Mammalian Genome 10, 194–196 (1999). Incorporating Mouse Genome © Springer-Verlag New York Inc. 1999 Murine Pkd1 introns 21 and 22 lack the extreme polypyrimidine bias present in human PKD1 Klaus B. Piontek, Gregory G. Germino The Johns Hopkins School of Medicine, Division of Nephrology Baltimore, Maryland 21205, USA Received: 17 July, 1998 / Accepted: 13 October 1998 Autosomal dominant polycystic kidney disease (ADPKD) is esti- mPkd1. Further mapping determined that each clone was unique, mated to affect between 1/200–1/1000 people, making it one of the but that only clone C contained exon 24 (data not shown). We next most common genetic disorders in humans (Gabow 1993). Muta- sought to determine whether the lengthy polypyrimidine tracts tions of PKD1 on Chromosome (Chr) 16p13.3 account for 85–95% present in human introns 21 and 22 were conserved in the corre- of all cases. PKD1 is a relatively compact gene, with its 46 exons sponding position in the mouse genome with hybridization meth- embedded within an ~ 50kb genomic segment. The gene has an ods. A Southern blot of restriction digests of clone C and cGGG10 unusual bipartite structure, with 70% of its 58 end duplicated in (included as a positive control because
Mammalian Genome – Springer Journals
Published: Feb 1, 1999
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