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Abstract：
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.
摘要：
XVII型胶原(COL17)是在基底表皮中表达的跨膜蛋白。COL17作为表皮干细胞的小生境，尽管它的减少与改变细胞极性和表皮老化有关，目前尚不清楚COL17如何影响表皮细胞极性。这里,我们发现COL17是aPKC-PAR复合物的结合伴侣，是细胞极性的关键调节因子。免疫沉淀-免疫印迹测定和蛋白质-蛋白质结合测定显示COL17与aPKC和PAR3相互作用。COL17缺乏或表皮特异性aPKCλ缺失使PAR3在表皮中的分布不稳定，而aPKCζ敲除没有。在COL17无效的新生儿爪表皮中，细胞分裂不对称。这些结果表明COL17对于维持表皮细胞极性至关重要。我们的研究强调了COL17在基底角质形成细胞中先前未被识别的作用。
