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Simian virus 40 mutants were constructed with deletions at the late side of the origin of DNA replication by partial Bal 31 digestion at the SphI site or at the PvuII site. Some of these mutants lost virtually all of both 72-base-pair repeat segments ("enhancer" sequences) and exhibited a decrease in viability from 20-to 300-fold; one particular mutant, dl1852, even showed a reduction of almost 10(4)-fold. The very poorly growing deletion mutants were unstable and gave rise to DNA rearrangements upon further growth. An essential region for viability, at least in the absence of a 72-base-pair repeat, was revealed at the distal side of the 72-base-pair elements (L250 through L272). The effect of the deletions on T-antigen expression was measured, and the decreased viability of the mutants correlated with the impairment of T-antigen expression in all cases. The study of these mutants also revealed that the 72-base-pair repeats are not required for late transcription.

Simian virus 40 mutants carrying extensive deletions in the 72-base-pair repeat region