Amino acid changes in P3, and not the overlapping pipo‐encoded protein, determine virulence of Soybean mosaic virus on functionally immune Rsv1‐genotype soybean

Wen, R.-H.; Maroof, M. A. Saghai; Hajimorad, M. R.

doi:10.1111/j.1364-3703.2011.00714.x

Cited by 38 publications

(50 citation statements)

References 38 publications

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“…and Hajimorad (2010) reported that mutation of the putative SMV (Soybean mosaic virus) PIPO inhibits cell-to-cell movement, but does not affect the virulence. This effect was the result of a mutation in the P3 cistron upstream of PIPO (Wen et al, 2011). Our results presented here support the previous observation that a single amino acid mutation at the position 917 affects the virus pathogenicity.…”

Section: Zymv-se04t (Mild) and Zymv-kuchyna (Moderate)supporting

confidence: 91%

Analysis of the complete sequences of two biologically distinct Zucchini yellow mosaic virus isolates further evidences the involvement of a single amino acid in the virus pathogenicity

Nováková¹,

Svobodá²,

Glasa³

2014

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Summary. -The complete genome sequences of two Slovak Zucchini yellow mosaic virus isolates (ZYMV-H and ZYMV-SE04T) were determined. These isolates differ significantly in their pathogenicity, producing either severe or very mild symptoms on susceptible cucurbit hosts. The viral genome of both isolates consisted of 9593 nucleotides in size, and contained an open reading frame encoding a single polyprotein of 3080 amino acids. Despite their different biological properties, an extremely high nucleotide identity could be noted (99.8%), resulting in differences of only 5 aa, located in the HC-Pro, P3, and NIb, respectively. In silico analysis including 5 additional fully-sequenced and phylogenetically closely-related isolates known to induce different symptoms in cucurbits was performed. This suggested that the key single mutation responsible for virus pathogenicity is likely located in the N-terminal part of P3, adjacent to the PIPO.

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Section: Zymv-se04t (Mild) and Zymv-kuchyna (Moderate)supporting

confidence: 91%

Analysis of the complete sequences of two biologically distinct Zucchini yellow mosaic virus isolates further evidences the involvement of a single amino acid in the virus pathogenicity

Nováková¹,

Svobodá²,

Glasa³

2014

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“…P3N-PIPO contributes to cell-to-cell movement of the virus in susceptible hosts (Chung et al, 2008;Wen and Hajimorad, 2010). HC-Pro, along with P3 and Cl, regulates SMV virulence Hajimorad et al, 2008;Seo et al, 2009;Zhang et al, 2009;Hajimorad et al, 2011;Seo et al, 2011;Chowda-Reddy et al, 2011;Wen et al, 2011). The precise biochemical function of SMV P3, and indeed the potyviral P3 protein in general, is largely uncharacterized due to the lack of structural or functional motifs in its sequence.…”

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confidence: 99%

The Potyviral P3 Protein Targets Eukaryotic Elongation Factor 1A to Promote the Unfolded Protein Response and Viral Pathogenesis

et al. 2016

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The biochemical function of the potyviral P3 protein is not known, although it is known to regulate virus replication, movement, and pathogenesis. We show that P3, the putative virulence determinant of soybean mosaic virus (SMV), targets a component of the translation elongation complex in soybean. Eukaryotic elongation factor 1A (eEF1A), a well-known host factor in viral pathogenesis, is essential for SMV virulence and the associated unfolded protein response (UPR). Silencing GmEF1A inhibits accumulation of SMV and another ER-associated virus in soybean. Conversely, endoplasmic reticulum (ER) stress-inducing chemicals promote SMV accumulation in wild-type, but not GmEF1A-knockdown, plants. Knockdown of genes encoding the eEF1B isoform, which is important for eEF1A function in translation elongation, has similar effects on UPR and SMV resistance, suggesting a link to translation elongation. P3 and GmEF1A promote each other's nuclear localization, similar to the nuclearcytoplasmic transport of eEF1A by the Human immunodeficiency virus 1 Nef protein. Our results suggest that P3 targets host elongation factors resulting in UPR, which in turn facilitates SMV replication and place eEF1A upstream of BiP in the ER stress response during pathogen infection.

