The Potyviral P3 Protein Targets Eukaryotic Elongation Factor 1A to Promote the Unfolded Protein Response and Viral Pathogenesis1[OPEN]
Soybean Mosaic Virus P3 targets soybean elongation factor EF1A to induce ER stress, which in turn facilitates SMV pathogenesis and this is linked to EF1A function in translation elongation. The biochemical function of the potyviral P3 protein is not known, although it is known to regulate virus repl...
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Published in | Plant physiology (Bethesda) Vol. 172; no. 1; pp. 221 - 234 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
American Society of Plant Biologists
29.06.2016
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Online Access | Get full text |
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Summary: | Soybean Mosaic Virus P3 targets soybean elongation factor EF1A to induce ER stress, which in turn facilitates SMV pathogenesis and this is linked to EF1A function in translation elongation.
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 nuclear-cytoplasmic 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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Bibliography: | H.L. and M.B.S. performed most of the experiments; X.Cu, X.Ch., and N.M. provided technical assistance; P.K. conceived some experiments and complemented the writing; H.Z. and A.K. conceived the project and supervised the experiments; and A.K. wrote the manuscript with contributions from H.L. and M.B.S. The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Aardra Kachroo (apkach@uky.edu) www.plantphysiol.org/cgi/doi/10.1104/pp.16.00505 |
ISSN: | 0032-0889 1532-2548 |
DOI: | 10.1104/pp.16.00505 |