Epithelial polarization in 3D matrix requires DDR1 signaling to regulate actomyosin contractility.

ABSTRACT: Epithelial cells form sheets and tubules in various epithelial organs and establish apicobasal polarity and asymmetric vesicle transport to provide functionality in these structures. However, the molecular mechanisms that allow epithelial cells to establish polarity are not clearly understood. Here, we present evidence that the kinase activity of the receptor tyrosine kinase for collagen, discoidin domain receptor 1 (DDR1), is required for efficient establishment of epithelial polarity, proper asymmetric protein secretion, and execution of morphogenic programs. Lack of DDR1 protein or inhibition of DDR1 kinase activity disturbed tubulogenesis, cystogenesis, and the establishment of epithelial polarity and caused defects in the polarized localization of membrane-type 1 matrix metalloprotein

SUBMITTER: Sogaard PP 

PROVIDER: S-EPMC6374992 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature