Repression of beta interferon gene expression in virus-infected cells is correlated with a poly(A) tail elongation.

摘要: Expression of beta interferon (IFN-beta) is transiently induced when Namalwa B cells (Burkitt lymphoma cell line) are infected by Sendai virus. In this study, we found that an elongation the IFN-beta mRNA could be detected in virus-infected and such a modification was not observed transcript nonviral agent, poly(I-C). Treatment with transcriptional inhibitor (actinomycin D or 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole) resulted further transcript. Characterization elongated primer extension RNase H treatment showed result poly(A) tail up to 400 nucleotides. We conclude associated viral infection. Furthermore, presence correlated decrease protein medium extracts. Sucrose gradient analysis cytoplasmic extracts transcripts tails were nonpolysomal fractions, whereas shorter both polysomal fractions. A longer form also fractions treated inhibitors. Thus, regulation entirely dependent on inhibition transcription. To our knowledge, study provides first example somatic negatively influences gene expression vivo.