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“…SMV strain G7 induces lethal systemic cell death in soybean carrying the dominant resistance gene Rsv1 (14). In this virus, P3, and not P3N-PIPO, determines virulence (40). TuMV induces lethal systemic cell death in A. thaliana Ler carrying the TuNI gene (15).…”

Section: Discussionmentioning

confidence: 99%

“…We compared the accumulation of Cl-RB with that of Cl-No.30 by using GFP-tagged versions of each virus. P3N-PIPO is an essential factor for potyviruses to move from cell to cell in infected leaves (40). Therefore, we anticipated that Cl-RB would accumulate more efficiently than ClNo.30 in PI 226564 if the level of Cl-RB P3N-PIPO was higher than that of Cl-No.30 P3N-PIPO.…”

Section: P3 Of CLmentioning

confidence: 99%

P3N-PIPO, a Frameshift Product from the P3 Gene, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas

Atsumi

Suzuki

Miyashita

et al. 2016

J Virol

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IMPORTANCEControl of plant viral disease has relied on the use of resistant cultivars; however, emerging mutant viruses have broken many types of resistance. Recently, we revealed that Cl-90-1 Br2 breaks the recessive resistance conferred by cyv1, mainly by accumulating a higher level of P3N-PIPO than that of the nonbreaking isolate Cl-No.30. Here we show that a susceptible pea line recognized the increased amount of P3N-PIPO produced by Cl-90-1 Br2 and activated the salicylic acid-mediated defense pathway, inducing lethal systemic cell death. We found a gradation of virulence among ClYVV isolates in a cyv1-carrying pea line and two susceptible pea lines. This study suggests a trade-off between breaking of recessive resistance (cyv1) and host viability; the latter is presumably regulated by the dominant Cyn1 gene, which may impose evolutionary constraints upon P3N-PIPO for overcoming resistance. We propose a working model of the host strategy to sustain the durability of resistance and control fast-evolving viruses.H ost plants protect themselves from virus infection by activating defense systems mediated by immune receptors (e.g., nucleotide-binding-site-leucine-rich-repeat [NB-LRR] proteins) (1). Plants have many NB-LRR immune receptors, each of which recognizes specific viral proteins. The activated immune response is referred to as a hypersensitive response (HR) and is often accompanied by cell death. When an HR is induced, the virus is localized in and around the infection locus. NB-LRR immune receptors are encoded by resistance genes that are genetically dominant.Another important defense against plant virus infection is genetically recessive resistance (2). The viral life cycle totally relies on host cells, and viruses require host factors in order to multiply within cells and move to neighboring cells. Therefore, the lack of a specific host-coopted factor required for the viral life cycle leads to host resistance against the virus, which would be recessively inherited. Many natural recessive resistance genes against viruses have been identified in diverse crops (2). Extensive studies have been carried out on viruses belonging to the Potyvirus genus, the major genus of the Potyviridae family, which is one of the two largest plant virus genera and is found in most climatic regions worldwide (3). These viruses infect a broad range of host plants, including both monocots and dicots. They cause considerable crop damage, resulting in severe economic losses. Most of the recessive

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Amino acid changes in P3, and not the overlapping pipo‐encoded protein, determine virulence of Soybean mosaic virus on functionally immune Rsv1‐genotype soybean

Cited by 38 publications

References 38 publications

Analysis of the complete sequences of two biologically distinct Zucchini yellow mosaic virus isolates further evidences the involvement of a single amino acid in the virus pathogenicity

Analysis of the complete sequences of two biologically distinct Zucchini yellow mosaic virus isolates further evidences the involvement of a single amino acid in the virus pathogenicity

The Potyviral P3 Protein Targets Eukaryotic Elongation Factor 1A to Promote the Unfolded Protein Response and Viral Pathogenesis

P3N-PIPO, a Frameshift Product from the P3 Gene, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas

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