Perinatal lethality with kidney and pancreas defects in mice with a targetted Pkd1 mutation View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-10

AUTHORS

Weining Lu, Bernard Peissel, Hermik Babakhanlou, Anna Pavlova, Lin Geng, Xiaohong Fan, Cecilia Larson, Gregory Brent, Jing Zhou

ABSTRACT

PKD1 is the most common site for mutations in human autosomal dominant polycystic kidney disease (ADPKD). ADPKD is characterized by progressive replacement of kidney tissue by epithelial cysts and eventual renal failure. Hepatic and pancreatic cysts are also common1. The PKD1 protein, poly cyst in, is a cell-surface protein2,3 of unknown function that is widely expressed in epithelia and in vascular smooth muscle and myocardium4–9. None of the genetic forms of murine polycystic disease map to the murine Pkd1 locus. We introduced into mice by homologous recombination a Pkd1 truncation mutation, Pkd1−, that mimics a mutation found in ADPKD. Pkd1− heterozygotes have no discernible phenotype, whereas homozygotes die during the perinatal period with massively enlarged cystic kidneys, pancreatic ductal cysts and pulmonary hypoplasia. Renal cyst formation begins at embryonic day 15.5 (E15.5) in proximal tubules and progresses rapidly to replace the entire renal parenchyma. The timing of cyst formation indicates that full-length polycystin is required for normal morphogenesis during elongation and maturation of tubular structures in the kidney and pancreas. More... »

PAGES

179-181

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng1097-179

DOI

http://dx.doi.org/10.1038/ng1097-179

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1042625074

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9326937


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