Abstract
Amino acid sequence analyses indicate that the Soilborne wheat mosaic virus (SBWMV) 19K protein is a cysteine-rich protein (CRP) and shares sequence homology with CRPs derived from furo-, hordei-, peclu- and tobraviruses. Since the hordei- and pecluvirus CRPs were shown to be pathogenesis factors and/or suppressors of RNA silencing, experiments were conducted to determine if the SBWMV 19K CRP has similar activities. The SBWMV 19K CRP was introduced into the Potato virus X (PVX) viral vector and inoculated to tobacco plants. The SBWMV 19K CRP aggravated PVX-induced symptoms and restored green fluorescent protein (GFP) expression to GFP silenced tissues. These observations indicate that the SBWMV 19K CRP is a pathogenicity determinant and a suppressor of RNA silencing.
Highlights
Viruses survive in their hosts either by evading or countering host defenses
Soilborne wheat mosaic virus (SBWMV) 19K protein is a conserved cysteine-rich protein (CRP) The Pfam Protein Families Database reports a family of CRPs with similar sequences which includes proteins from Barley stripe mosaic virus (BSMV), Poa semilatent virus (PSLV), Peanut clump virus (PCV) and SBWMV (Pfam 04521.5)
Further examination in this study reveals that the CRPs encoded by all known hordei, peclu- and furoviruses share significant sequence similarity (Fig. 1)
Summary
Viruses survive in their hosts either by evading or countering host defenses. Viral evasion is a passive mechanism by which viruses overwhelm host defenses, or invade organs or cells where the host defenses cannot reach them. The ability of a virus to counter host defenses requires an active mechanism to either bypass or disarm the host machinery. Viruses invading vertebrate hosts produce virokines and viroceptors which interact with immune response molecules to inhibit or modulate their anti-viral activities [1,2]. Recent studies have shown many viruses infecting a wide range of eukaryotic hosts encode proteins that suppress the RNA silencing, anti-viral defense response [3,4,5,6]. Some silencing suppressor proteins affect symptom development and increase virus titer. The TBSV P19 protein was unique because it affects disease severity in a host specific manner [11,12]
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