SV40 deletion mutants lacking the 21-bp repeated sequences are viable, but have noncomplementable deficiencies.
We have constructed deletion mutants of simian virus 40 (SV40) lacking the two tandemly repeated copies or all three copies of the 21-bp repeated sequence located in the origin region. The mutants were viable, but had lower infectivities compared to the wild type. The mutant lacking two copies of the 21-bp repeat grew fairly well indicating that the one copy of the 21-bp repeat it contains is adequate. The other mutant lacking all the three copies of the 21-bp repeat was also viable but grew poorly. The viability of this mutant suggests that the upstream 72-bp repeated sequence compensates, though only partially, for the absence of the 21-bp repeat. The growth deficiencies of the deletion mutants could not be overcome by complementation with temperature-sensitive helper mutants providing either the early or the late functions of the virus, suggesting that the deficiencies lie in both early and late gene expression and/or in replication.
D000818:Animals; D001482:Base Composition; D002460:Cell Line; D002522:Chlorocebus aethiops; D004262:DNA Restriction Enzymes; D004279:DNA, Viral / Q000235:genetics*; D007668:Kidney; D009154:Mutation; D012333:RNA, Messenger / Q000235:genetics; D012091:Repetitive Sequences, Nucleic Acid; D013539:Simian virus 40 / Q000235:genetics*; D014158:Transcription, Genetic
D004279:DNA, Viral; D012333:RNA, Messenger; D004262:DNA Restriction Enzymes