Identification of a novel mechanism that regulates replication and transcription at the RNA level in wild-type rabies virus

2016 Fiscal Year Final Research Report

• Project/Area Number: 26850187
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Veterinary medical science
• Research Institution: Nihon University
• Principal Investigator: SUZUKI Yuki 日本大学, 生物資源科学部, 助教 (30712492)
• Research Collaborator: INOUE Satoshi
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 狂犬病ウイルス / 複製・転写制御 / 3' UTR / RNAモチーフ

Outline of Final Research Achievements

The aim of this study was to find a novel mechanism that regulates replication and transcription in rabies virus (RABV) at the RNA level. The RNA motifs conserved among 119 wild-type RABV strains were found at the 5’ end of N CDS and 3’-UTR of M gene. Since the reporter activities using the luciferase mRNAs with the 3’UTR of RABV genes were lower than that of control luciferase mRNA, the 3’-UTR of M and G mRNAs may promote the degradation of M and G mRNAs, respectively. The mini genome reporter assay showed that the synonymous mutations in conserved motif at the 5’ end of N CDS reduced the luciferase activities. In addition, the replication yield of recombinant RABV with synonymous mutations in the conserved motif was lower than that of parental RABV strain. These results suggest that the conserved motif at the 5’ end of N CDS encode nucleotide sequences are required for the effective replication of RABV.

Free Research Field

ウイルス学