Abstract
Several transformation defective ( td) mutants of the Prague strain of Rous sarcoma virus, which had been previously shown to have deletions of varying sizes and positions within the src gene, were tested for their ability to induce disease in chickens. Several of the mutants induced sarcomas after long latency, in particular two mutants which had deletions spanning the presumed active site (i.e., the phosphotyrosine residue) of the RSV transforming protein, pp60 src . Viruses recovered from these tumors, as well as the tumors themselves, were analyzed to study the mechanism of tumor induction. In some examples proviral DNA structurally similar to wild-type virus was found in tumors and virus recovered from these tumors was shown to transform chick cells in vitro. Transformation specific proteins of 55,000 Da immunoprecipitable with antisera against pp60 src were encoded by the recovered viruses. These proteins displayed a protein kinase activity, appeared to have small deletions in the amino termini, and by phosphotryptic peptide mapping appeared to contain novel phosphotyrosine tryptic peptides, when compared to wild-type virus, which were presumably derived from endogenous c-src.
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