Regulated transcription of the genomes of defective virions and temperature-sensitive mutants of reovirus.

Defective reovirus, which lacks the largest (L1) of the 10 double-stranded (ds) RNA genomic segments, attaches to L cells and is uncoated in the same way as reovirus. The defective genome does not replicate in the cells, but it is transcribed. During the first 5 h after infection, three of the genomic segments, M3, S3, and S4, are more frequently transcribed than the remaining six segments. During the succeeding 5 h, there is a transition to a situation in which all nine segments are transcribed at the same relative frequencies. Since the class C ts mutation has been allocated to the L1 segment (Spandidos and Graham, 1975) the transcription of the C mutant genome was investigated in cells infected with it at the nonpermissive temperature, at which the parental genome does not replicate. Genomic segments L1, M3, S3, and S4 are predominantly transcribed at early times, and later all 10 segments are transcribed with the same relative frequencies. Transcription of the defective viral genome and the C mutant genome is therefore regulated in the same way as previously found for wild-type virus (Nonoyama, Millward, and Graham, 1974), and the regulation is independent of genome replication. Apparently the L1 segment function is involved in dsRNA synthesis but not in regulating the early to late transcription. It is suggested that a cellular repressor may be involved in this regulation and that derepression might be effected by one of the early viral gene products. Virion transcriptase activity was studied in vitro with cores prepared by chymotrypsin digestion of purified defective and standard virions. For both genomes the relative frequencies of transcription of the dsRNA segments are inversely proportional to their molecular weights. These results can be accounted for in a model that postulates each segment to be transcribed independently of the other. The same model with certain restrictions can describe the in vivo transcription of the viral genome.