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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Targeted ablation of the murine alpha-tropomyosin gene.

We created a mouse that lacks a functional alpha-tropomyosin gene using gene targeting in embryonic stem cells and blastocyst-mediated transgenesis. Homozygous alpha-tropomyosin "knockout" mice die between embryonic day 9.5 and 13.5 and lack alpha-tropomyosin mRNA. Heterozygous alpha-tropomyosin knockout mice have approximately 50% as much cardiac alpha-tropomyosin mRNA as wild-type littermates but similar alpha-tropomyosin protein levels. Cardiac gross morphology, histology, and function (assessed by working heart preparations) of heterozygous alpha-tropomyosin knockout and wild-type mice were indistinguishable. Mechanical performance of skinned papillary muscle strips derived from mutant and wild-type hearts also revealed no differences. We conclude that haploinsufficiency of the alpha-tropomyosin gene produces little or no change in cardiac function or structure, whereas total alpha-tropomyosin deficiency is incompatible with life. These findings imply that in heterozygotes there is a regulatory mechanism that maintains the level of myofibrillar tropomyosin despite the reduction in alpha-tropomyosin mRNA.[1]

References

  1. Targeted ablation of the murine alpha-tropomyosin gene. Blanchard, E.M., Iizuka, K., Christe, M., Conner, D.A., Geisterfer-Lowrance, A., Schoen, F.J., Maughan, D.W., Seidman, C.E., Seidman, J.G. Circ. Res. (1997) [Pubmed]
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