The abnormal morphology of polyoma-transformed baby hamster kidney cells is due to a failure to respond to 70K spreading factor.
The typical elongated bipolar morphology of baby hamster kidney (BHK) cells is not shown by polyoma-transformed BHK (Py-BHK) cells. Instead, the transformed line adheres poorly to tissue-culture plastic and cells have a more rounded morphology than the parent line. Plasma fibronectin is known to mediate the spreading of BHK cells, but when human serum is subjected to Sephacryl S-300 chromatography two peaks of spreading activity are eluted; the first is fibronectin and the second, which is quantitatively more significant, is a 70 K protein that is not related to fibronectin and stimulates spreading by a different mechanism. Py-BHK cells spread well in low concentrations of purified fibronectin but will not spread well in levels of serum that contain similar or greater concentrations of fibronectin. This is because fibronectin-mediated spreading of both BHK and Py-BHK cells occurs only in the presence of low concentrations of other proteins; albumin and other serum proteins inhibit fibronectin-mediated spreading. BHK cells spread under routine culture conditions in response to the 70 K factor rather than fibronectin. The altered morphology that results from viral transformation is due to a failure of the cells to respond to the 70 K spreading factor.