AbstractA colchicine‐resistant clone, CHRE5, has been isolated in a single step from a mutagenized culture of Chinese hamster ovary cells. Its resistance correlates with reduced colchicine permeability. At the same time, CHRE5 cells display a pattern of cross‐resistance to unrelated drugs similar to other membrane‐altered drug‐resistant mutants previously described (Ling and Thompson, 1974). However, CHRE5 cells also express a cold‐sensitivity for growth in that at 34° they do not double in number while at 38.5° they grow with a doubling time of about 22 hours. Employing synchronous cultures, the cold sensitive block in CHRE5 cells has been determined to be located prior to S in the G1 phase of the cell cycle. Mutant cells at 33.5° are not able to initiate DNA synthesis, however, cells already synthesizing DNA are able to complete the whole course of S. This cold sensitive block is reversed by shifting cells back to the higher temperature. Additonal clones with the CHRE5 phenotype have been isolated from non‐mutagenized cultures of wild‐type cells. Moreover, partial revertants of CHRE5 with increased ability to grow at 34° have been isolated and found to display increased colchicine sensitivity. These results are consistent with the hypothesis that the two phenotypes observed in CHRE5, namely, an altered plasma membrane (reduced drug permeability) and an altered ability to initiate DNA synthesis are the result of
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