Small deletion in src of Rous sarcoma virus modifying transformation phenotypes: identification of 207-nucleotide deletion and its smaller product with protein kinase activity.
Partial deletion in the src gene and the gene product were characterized in a deletion mutant, dl5, isolated from the Prague strain of Rous sarcoma virus. The mutant induced fusiform-like transformed cells, unlike the parental Prague strain, which induced round transformed cells. Determination of the total nucleotide sequences of src in dl5 and the Prague strain of Rous sarcoma virus demonstrated that in the former two deletions of 196 and 11 nucleotides had occurred at positions 403 and 696, respectively, from the 5' end of src. A protein with a molecular weight of 52,000 (p52src) was detected in cells infected with dl5, as predicted from the deletion size in src. From the nucleotide sequence, it was predicted that p52src had two deletions of 65 and 4 amino acids at positions 135 and 232, respectively, from the N-terminal methionine of p60src and also had 33 amino acid changes between these two deletion sites due to alteration of the reading frame. p52src, which contained deletions and alterations of amino acids near the N-terminus, showed protein kinase activity similar to that of p60src and functioned in the infected cells. These results strongly suggest that changes in the N-terminal region of p60src modified its transforming ability, causing induction of the fusiform-like transformation phenotype.