[Role of the nucleus and the cytoplasm in determining the change in the permeability for colchichine of the plasma membrane of mouse cells].

A mouse cell line, B-82CH/CAP, with three genetic markers - resistance to 5-bromodeoxyuridine (5-BUdR), due to the deficiency in thymidine kinase (TK); resistance to colchicine, due to a decrease in membrane permeability to the drug; and resistance to chloramphenicol (CAP), was obtained. The capacity of cytoplasts and karyoplasts prepared from this cell line, to transfer resistance to colchicine and CAP was studied. Cytoplasts prepared from B-82CH/CAP cells were fused to karyoplasts prepared either from the mouse L or hamster DM-15 cell line, both of which are sensitive to colchicine and to CAP. The hybrid cells were resistant to CAP, but sensitive to colchicine. However, when karyoplasts prepared from B-82CH/CAP cells were fused to cytoplasts prepared from L cells, the hybrids retained the capacity to proliferate in the medium containing colchicine and 5-BUdR, but were greatly reduced in their ability to grow in the medium containing CAP. These results indicate that the resistance of B-82CH/CAP cells to CAP can be cytoplasmically transmitted and, as in other CAP-resistant cell lines, is probably due to a mutation in mitochondrial DNA. Changes in membrane permeability associated with colchicine-resistance appear to be determined by the nucleus.