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Abstract
Expression of GTPase-deficient Gi2 α subunit (αi2) mutant polypeptides and overexpression of the wild-type αi2 polypeptide in Rat la, Swiss 3T3, and NIH 3T3 fibroblasts altered normal growth regulation and induced a loss of contact inhibition. In Rat la cells (but not in NIH 3T3 or Swiss 3T3 cells), expression of the GTPase-deficient αi2 mutant polypeptides allowed colony formation in soft agar, which correlated with a loss in anchorage dependence and a decreased serum requirement. The altered growth regulatory properties of Rat la cells induced by expression of αi2 mutant polypeptides was not significantly inhibited by cotransfection with a dominant negative Ha-ras mutant polypeptide (Asn-17rasH), indicating that the activated Gi2 membrane signal transduction protein is uniquely capable of altering the regulation of Rat la cell growth by a predominantly c-ras-independent mechanism. The results show that GTPase-deficient αi2 mutant polypeptides have the properties of an oncogene that can induce the phenotypic characteristics of transformation in Rat la cells but that only a subset of these changes is observed with NIH 3T3 and Swiss 3T3 cells.