Department of Microbiology, School of Medicine, Wakayama Medical University, Wakayama 641-8509, Japan.
Department of Microbiology and Molecular Medicine, University of Geneva School of Medicine, 1211 Geneva, Switzerland.
RNA. 2018 Apr;24(4):461-467. doi: 10.1261/rna.065243.117. Epub 2018 Jan 22.
The unusual ability of a human parainfluenza virus type 2 (hPIV2) nucleoprotein point mutation (NP) to strongly enhance minigenome replication was found to depend on the absence of a functional, internal element of the bipartite replication promoter (CRII). This point mutation allows relatively robust CRII-minus minigenome replication in a CRII-independent manner, under conditions in which NP is essentially inactive. The nature of the amino acid at position 202 apparently controls whether viral RNA-dependent RNA polymerase (vRdRp) can, or cannot, initiate RNA synthesis in a CRII-independent manner. By repressing genome synthesis when vRdRp cannot correctly interact with CRII, gln of N, the only residue of the RNA-binding groove that contacts a nucleotide base in the N-RNA, acts as a gatekeeper for wild-type (CRII-dependent) RNA synthesis. This ensures that only hexamer-length genomes are replicated, and that the critical hexamer phase of the -acting mRNA editing sequence is maintained.
人类副流感病毒 2 型（hPIV2）核蛋白点突变（NP）具有很强的增强小基因组复制的异常能力，这一发现依赖于二分体复制启动子（CRII）的无功能内部元件。该点突变允许 NP 基本失活的情况下，以不依赖于 CRII 的方式进行相对强大的 CRII 缺失小基因组复制。第 202 位氨基酸的性质显然控制着病毒 RNA 依赖性 RNA 聚合酶（vRdRp）是否能够以不依赖于 CRII 的方式起始 RNA 合成。通过当 vRdRp 不能与 CRII 正确相互作用时抑制基因组合成，N 中的谷氨酰胺（唯一与 N-RNA 中的核苷酸碱基接触的 RNA 结合槽的残基）作为野生型（依赖于 CRII）RNA 合成的守门员。这确保了只有六聚体长度的基因组被复制，并且 - 作用的 mRNA 编辑序列的关键六聚体相得以维持。
