[Genetic study of stable inheritable cell resistance to colchicine. Chromosomal and hybridization analysis]

The karyotype of mouse B-82CH-9 and B-82CH-9/CAP cell lines as well as the inheritance of their colchicine resistance in somatic cell hybrids were studied. We found earlier that these cell lines differ from other colchicine-resistant mouse and Djungarian hamster cell lines in stability of drug resistance and the lack of overproduction of the p22 polypeptide. The analysis of chromosomes stained by trypsin G-banding technique showed that, unlike mouse L-53 cells possessing unstable colchicine resistance, the B-82CH-9 and its B-82CH-9/CAP derivative had neither chromosomes with long homogeneously staining regions (HSRs) nor other cytological manifestations of gene amplification, such as double-minute chromosomes and small chromatin bodies. The hybrids of B-82CH-9/CAP and sensitive to colchicine Djungarian hamster DM-15 cells appeared in the HAT medium 10-fold more frequently than in the HAT medium containing colchicine. The hybrids grown in the HAT medium had complete chromosome complements of parent cells, while hybrids isolated from the medium with colchicine lacked some Djungarian hamster and mouse chromosomes. 4 independent clones and the cell line originated from the mixture of about 100 clones grown in HAT medium were sensitive to colchicine. We failed to transfer colchicine resistance with B-82CH-9/CAP microcells, while they were able to transfer HPRT+. At the same time, microcells of DM2/1 cells, possessing unstable colchicine resistance connected with gene amplification, could transfer both TK+ and resistance to colchicine. These results indicate that colchicine resistance of B-82CH-9 is suppressed in somatic cell hybrids. Stability of the trait, the absence of cytological manifestations of gene amplification, the lack of overproduction of p22 polypeptide and recessive inheritance suggest that colchicine resistance in these cells is not connected with gene amplification but rather results from another genetic alteration, possibly, gene mutation.