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Signed, sealed, undelivered: Mechanisms underlying polycystic kidney disease

In an article published online ahead of print on Feb. 19, 2015 in the Journal of Biological Chemistry (JBC), investigators at the Medical University of South Carolina (MUSC) and the Ralph H. Johnson VA Medical Center report findings from in vitro and in vivo studies that elucidate the mechanisms underlying the impaired ciliogenesis and abnormal kidney development characteristic of polycystic kidney disease (PKD). Depletion of dynamin-binding protein or Tuba, a guanine nucleotide exchange factor, disrupted renal ciliogenesis in cell culture and led to abnormal kidney morphology in a Tuba knockdown zebrafish model of PKD.

Aberrant Phenotypes Resulting from Tuba Knockdown in Zebrafish
Knockdown of dynamin-binding protein or Tuba results in abnormal kidney development and other aberrant phenotypes in zebrafish models (middle and right panels) compared with controls (left panel).
Credit: Image courtesy of Joshua Lipschutz, M.D., of the Medical University of South Carolina