Gallwitz D, Traub U, Traub P
Eur J Biochem. 1977 Dec 1;81(2):387-93. doi: 10.1111/j.1432-1033.1977.tb11963.x.
Histone mRNA was isolated from mengovirus-infected Ehrlich ascites tumor cells at various times postinfection and quantitated in a reticulocyte cell-free protein-synthesizing system. The amount of translatable histone mRNA decreases during the first hour postinfection by 30%, rises during the following 1-1.5 h by 10-15%, drops progressively in the further course of infection, and reaches 20% of the control at the end of the infectious cycle (8-9 h postinfection). On the basis of the relative histone mRNA contents, the histone-synthesizing potentials of mengovirus-infected Ehrlich ascites tumor cells are substantially higher throughout infection than actually expressed in vivo. This result indicates that the virus-induced shutoff of histone synthesis is not directly the consequence of inactivation or degradation of histone mRNA. Most of the histone mRNA recovered from mengovirus-infected Ehrlich ascites tumor cells is bound to ribosomes. Late in infection, certain mRNAs are co-isolated with histone mRNAs, very likely due to loss or shortening of poly(A) occurring after release of the mRNAs from polyribosomes.
在感染后不同时间从感染脑心肌炎病毒的艾氏腹水瘤细胞中分离组蛋白mRNA，并在无细胞网织红细胞蛋白质合成系统中进行定量。可翻译的组蛋白mRNA量在感染后第一小时内下降30%，在随后的1 - 1.5小时内上升10 - 15%，在感染的进一步过程中逐渐下降，在感染周期结束时（感染后8 - 9小时）降至对照的20%。根据相对组蛋白mRNA含量，感染脑心肌炎病毒的艾氏腹水瘤细胞在整个感染过程中的组蛋白合成潜力比体内实际表达的要高得多。这一结果表明，病毒诱导的组蛋白合成关闭并非直接由于组蛋白mRNA的失活或降解。从感染脑心肌炎病毒的艾氏腹水瘤细胞中回收的大部分组蛋白mRNA与核糖体结合。在感染后期，某些mRNA与组蛋白mRNA共同分离，很可能是由于mRNA从多核糖体释放后发生的聚腺苷酸（poly(A)）丢失或缩短所致。
