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(Circulation Research. 1997;80:751-753.)
© 1997 American Heart Association, Inc.

Articles

Manipulating Myosin Light Chain 2 Isoforms In Vivo

A Transgenic Approach to Understanding Contractile Protein Diversity

Robert Kelly, , Margaret Buckingham

Correspondence to Dr Margaret Buckingham, CNRS URA 1947, Department of Molecular Biology, Pasteur Institute, 28 rue du Dr Roux, 75724 Paris Cedex 15, France.

Key Words: myosin light chain • transgenic mice • isoform diversity • editorial

	Introduction

 
The evolution of the contractile apparatus of striated muscle, from cytoskeletal systems involved in cell motility to the specialized structure of the sarcomere, has been achieved largely by the diversification of contractile protein isoforms. Despite the distinct embryological origins and transcriptional regulatory pathways of skeletal and cardiac muscle, there is a considerable overlap in the contractile protein isoforms expressed in these two striated muscle types (see Reference 1¹ ). Isoform switching occurs during striated muscle development and mediates plasticity in adult skeletal and cardiac myocytes. Functional diversity in different muscle types is therefore largely the result of differential expression of interchangeable sarcomeric components.

Cardiac and skeletal muscle programs are finely tuned to the functional requirements of these striated muscles. Forced activation of the skeletal muscle program in myocardial cells of mice expressing transgenes coding for skeletal muscle regulatory factors in the heart leads to varying degrees of abnormal heart morphology and cardiomyopathy, demonstrating at a gross level the incompatibility of these programs for correct sarcomeric function.^{2 3} There are few examples to date where specific skeletal muscle contractile protein isoforms have been targeted to the heart. In transgenic mice expressing skeletal troponin C (TnC) in the myocardium, it has been shown that contractile sensitivity to acidosis was reduced, identifying functional differences between TnC isoforms.⁴ In a naturally occurring model, the BALB/c line of inbred mice, a duplication upstream from the cardiac -actin gene results in reduced cardiac -actin expression and abnormally high levels of skeletal -actin in the adult heart.⁵ Overexpression . . . [Full Text of this Article]

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