Lazaridis I, Babich A, Nevins J R
Howard Hughes Medical Institute, Rockefeller University, New York, New York 10021.
Virology. 1988 Aug;165(2):438-45. doi: 10.1016/0042-6822(88)90587-9.
Previous experiments have shown that the early adenovirus E1A and E1B mRNAs decay with a half-life of 20 min in a lytic infection dependent on the action of the viral 72-kDa DNA binding protein. In contrast, the same E1A and E1B mRNAs are stable when synthesized in 293 cells, an adenovirus-transformed cell line that is devoid of the 72-kDa protein. If 293 cells are infected with the E1A deletion mutant dl312, the endogenous E1A RNA disappears after 4 hr of infection, a time coincident with the appearance of the 72-kDa protein. The induction of decay is specific since there is no decrease in the level of actin or certain other cellular mRNAs. Thus, the stability of the early RNAs is variable and correlates with the presence of the 72-kDa protein. An interaction of the 72-kDa DNA binding protein with RNA inside the cell has been demonstrated by in vivo crosslinking of protein to RNA. However, the protein is found in association with actin mRNA as well as E1A mRNA. Thus, although the 72-kDa protein appears to be required for the rapid decay of viral mRNA it apparently does not impart specificity to the process.
