The stability of early adenovirus mRNA is controlled by the viral 72 kd DNA-binding protein.

H5ts125, a temperature-sensitive mutant of adenovirus type 5, is restricted to the early phase of infection when grown at the nonpermissive temperature. One phenotype of the virus is the overproduction of early viral mRNA at the nonpermissive temperature relative to levels found in wild-type-infected cells, although normal levels are found at the permissive temperature. We have analyzed this phenomenon for the production of RNA from two specific early viral transcription units, E1A and E1B. Transcription rates from both of these regions were found to be the same in ts125-infected cells as in wild-type-infected cells at the nonpermissive temperature. However, when the cytoplasmic stabilities of the E1A and E1B mRNAs were measured in wild-type- and ts125-infected cells, it was found that at the nonpermissive temperature, the RNAs were 3 to 5 times more stable in a ts125 infection than in a wild-type infection. Since the mutation in ts125 maps to the gene for the 72 kd DNA-binding protein, these results imply that a functional 72 kd protein is required for the rapid turnover of early viral mRNA in wild-type-infected cells, indicating that the abundance of early viral mRNA is controlled by the 72 kd DNA-binding protein.