Wongabel rhabdovirus accessory protein U3 targets the SWI/SNF chromatin remodeling complex

D Albert Joubert, Julio Rodriguez-Andres, Paul Monaghan, Michelle Cummins, William J McKinstry, Prasad N Paradkar, Gregory W Moseley, Peter J Walker

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Wongabel virus (WONV) is an arthropod-borne rhabdovirus that infects birds. It is one of the growing array of rhabdoviruses with complex genomes that encode multiple accessory proteins of unknown function. In addition to the five canonical rhabdovirus structural protein genes (N, P, M, G, and L), the 13.2-kb negative-sense single-stranded RNA (ssRNA) WONV genome contains five uncharacterized accessory genes, one overlapping the N gene (Nx or U4), three located between the P and Mgenes (U1 to U3), and a fifth one overlapping the G gene (Gx or U5). Here we show that WONV U3 is expressed during infection in insect and mammalian cells and is required for efficient viral replication. A yeast two-hybrid screen against a mosquito cell cDNA library identified that WONV U3 interacts with the 83-amino-acid (aa) C-terminal domain of SNF5, a component of the SWI/SNF chromatin remodeling complex. The interaction was confirmed by affinity chromatography, and nuclear colocalization was established by confocal microscopy. Gene expression studies showed that SNF5 transcripts are upregulated during infection of mosquito cells with WONV, as well as West Nile virus (Flaviviridae) and bovine ephemeral fever virus (Rhabdoviridae), and that SNF5 knockdown results in increased WONV replication. WONV U3 also inhibits SNF5-regulated expression of the cytokine gene CSF1. The data suggest that WONV U3 targets the SWI/SNF complex to block the host response to infection.
Original languageEnglish
Pages (from-to)1377-1388
Number of pages12
JournalJournal of Virology
Volume89
Issue number2
DOIs
Publication statusPublished - 2015

Cite this

Joubert, D. A., Rodriguez-Andres, J., Monaghan, P., Cummins, M., McKinstry, W. J., Paradkar, P. N., ... Walker, P. J. (2015). Wongabel rhabdovirus accessory protein U3 targets the SWI/SNF chromatin remodeling complex. Journal of Virology, 89(2), 1377-1388. https://doi.org/10.1128/JVI.02010-14
Joubert, D Albert ; Rodriguez-Andres, Julio ; Monaghan, Paul ; Cummins, Michelle ; McKinstry, William J ; Paradkar, Prasad N ; Moseley, Gregory W ; Walker, Peter J. / Wongabel rhabdovirus accessory protein U3 targets the SWI/SNF chromatin remodeling complex. In: Journal of Virology. 2015 ; Vol. 89, No. 2. pp. 1377-1388.
@article{26f75bea3f4644e59266b243919a8624,
title = "Wongabel rhabdovirus accessory protein U3 targets the SWI/SNF chromatin remodeling complex",
abstract = "Wongabel virus (WONV) is an arthropod-borne rhabdovirus that infects birds. It is one of the growing array of rhabdoviruses with complex genomes that encode multiple accessory proteins of unknown function. In addition to the five canonical rhabdovirus structural protein genes (N, P, M, G, and L), the 13.2-kb negative-sense single-stranded RNA (ssRNA) WONV genome contains five uncharacterized accessory genes, one overlapping the N gene (Nx or U4), three located between the P and Mgenes (U1 to U3), and a fifth one overlapping the G gene (Gx or U5). Here we show that WONV U3 is expressed during infection in insect and mammalian cells and is required for efficient viral replication. A yeast two-hybrid screen against a mosquito cell cDNA library identified that WONV U3 interacts with the 83-amino-acid (aa) C-terminal domain of SNF5, a component of the SWI/SNF chromatin remodeling complex. The interaction was confirmed by affinity chromatography, and nuclear colocalization was established by confocal microscopy. Gene expression studies showed that SNF5 transcripts are upregulated during infection of mosquito cells with WONV, as well as West Nile virus (Flaviviridae) and bovine ephemeral fever virus (Rhabdoviridae), and that SNF5 knockdown results in increased WONV replication. WONV U3 also inhibits SNF5-regulated expression of the cytokine gene CSF1. The data suggest that WONV U3 targets the SWI/SNF complex to block the host response to infection.",
author = "Joubert, {D Albert} and Julio Rodriguez-Andres and Paul Monaghan and Michelle Cummins and McKinstry, {William J} and Paradkar, {Prasad N} and Moseley, {Gregory W} and Walker, {Peter J}",
year = "2015",
doi = "10.1128/JVI.02010-14",
language = "English",
volume = "89",
pages = "1377--1388",
journal = "Journal of Virology",
issn = "0022-538X",
publisher = "American Society for Microbiology",
number = "2",

