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First published online November 27, 2006
doi: 10.1242/10.1242/jcs.03269

Journal of Cell Science 119, 4797-4801 (2006)
Published by The Company of Biologists 2006
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Commentary

Differentiation of columnar epithelia: the hensin pathway

Soundarapandian Vijayakumar1, Jiro Takito1,*, XiaoBo Gao1, George J. Schwartz2 and Qais Al-Awqati1,{ddagger}

1 Departments of Medicine and Physiology and Cellular Biophysics, College of Physicians and Surgeons of Columbia University, 630 W 168th St, New York, NY 10032, USA
2 Department of Pediatrics, University of Rochester School of Medicine, Rochester, NY, USA

{ddagger} Author for correspondence (e-mail: qa1{at}columbia.edu)

Accepted 20 September 2006

Epithelia, the most common variety of cells in complex organisms exist in many shapes. They are sheets of polarized cells that separate two compartments and selectively transport materials from one to the other. After acquiring these general characteristics, they differentiate to become specialized types such as squamous columnar or transitional epithelia. High density seeding converts a kidney-derived cell line from flat `generic' epithelial cells to columnar cells. The cells acquire all the characteristics of differentiated columnar cells, including microvilli, and the capacity for apical endocytosis. The high seeding density induces the deposition of a new protein termed hensin and polymerization of hensin is the crucial event that dictates changes in epithelial phenotype. Hensin is widely expressed in most epithelia. Its deletion in mice leads to embryonic lethality at the time of generation of the first columnar epithelium, the visceral endoderm. Moreover many human cancers have deletions in the hensin gene, which indicates that it is a tumor suppressor.

Key words: Hensin, DMBT1, Epithelial terminal differentiation, Columnar epithelia




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