The virulence of Newcastle disease virus varies greatly and is determined by multiple genetic factors. In this study, we systematically evaluated the roles of the polymerase-associated (NP, P and L) protein genes in genotype VII NDV virulence after confirming the envelope-associated (F and HN) proteins contributed greatly to NDV virulence. The results revealed that the polymerase-associated protein genes individually had certain effect on virulence, while transfer of these three genes in combination significantly affected the chimeric virus virulence, especially when the L gene was involved. These results indicated that the L protein was a major contributor to NDV virulence when combined with the homologous NP and P proteins. We also investigated viral RNA synthesis using NDV minigenome systems to assess the interaction between the NP, P, and L proteins, which showed that the activity of the polymerase-associated proteins were directly related to viral RNA transcription and replication.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5292418 | PMC |
| http://dx.doi.org/10.3389/fmicb.2017.00161 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Recent advancements in the diverse roles of polymerase-associated proteins in the replication and pathogenesis of Newcastle disease virus.
Vet Res
January 2025
Key Laboratory of Animal Genetics, Breeding and Reproduction in The Plateau Mountainous Region, Ministry of Education, Guizhou University, Guiyang, 550025, China.
Newcastle disease virus (NDV) is a significant member of the Paramyxoviridae family, known for causing epidemics and substantial economic losses in the poultry industry worldwide. The NDV RNA genome primarily encodes six structural proteins (N, P, M, F, HN, and L) and two non-structural proteins (V and W). Among these, the polymerase-associated proteins (N, P, and L) and the viral RNA (vRNA) genome form the ribonucleoprotein complex, which plays a crucial role in the synthesis and transcription of NDV vRNA.
View Article and Find Full Text PDFCrystal structure of F10 core protein from Mpox virus reveals its potential inhibitors.
Int J Biol Macromol
January 2025
Department of Cardiology, the First hospital of Shanxi Medical University, and Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, China; Guangxi Key Laboratory of Precision Medicine for Genetic Diseases, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Nanning, China. Electronic address:
Article Synopsis
- Mpox virus (MPXV) is a rare zoonotic disease that has resulted in over 15,600 cases and 537 deaths to date.
- The study focuses on the RNA polymerase (RNAP) of MPXV, which is crucial for early transcription, and reveals the high-resolution crystal structure of the F10 core protein, which stabilizes essential components of the RNAP complex.
- The research identified a cavity in the RNAP structure and screened 28 potential inhibitors, marking a significant step towards developing treatments for MPXV and similar emerging pathogens.*
CELL DIVISION CYCLE 5 controls floral transition by regulating flowering gene transcription and splicing in Arabidopsis.
Plant Physiol
December 2024
State Key Laboratory of Wheat Improvement, College of Life Sciences, Shandong Agricultural University, Tai' an 271018, China.
CELL DIVISION CYCLE 5 (CDC5) is a R2R3-type MYB transcription factor, serving as a key component of modifier of snc1, 4-associated complex/NineTeen complex, which is associated with plant immunity, RNA splicing, and miRNA biogenesis. In this study, we demonstrate that mutation of CDC5 accelerates flowering in Arabidopsis (Arabidopsis thaliana). CDC5 activates the expression of FLOWERING LOCUS C (FLC) by binding to and affecting the enrichment of RNA polymerase II on FLC chromatin.
View Article and Find Full Text PDFARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss.
Mol Cell
December 2024
Department of Microbiology, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address:
The polymerase associated factor 1 (PAF1) complex (PAF1c) promotes RNA polymerase II (RNA Pol II) transcription at the elongation step; however, how PAF1c transcription activity is selectively regulated during cell fate transitions remains poorly understood. Here, we reveal that the alternative reading frame (ARF) tumor suppressor operates at two levels to restrain PAF1c-dependent oncogenic transcriptional programs upon p53 loss in mouse cells. First, ARF assembles into homo-oligomers to bind the PAF1 subunit to promote PAF1c disassembly, consequently dampening PAF1c interaction with RNA Pol II and PAF1c-dependent transcription.
View Article and Find Full Text PDFhnRNPA2B1 deacetylation by SIRT6 restrains local transcription and safeguards genome stability.
Cell Death Differ
November 2024
Department of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Repair of double strand breaks (DSBs) by RNA-binding proteins (RBPs) is vital for ensuring genome integrity. DSB repair is accompanied by local transcriptional repression in the vicinity of transcriptionally active genes, but the mechanism by which RBPs regulate transcriptional regulation is unclear. Here, we demonstrated that RBP hnRNPA2B1 functions as a RNA polymerase-associated factor that stabilizes the transcription complex under physiological conditions.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!