Activation of the trk oncogene by alternatively spliced muscle and non-muscle tropomyosin sequences.

We have constructed a derivative of the trk oncogene in which the cytoskeletal tropomyosin sequences are replaced with skeletal muscle alpha-tropomyosin sequences derived from the same tropomyosin gene by alternative splicing. The biochemical and biological properties of this derivative are indistinguishable from those of the naturally occurring trk oncogene. Thus activation of the oncogenic activity of trk is a function of structural features of tropomyosin which are common to both skeletal muscle and non-muscle isoforms.