Intracistronic complementation in the simian virus 40 A gene.

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Abstract
A set of 8 SV40 mutants was constructed with lesions in the A gene, which encodes the large tumor (T) antigen. These mutants have small deletions (3-20 base pairs) at either 0.497, 0.288 or 0.243 map units. Mutants having both in-phase and frameshift mutations at each site were isolated. Neither plaque formation nor replication of the mutant DNA could be detected after transfection of monkey kidney cells. Another nonviable mutant, dlA2459, had a 14-base-pair deletion at 0.193 map unit and was positive for viral DNA replication. Each of the 8 mutants was tested for ability to form plaques after cotransfection with dlA2459 DNA. The 4 mutants that had in-phase deletions were able to complement dlA2459. The other 4, which had frameshift deletions, did not. No plaques were formed after cotransfection of cells with any other pair of group A mutants. This suggests that the defect in dlA2459 defines a distinct functional domain of SV40 T antigen.