REGULATION OF C-MYC RNA AND ITS PROTEINS IN DAUDI CELLS BY INTERFERON-BETA

It has been shown previously that interferons (IFNs)-.alpha. and -.beta. cause a reduction in the steady-state level of poly(A) c-myc RNA in the Burkitt lymphoma, Daudi. In this report we show that the c-myc RNA reduction is not mediated by simple changes in the polyadenylation of either nascent or existing c-myc transcripts, since similar reductions of c-myc sequences were observed in poly(A) and total cellular RNA preparations from IFN-.beta.-treated cells. Furthermore, the first exon of c-myc RNA in Daudi cells contains several mutations, suggesting that the germ line configuration of the first exon is not essential for the IFN-.beta.-mediated regulation. The c-myc RNA reduction was also detected in cells whose protein synthesis was inhibited by more than 95% with cycloheximide or emetine. We surmise that neither sustained nor IFN-induced protein synthesis is required for the c-myc RNA regulation. Antisera raised against either the carboxy- or amino-terminal c-myc peptides precipitate in Daudi cells proteins of 66,000 and 63,000 daltons. In cells treated with IFN-.beta., the amounts of these proteins are reduced by 46-74% which is in agreement with the reduction detected at the level of c-myc RNA.