Abstract

With the single exception of BE1 (Bader et al. 1974), transformation-defective, temperature-sensitive mutants of Rous sarcoma virus (RSV) were assumed to carry lesions in the src gene responsible for a thermolabile product, which becomes irreversibly inactivated at the nonpermissive temperature. This was concluded from studies in which a variety of different transformation parameters were examined, using different mutants in temperature-shift experiments performed in the presence of inhibitors of protein synthesis. The results of these experiments seemed to show that transformation was dependent on new protein synthesis (Kawai and Hanafusa 1971; Biquard and Vigier 1972; Rifkin et al. 1975; Ash et al. 1976). Irreversible inactivation of the src-gene product has remained, however, a matter of belief, not of certainty, since there was no direct assay for its function, and the parameters that were used to monitor transformation were probably induced in the host cell rather than being primary effects.

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