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Molecular and Cellular Biology, January 2003, p. 70-79, Vol. 23, No. 1
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.1.70-79.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Targeted Disruption of the Murine zyxin Gene

Laura M. Hoffman,1 David A. Nix,1 Beverly Benson,1 Ray Boot-Hanford,2 Erika Gustafsson,2 Colin Jamora,3 A. Sheila Menzies,4 Keow Lin Goh,4 Christopher C. Jensen,1 Frank B. Gertler,4 Elaine Fuchs,3 Reinhard Fässler,2,1 and Mary C. Beckerle1*

Huntsman Cancer Institute and Department of Biology, University of Utah, Salt Lake City, Utah 84112,1 Department of Experimental Pathology, Lund University, 221 85 Lund, Sweden,2 Department of Molecular Genetics and Cell Biology and Howard Hughes Medical Institute, University of Chicago, Chicago, Illinois 60637,3 Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 021394

Received 8 July 2002/ Returned for modification 15 August 2002/ Accepted 27 September 2002

Zyxin is an evolutionarily conserved protein that is concentrated at sites of cell adhesion, where it associates with members of the Enabled (Ena)/vasodilator-stimulated phosphoprotein (VASP) family of cytoskeletal regulators and is postulated to play a role in cytoskeletal dynamics and signaling. Zyxin transcripts are detected throughout murine embryonic development, and the protein is widely expressed in adults. Here we used a reverse genetic approach to examine the consequences of loss of zyxin function in the mouse. Mice that lack zyxin function are viable and fertile and display no obvious histological abnormalities in any of the organs examined. Because zyxin contributes to the localization of Ena/VASP family members at certain subcellular locations, we carefully examined the zyxin-/- mice for evidence of defects that have been observed when Ena/VASP proteins are compromised in the mouse. Specifically, we evaluated blood platelet function, nervous system development, and skin architecture but did not detect any defects in these systems. Zyxin is the founding member of a family of proteins that also includes the lipoma preferred partner (LPP) and thyroid receptor-interacting protein 6 (TRIP6). These zyxin family members display patterns of expression that significantly overlap that of zyxin. Western blot analysis indicates that there is no detectable upregulation of either LPP or TRIP6 expression in tissues derived from zyxin-null mice. Because zyxin family members may have overlapping functions, a comprehensive understanding of the role of these proteins in the mouse will require the generation of compound mutations in which multiple zyxin family members are simultaneously compromised.

* Corresponding author. Mailing address: Huntsman Cancer Institute, University of Utah, 2000 Circle of Hope, Salt Lake City, UT 84112-5550. Phone: (801) 581-4485. Fax: (801) 581-2175. E-mail: mary.beckerle{at}hci.utah.edu.

{dagger} Present address: Department of Molecular Medicine, Max Planck Institute for Biochemistry, 82152 Martinsreid, Germany.

Molecular and Cellular Biology, January 2003, p. 70-79, Vol. 23, No. 1
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.1.70-79.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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