International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


Sarah J. Price
Department of Microbiology, Immunology, and Molecular Genetics
Joan C. Edwards School of Medicine
Marshall University
Huntington WV

Co-Authors: Elizabeth C. Bryda
Institutions: Department of Microbiology, Immunology, and Molecular Genetics.  Joan C. Edwards School of Medicine, Marshall University

The mouse juvenile congenital polycystic kidney disease (jcpk) gene causes an aggressive, early-onset form of polycystic kidney disease (PKD) characterized by fluid-filled cysts in all segments of the nephron.  When inherited in an autosomal recessive manner, this disease is the most severe of all the known mouse mutations for PKD, with death occurring within 10 days after birth. Expression studies have shown that the jcpk gene is expressed in a variety of tissues including kidney, heart, lung, ovary, testis and brain.  This gene is also expressed in the developing embryo as early as 7 days post coitum.

The pathogenesis of cyst formation in jcpk homozygous mice is unknown. To unravel some of the molecular mechanisms underlying cystogenesis in this model, cDNA microarray analysis was performed to simultaneously profile expression differences between kidney mRNA from a homozygous jcpk animal versus that of a wildtype littermate.  Over 1500 different genes were profiled and a subset of both up- and down-regulated genes were chosen for further analysis. Currently, efforts are focused on using real-time PCR to determine whether the differential expression of these genes are primary factors involved in cystogenesis or are secondary to the pathology of cyst formation.

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