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Evaluation of Zebrafish Kidney Function Using a Fluorescent Clearance Assay
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Published on: February 20, 2015

Cdc42 deficiency causes ciliary abnormalities and cystic kidneys.

Soo Young Choi1, Maria F Chacon-Heszele, Liwei Huang

  • 1Department of Medicine, University of Pennsylvania, Philadelphia, USA.

Journal of the American Society of Nephrology : JASN
|June 15, 2013
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Summary

The small GTPase Cdc42 and the exocyst complex cooperate in ciliogenesis and prevent polycystic kidney disease. This study reveals Cdc42

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Ciliogenesis and cystogenesis depend on the exocyst complex for ciliary protein trafficking.
  • The in vivo role of the small GTPase Cdc42 in these processes is largely unknown.
  • Cdc42 interacts with the exocyst component Sec10 at primary cilia in vitro.

Purpose of the Study:

  • To investigate the in vivo function of Cdc42 in ciliogenesis and cystogenesis.
  • To determine the relationship between Cdc42 and the exocyst complex in vivo.
  • To explore the role of Cdc42 in polycystic kidney disease (PKD).

Main Methods:

  • Knockdown of cdc42 in zebrafish.
  • Genetic interaction studies between cdc42 and sec10 in zebrafish.
  • Generation and analysis of mice with Cdc42 deficiency in kidney tubular epithelial cells.
  • Histological examination of kidney tissues.

Main Results:

  • Zebrafish cdc42 knockdown phenocopied sec10 knockdown, causing tail curvature, glomerular expansion, and MAPK activation, indicating cooperation in ciliogenesis.
  • cdc42 knockdown in zebrafish led to hydrocephalus and loss of photoreceptor cilia.
  • Zebrafish cdc42 and sec10 exhibited synergistic genetic interaction, supporting their role in the same pathway.
  • Mice lacking Cdc42 in kidney tubular cells developed PKD with cystogenesis, reduced ciliogenesis, increased proliferation, apoptosis, fibrosis, and MAPK activation.
  • Cdc42 appears to localize the exocyst to primary cilia for vesicle targeting of ciliary proteins.

Conclusions:

  • Cdc42 is essential for ciliogenesis and preventing polycystic kidney disease.
  • Cdc42 and Sec10 function in the same pathway to regulate ciliogenesis.
  • Disruptions in the Cdc42-exocyst pathway lead to aberrant ciliogenesis and PKD.