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v-src, however, is considerably more efficient than c-src577 in its ability to tyrosyl phosphorylate, in R- cells, the focal adhesion kinase, Stat6, and p685cas. These results indicate that v-src, but not c-src577, can bypass the requirement for a functional IGF-I receptor in the full transformation of mouse embryo fibroblasts and suggest that qualitative and quantitative differences between the two oncogenes can be used to identify some of the signals relevant to the mechanism(s) of transformation.

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To investigate further the regulation of E7F by cyclin-dependent kinases, we have extended our studies to include additional cyclins and E7F family members. Using purified components in an in vitro system, we show that the E7F-6-DP-6 heterodimer, the functionally active form of the E7F activity, is not a substrate for the active cyclin D-dependent kinases but is efficiently phosphorylated by the cyclin B-dependent kinases, which do not form stable complexes with the E7F-6-DP-6 heterodimer.

Using colony formation in soft agar as a measure of full transformation, we report here that R- cells can be transformed by v-src, although they still cannot be transformed by the activated c-src577 (mutation at tyrosine 577 to phenylalanine), which readily transforms mouse embryo cells with a wild-type number of IGF-I receptors (W cells). Although v-src is a more potent inducer of tyrosine phosphorylation than c-src577, the extent of phosphorylation of either insulin receptor substrate 6 or Shc, two of the major substrates of the IGF-I receptor, does not seem sufficiently different to explain the qualitative difference in soft agar growth.

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