This Article Full Text Full Text (PDF) Supplemental material Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wei, T. Articles by Wang, A. Search for Related Content PubMed PubMed Citation Articles by Wei, T. Articles by Wang, A.

 Previous Article  |  Next Article 

Journal of Virology, December 2008, p. 12252-12264, Vol. 82, No. 24
0022-538X/08/$08.00+0     doi:10.1128/JVI.01329-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Biogenesis of Cytoplasmic Membranous Vesicles for Plant Potyvirus Replication Occurs at Endoplasmic Reticulum Exit Sites in a COPI- and COPII-Dependent Manner ^,

Taiyun Wei^1,2 and Aiming Wang^1,2*

Southern Crop Protection and Food Research Centre, Agriculture and Agri-Food Canada, 1391 Sandford Street, London, Ontario, Canada N5V 4T3,¹ Department of Biology, The University of Western Ontario, 1151 Richmond Street, London, Ontario, Canada N6A 5B7²

Received 25 June 2008/ Accepted 29 September 2008

Single-stranded positive-sense RNA viruses induce the biogenesis of cytoplasmic membranous vesicles, where viral replication takes place. However, the mechanism underlying this characteristic vesicular proliferation remains poorly understood. Previously, a 6-kDa potyvirus membrane protein (6K) was shown to interact with the endoplasmic reticulum (ER) and to induce the formation of the membranous vesicles. In this study, the involvement of the early secretory pathway in the formation of the 6K-induced vesicles was investigated in planta. By means of live-cell imaging, it was found that the 6K protein was predominantly colocalized with Sar1, Sec23, and Sec24, which are known markers of ER exit sites (ERES). The localization of 6K at ERES was prevented by the coexpression of a dominant-negative mutant of Sar1 that disables the COPII activity or by the coexpression of a mutant of Arf1 that disrupts the COPI complex. The secretion of a soluble secretory marker targeting the apoplast was arrested at the level of the ER in cells overexpressing 6K or infected by a potyvirus. This blockage of protein trafficking out of the ER by 6K and the distribution of 6K toward the ERES may account for the aggregation of the 6K-bound vesicles. Finally, virus infection was reduced when the accumulation of 6K at ERES was inhibited by impairing either the COPI or COPII complex. Taken together, these results imply that the cellular COPI and COPII coating machineries are involved in the biogenesis of the potyvirus 6K vesicles at the ERES for viral-genome replication.

---

* Corresponding author. Mailing address: Southern Crop Protection and Food Research Centre, AAFC, 1391 Sandford Street, London, Ontario N5V 4T3, Canada. Phone: (519) 457-1470, ext. 313. Fax: (519) 457-3997. E-mail: wanga{at}agr.gc.ca

Published ahead of print on 8 October 2008.

Supplemental material for this article may be found at http://jvi.asm.org/.

---

Journal of Virology, December 2008, p. 12252-12264, Vol. 82, No. 24
0022-538X/08/$08.00+0     doi:10.1128/JVI.01329-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

This article has been cited by other articles:

• Cotton, S., Grangeon, R., Thivierge, K., Mathieu, I., Ide, C., Wei, T., Wang, A., Laliberte, J.-F. (2009). Turnip Mosaic Virus RNA Replication Complex Vesicles Are Mobile, Align with Microfilaments, and Are Each Derived from a Single Viral Genome. J. Virol. 83: 10460-10471 [Abstract] [Full Text]