4.7 Article

p120 catenin is required for normal renal tubulogenesis and glomerulogenesis

Journal

DEVELOPMENT
Volume 138, Issue 10, Pages 2099-2109

Publisher

COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/dev.056564

Keywords

Cadherins; Glomerulogenesis; Kidney development; p120 catenin; Polycystic disease; Mouse

Funding

  1. National Kidney Foundation
  2. March of Dimes
  3. NIH [DK081668, DK068358, DK074398, DK067153, DK064338]

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Defects in the development or maintenance of tubule diameter correlate with polycystic kidney disease. Here, we report that absence of the cadherin regulator p120 catenin (p120ctn) from the renal mesenchyme prior to tubule formation leads to decreased cadherin levels with abnormal morphologies of early tubule structures and developing glomeruli. In addition, mutant mice develop cystic kidney disease, with markedly increased tubule diameter and cellular proliferation, and detached luminal cells only in proximal tubules. The p120ctn homolog Arvcf is specifically absent from embryonic proximal tubules, consistent with the specificity of the proximal tubular phenotype. p120ctn knockdown in renal epithelial cells in 3D culture results in a similar cystic phenotype with reduced levels of E-cadherin and active RhoA. We find that E-cadherin knockdown, but not RhoA inhibition, phenocopies p120ctn knockdown. Taken together, our data show that p120ctn is required for early tubule and glomerular morphogenesis, as well as control of luminal diameter, probably through regulation of cadherins.

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