AbstractAttempts to synchronize the BHK21 hamster cell C‐13 and its polyoma‐transformed derivative P‐183 with excess thymidine resulted in the observation that the parent cell line could be readily synchronized but the transformed derivative could not. Differences in the growth pattern indicate that excess thymidine (10 mM) stops progress of the virus‐transformed derivative at all stages in the life cycle rather than exclusively in S. The data are suggestive but do not establish that the difference is a result of the presence of the virus
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