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First published online December 22, 2006; 10.1104/pp.106.091488

Plant Physiology 143:801-811 (2007)
© 2007 American Society of Plant Biologists

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PLANTS INTERACTING WITH OTHER ORGANISMS

MPB2C, a Microtubule-Associated Plant Factor, Is Required for Microtubular Accumulation of Tobacco Mosaic Virus Movement Protein in Plants1

Mirela Curin, Eve-Ly Ojangu, Kateryna Trutnyeva2, Birger Ilau, Erkki Truve and Elisabeth Waigmann*

Max F. Perutz Laboratories, University Departments at the Vienna Biocenter, Department of Medical Biochemistry, Medical University of Vienna, A–1030 Vienna, Austria (M.C., K.T., E.W.); and Department of Gene Technology, Tallinn University of Technology, 19086 Tallinn, Estonia (E.-L.O., B.I., E.T.)

Movement protein binding 2C (MPB2C) is a plant endogenous microtubule-associated protein previously identified as an interaction partner of tobacco (Nicotiana tabacum) mosaic virus movement protein (TMV-MP). In this work, the role of MPB2C in cell-to-cell transport of TMV-MP, viral spread of TMV, and subcellular localization of TMV-MP was examined. To this end, plants with reduced MPB2C levels were generated by a gene-silencing strategy. Local and systemic spread of TMV and cell-to-cell movement of TMV-MP were unimpaired in MPB2C-silenced plants as compared to nonsilenced plants, indicating that MPB2C is not required for intercellular transport of TMV-MP itself or spread of TMV. However, a clear change in subcellular distribution of TMV-MP characterized by a nearly complete loss of microtubular localization was observed in MPB2C-silenced plants. This result shows that the MPB2C is a central player in determining the complex subcellular localization of TMV-MP, in particular its microtubular accumulation, a phenomenon that has been frequently observed and whose role is still under discussion. Clearly, MPB2C mediated accumulation of TMV-MP at microtubules is not required for intercellular spread but may be a means to withdraw the TMV-MP from the cell-to-cell transport pathway.


1 This work was supported by the Austrian Science Foundation (Spezialforschungsbereich 17, project part 08 to E.W.), by the Wiener Wissenschafts-, Forschungs- und Technologiefonds (project LS123 to E.W.), and by the Estonian Science Foundation (grant no. 6559 to E.T.).

2 Present address: Clinical Institute for Medical and Chemical Laboratory Diagnostics, Department of Human Genetics, Medical University of Vienna, Waehringerstr. 10, 1090 Vienna, Austria.

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: Elisabeth Waigmann (elisabeth.waigmann{at}meduniwien.ac.at).

www.plantphysiol.org/cgi/doi/10.1104/pp.106.091488

* Corresponding author; e-mail elisabeth.waigmann{at}meduniwien.ac.at; fax 43–1–4277–9616.

Received October 19, 2006; accepted November 22, 2006; published December 22, 2006.




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