v-Abl utilizes multiple mechanisms to drive G1/S progression in fibroblasts

Transformation of 3T3 fibroblasts by the v-Abl tyrosine kinase replaces mit ogenic and adhesion signals normally required for cell cycle progression. A 3T3 cell line conditionally transformed with v-Abl has been used to study v-Abl's effects on cell cycle in the context of either serum depletion or a bsence of adhesion signals. We show that E2F-dependent mRNAs, encoding prot eins required for cell cycle progression, are induced by v-Abl, In addition , we identify two previously unknown targets of v-Abl signaling: (1) cyclin D1 and D2 mRNAs are induced upon v-Abl activation; and (2) the CDK inhibit or p27 is decreased upon v-Abl activation.