watanabe;H. Kosumi;S. Osada;S. Takashima;Yunan Wang;W. Nishie;Tsukasa Oikawa;Tomonori Hirose;H. Shimizu;K. Natsuga
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文献类型：
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作者：
M. Watanabe;H. Kosumi;S. Osada;S. Takashima;Yunan Wang;W. Nishie;Tsukasa Oikawa;Tomonori Hirose;H. Shimizu;K. Natsuga
XVII型胶原（COL 17）是在基底表皮中表达的跨膜蛋白。COL 17作为表皮干细胞的小生境，尽管其减少与改变细胞极性和表皮老化有关，但尚不清楚COL 17如何影响表皮细胞极性。在这里，我们发现COL 17是aPKC-PAR复合物的结合伴侣，这是细胞极性的关键调节因子。免疫沉淀-免疫印迹试验和蛋白-蛋白结合试验表明，COL 17与aPKC和PAR 3相互作用。COL 17缺陷或表皮特异性aPKCλ缺失使PAR 3在表皮中的分布不稳定，而aPKC λ敲除则没有。在COL 17缺失的新生儿爪表皮中，不对称细胞分裂明显。这些结果表明，COL 17是维持表皮细胞极性的关键。我们的研究强调了以前未被认识到的COL 17在基底角质形成细胞中的作用。
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.