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Published ahead of print on November 12, 2008
J Am Soc Nephrol 20: 86-94, 2009
© 2009 American Society of Nephrology
doi: 10.1681/ASN.2007111172
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BASIC RESEARCH

Disruption of Myosin 1e Promotes Podocyte Injury

Mira Krendel*, Sangwon V. Kim{dagger}, Tim Willinger{dagger}, Tong Wang{ddagger}, Michael Kashgarian§, Richard A. Flavell{dagger},|| and Mark S. Mooseker*,§,¶

* Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut, and Departments of {dagger} Immunobiology, {ddagger} Cellular and Molecular Physiology, § Pathology, and Cell Biology, School of Medicine, Yale University, New Haven, Connecticut; and || Howard Hughes Medical Institute, Chevy Chase, Maryland

Correspondence: Dr. Mira Krendel, Department Cell and Developmental Biology, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210. Phone: 315-464-8527; Fax: 315-464-8535; E-mail krendelm{at}upstate.edu

Received for publication November 6, 2007. Accepted for publication August 28, 2008.

Myosin 1e (Myo1e) is one of two Src homology 3 domain–containing "long-tailed" type I myosins in vertebrates, whose functions in health and disease are incompletely understood. Here, we demonstrate that Myo1e localizes to podocytes in the kidney. We generated Myo1e-knockout mice and found that they exhibit proteinuria, signs of chronic renal injury, and kidney inflammation. At the ultrastructural level, renal tissue from Myo1e-null mice demonstrates changes characteristic of glomerular disease, including a thickened and disorganized glomerular basement membrane and flattened podocyte foot processes. These observations suggest that Myo1e plays an important role in podocyte function and normal glomerular filtration.






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Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673