Poster: Plant Pathogen/Symbiont Interactions

Abs # 718: The Role of Microfilaments in Inclusion Body Formation by 126-kDa protein of Tobacco mosaic virus (TMV) and in TMV Pathogenicity

Presenter:	Liu, Jian-zhong , jzliu@noble.org
Authors	Liu, Jian-zhong  (A)   Nelson, Richard S. (A)
Affiliations:	(A): The Samuel Roberts Noble Foundation

It has been reported that the host cytoskeleton is used by viruses to aid in their accumulation. There is substantial evidence that microtubules (MT) aid cell-to-cell movement of TMV. However, there is some evidence that cell-to-cell trafficking of TMV occurs independently of MT and microfilaments (MF) may be important. Therefore, the mechanism of TMV cell-to-cell movement still remains controversial. The fact that TMV 126-kDa protein is in large excess to the 183-kDa protein (10-fold more) in virus infected cells suggests that the 126-kDa protein has functions additional to the formation of 126/183-kDa heterodimer replicase. Previously we have investigated the relationship of cytoplasmic inclusion bodies formed by 126-kDa protein in the absence of other viral factors and cytoplasmic bodies formed during virus infection, specifically, viroplasms and X-bodies, which also contain 126-kDa protein. Here, we show that both types of inclusion bodies were co-aligned with MF. MF depolymerizing agents, latrunculin B and cytochalasin D, not only disrupted cytoplasmic inclusion body formation when the 126-kDa protein was expressed alone, but also resulted in the inability of an infectious TMV clone expressing GFP (TMV-MP:GFP) to form fluorescent rings in N. benthamiana cells. Furthermore, de-polymerization of MF delayed or alleviated the formation of necrotic lesions on the leaves of local lesion host, N. tabacum, cv Xanthi NN. These data indicated that MF has an important role in the formation of the viral replication complex and viral intra- or inter-cellular movement, and thus in viral pathogenicity.