Clemens K E, Pintel D
Department of Microbiology, School of Medicine, University of Missouri--Columbia 65212.
Virology. 1987 Oct;160(2):511-4. doi: 10.1016/0042-6822(87)90028-6.
The polyadenylation sites for MVM(p) and MVM(i) mRNAs were determined by a quantitative hybridization-S1 protection assay. mRNAs produced by MVM(p) both early and late in infection of mouse A9 fibroblasts, and by MVM(p) and MVM(i) late in infection of human NB324K cells, polyadenylate predominantly at a single site, at nucleotide 4908 +/- 2 for MVM(p) and 4843 +/- 2 for MVM(i), shortly downstream of the final AATAAA in each viral genome. These results demonstrate that although the right-hand end of MVM has multiple AATAAA signals, and MVM(p) and MVM(i) vary significantly within this region, 3' end processing of viral mRNAs is not a prevalent mechanism for the regulation of MVM gene expression.
通过定量杂交-S1核酸酶保护试验确定了微小病毒M（p）和M（i）mRNA的聚腺苷酸化位点。在小鼠A9成纤维细胞感染的早期和晚期由MVM（p）产生的mRNA，以及在人NB324K细胞感染晚期由MVM（p）和MVM（i）产生的mRNA，主要在单个位点进行聚腺苷酸化，对于MVM（p）在核苷酸4908±2处，对于MVM（i）在4843±2处，在每个病毒基因组中最终的AATAAA下游不久。这些结果表明，尽管微小病毒M的右端有多个AATAAA信号，并且MVM（p）和MVM（i）在该区域内有显著差异，但病毒mRNA的3'末端加工并不是微小病毒M基因表达调控的普遍机制。
