Cellular targets of functional and dysfunctional mutants of tobacco mosaicvirus movement protein fused to green fluorescent protein

Citation
V. Boyko et al., Cellular targets of functional and dysfunctional mutants of tobacco mosaicvirus movement protein fused to green fluorescent protein, J VIROLOGY, 74(23), 2000, pp. 11339-11346
Citations number
54
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Microbiology
Journal title
JOURNAL OF VIROLOGY
ISSN journal
0022-538X → ACNP
Volume
74
Issue
23
Year of publication
2000
Pages
11339 - 11346
Database
ISI
SICI code
0022-538X(200012)74:23<11339:CTOFAD>2.0.ZU;2-P
Abstract
Intercellular transport of tobacco mosaic virus (TNM RNA involves the accum ulation of virus-encoded movement protein (MP) in plasmodesmata (Pd), in en doplasmic reticulum (ER)-derived inclusion bodies, and on microtubules. The functional significance of these interactions in viral RNA (vRNA) movement was tested in planta and in protoplasts with TMV derivatives expressing N- and C-terminal deletion mutants of MP fused to the green fluorescent prote in. Deletion of 55 amino acids from the C terminus of MP did not interfere with the vRNA transport function of MP:GFP but abolished its accumulation i n inclusion bodies, indicating that accumulation of MP at these ER-derived sites is not a requirement for function in vRNA intercellular movement. Del etion of 66 amino acids from the C terminus of MP inactivated the protein, and viral infection occurred only upon complementation in plants transgenic for MP. The functional deficiency of the mutant protein correlated with it s inability to associate with microtubules and, independently, with its abs ence from Pd at the leading edge of infection. Inactivation of MP by N-term inal deletions was correlated with the inability of the protein to target I 'd throughout the infection site, whereas its associations with microtubule s and inclusion bodies were unaffected. The observations support a role of MP-interacting microtubules in TMV RNA movement and indicate that MP target s microtubules and Pd by independent mechanisms. Moreover, accumulation of MP in Pd late in infection is insufficient to support viral movement, confi rming that intercellular transport of vRNA relies on the presence of MP in I'd at the leading edge of infection.