Myh9 (myosin, heavy chain 9, non-muscle) encodes a nonmuscle myosin IIA heavy chain involved in several functions including cytokinesis, cell motility and maintenance of cell shape. Genome wide association studies associate single nucleotide polymorphisms (SNPs) in MYH9 with chronic kidney disease in African-Americans. Myh9flox mutant mice possess loxP sites flanking exon 1. Homozygous mice are viable and fertile. 
 
When Myh9flox mice are crossed with Pod::Cre mice the resulting offspring will have exon 1 deleted in kidney podocytes. Double mutant mice on the C57BL/6 background do not develop spontaneous proteinuria or renal insufficiency, however, when subjected to environmental stress via doxyrubicin hydrochloride (Adriamycin), Myh9 podocyte-deleted mice develop albuminuria, focal and segmental glomerulosclerosis, foot process fusion and foot process effacement. When crossed to mice with widespread Cre recombinase expression, deletion of Myh9 is lethal.


This strain is unpublished on the FVB background. The donating investigator indicates that FVB mice are more sensitive to glomerular disease than C57BL/6 mice

Myh9flox mutant mice possess loxP sites flanking exon 1. Genome wide association studies associate single nucleotide polymorphisms (SNPs) in MYH9 with chronic kidney disease in African-Americans. These mice may be useful in generating conditional mutations to study hemostasis, glomerulosclerosis and kidney disease.

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