Point mutations in the ICR2 motif of brome mosaic virus RNAs debilitate (+)-strand replication.
Point mutations in the ICR2 motif of brome mosaic virus RNAs debilitate (+)-strand replication.
复制标题
雀麦花叶病毒 RNA 的 ICR2 基序中的点突变会削弱 ( ) 链复制。
DOI:
10.1016/0042-6822(90)90388-8
复制
发表时间:
1990
期刊:
影响因子:
3.7
通讯作者:
Hall,TC
中科院分区:
文献类型:
--
作者:
Pogue,GP;Marsh,LE;Hall,TC
Sequences at the 5′ termini of the genomic RNAs of brome mosaic virus (BMV) and other (+)-stranded RNA viruses have been shown (L. E. Marsh and T. C. Hall, 1987,Cold Spring Harbor Symp. Quant. Biol.52, 331–341) to resemble the ICRs 1 and 2 (A and B boxes) of tRNA genes, with the complementary sequences at the 3′ termini of the (−) strands resembling the ICR2 motif of methionine initiator tRNA genes (L. E. Marsh, G. P. Pogue, and T. C. Hall, 1989,Virology172, 415–427). In order to examine the role of these sequences in viral replication, point mutations have been introduced into the ICR2-like sequence of a BMV RNA-2 deletion mutant, pRNA ΔM/S (parasitic RNA), that does not encode a functional viral protein but replicates in the presence of genomic RNA-1 and -2. Single-base substitutions introduced at positions A7or T8of the (+)-sense ICR2-like motif reduced pRNA ΔM/S replication by 70–82%, the primary effect being shown by kinetic analyses to be debilitation of (+)-strand synthesis. Whether these motifs act in their (+)-sense orientation in a manner analogous to tRNA genes or through the tRNAMeti-like sequence on the 3′ (−) strand remains to be determined, but the data clearly demonstrate that the base composition within the ICR-like region of BMV RNAs contributes greatly to (+)-strand promoter function.