}

Joubert, DA, Rodriguez-Andres, J, Monaghan, P, Cummins, M, McKinstry, WJ, Paradkar, PN, Moseley, GW & Walker, PJ 2015, 'Wongabel rhabdovirus accessory protein U3 targets the SWI/SNF chromatin remodeling complex' Journal of Virology, vol. 89, no. 2, pp. 1377-1388. https://doi.org/10.1128/JVI.02010-14

Wongabel rhabdovirus accessory protein U3 targets the SWI/SNF chromatin remodeling complex. / Joubert, D Albert; Rodriguez-Andres, Julio; Monaghan, Paul; Cummins, Michelle; McKinstry, William J; Paradkar, Prasad N; Moseley, Gregory W; Walker, Peter J.

In: Journal of Virology, Vol. 89, No. 2, 2015, p. 1377-1388.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Wongabel rhabdovirus accessory protein U3 targets the SWI/SNF chromatin remodeling complex

AU - Joubert, D Albert

AU - Rodriguez-Andres, Julio

AU - Monaghan, Paul

AU - Cummins, Michelle

AU - McKinstry, William J

AU - Paradkar, Prasad N

AU - Moseley, Gregory W

AU - Walker, Peter J

PY - 2015

Y1 - 2015

N2 - Wongabel virus (WONV) is an arthropod-borne rhabdovirus that infects birds. It is one of the growing array of rhabdoviruses with complex genomes that encode multiple accessory proteins of unknown function. In addition to the five canonical rhabdovirus structural protein genes (N, P, M, G, and L), the 13.2-kb negative-sense single-stranded RNA (ssRNA) WONV genome contains five uncharacterized accessory genes, one overlapping the N gene (Nx or U4), three located between the P and Mgenes (U1 to U3), and a fifth one overlapping the G gene (Gx or U5). Here we show that WONV U3 is expressed during infection in insect and mammalian cells and is required for efficient viral replication. A yeast two-hybrid screen against a mosquito cell cDNA library identified that WONV U3 interacts with the 83-amino-acid (aa) C-terminal domain of SNF5, a component of the SWI/SNF chromatin remodeling complex. The interaction was confirmed by affinity chromatography, and nuclear colocalization was established by confocal microscopy. Gene expression studies showed that SNF5 transcripts are upregulated during infection of mosquito cells with WONV, as well as West Nile virus (Flaviviridae) and bovine ephemeral fever virus (Rhabdoviridae), and that SNF5 knockdown results in increased WONV replication. WONV U3 also inhibits SNF5-regulated expression of the cytokine gene CSF1. The data suggest that WONV U3 targets the SWI/SNF complex to block the host response to infection.

AB - Wongabel virus (WONV) is an arthropod-borne rhabdovirus that infects birds. It is one of the growing array of rhabdoviruses with complex genomes that encode multiple accessory proteins of unknown function. In addition to the five canonical rhabdovirus structural protein genes (N, P, M, G, and L), the 13.2-kb negative-sense single-stranded RNA (ssRNA) WONV genome contains five uncharacterized accessory genes, one overlapping the N gene (Nx or U4), three located between the P and Mgenes (U1 to U3), and a fifth one overlapping the G gene (Gx or U5). Here we show that WONV U3 is expressed during infection in insect and mammalian cells and is required for efficient viral replication. A yeast two-hybrid screen against a mosquito cell cDNA library identified that WONV U3 interacts with the 83-amino-acid (aa) C-terminal domain of SNF5, a component of the SWI/SNF chromatin remodeling complex. The interaction was confirmed by affinity chromatography, and nuclear colocalization was established by confocal microscopy. Gene expression studies showed that SNF5 transcripts are upregulated during infection of mosquito cells with WONV, as well as West Nile virus (Flaviviridae) and bovine ephemeral fever virus (Rhabdoviridae), and that SNF5 knockdown results in increased WONV replication. WONV U3 also inhibits SNF5-regulated expression of the cytokine gene CSF1. The data suggest that WONV U3 targets the SWI/SNF complex to block the host response to infection.

UR - http://jvi.asm.org/content/89/2/1377.full.pdf+html

U2 - 10.1128/JVI.02010-14

DO - 10.1128/JVI.02010-14

M3 - Article

VL - 89

SP - 1377

EP - 1388

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 2

ER -

Joubert DA, Rodriguez-Andres J, Monaghan P, Cummins M, McKinstry WJ, Paradkar PN et al. Wongabel rhabdovirus accessory protein U3 targets the SWI/SNF chromatin remodeling complex. Journal of Virology. 2015;89(2):1377-1388. https://doi.org/10.1128/JVI.02010-14