Production of the tobacco mosaic virus (TMV) transport protein in transgenic plants is essential but insufficient for complementing foreign virus transport: a need for the full-length TMV genome or some other TMV-encoded product

Previously, we identified a correlation between the interaction of the Tobacco mosaic virus (TMV) 126/183-kDa replicase with the auxin response regulator indole acetic acid (IAA)26/PAP1 and the development of disease symptoms. In this study, the TMV replicase protein is shown to colocalize with IAA26 in the cytoplasm and prevent its accumulation within the nucleus. Furthermore, two additional auxin (Aux)/IAA family members, IAA27 and IAA18, were found to interact with the TMV replicase and displayed alterations in their cellular localization or accumulation that corresponded with their ability to interact with the TMV replicase. In contrast, the localization and accumulation of noninteracting Aux/IAA proteins were unaffected by the presence of the viral replicase. To investigate the effects of the replicase interaction on Aux/IAA function, transgenic plants expressing a proteolysis-resistant IAA26-P108H-green fluorescent protein (GFP) protein were created. Transgenic plants accumulating IAA26-P108H-GFP displayed an abnormal developmental phenotype that included severe stunting and leaf epinasty. However, TMV infection blocked the nuclear localization of IAA26-P108H-GFP and attenuated the developmental phenotype displayed by the transgenic plants. Combined, these findings suggest that TMV-induced disease symptoms can be attributed, in part, to the ability of the viral replicase protein to disrupt the localization and subsequent function of interacting Aux/IAA proteins.

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In vitro transcription of infectious RNAs from full-length cDNAs of tobacco mosaic virus

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.83.14.5043 ◽

1986 ◽

Vol 83 (14) ◽

pp. 5043-5047 ◽

Cited By ~ 71

Author(s):

T. Meshi ◽

M. Ishikawa ◽

F. Motoyoshi ◽

K. Semba ◽

Y. Okada

Keyword(s):

Tobacco Mosaic Virus ◽

Mosaic Virus ◽

In Vitro Transcription ◽

Full Length

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Tobacco mosaic virus (TMV) and potato virus X (PVX) coat proteins confer heterologous interference to PVX and TMV infection, respectively

Journal of General Virology ◽

10.1099/vir.0.81396-0 ◽

2006 ◽

Vol 87 (4) ◽

pp. 1005-1012 ◽

Cited By ~ 16

Author(s):

A. A. Bazzini ◽

S. Asurmendi ◽

H. E. Hopp ◽

R. N. Beachy

Keyword(s):

Transgenic Plants ◽

Tobacco Mosaic Virus ◽

Mosaic Virus ◽

Potato Virus ◽

Quaternary Structure ◽

Systemic Infection ◽

Potato Virus X ◽

Coat Proteins ◽

Local Cell ◽

Cell Spread

Replication of Potato virus X (PVX) was reduced in transgenic protoplasts that accumulated wild-type coat protein (CPWT) of Tobacco mosaic virus (TMV) or a mutant CP, CPT42W, that produced highly ordered states of aggregation, including pseudovirions. This reaction is referred to as heterologous CP-mediated resistance. However, protoplasts expressing a CP mutant that abolished aggregation and did not produce pseudovirions, CPT28W, did not reduce PVX replication. Similarly, in transgenic tobacco plants producing TMV CPWT or CPT42W, there was a delay in local cell-to-cell spread of PVX infection that was not observed in CPT28W plants or in non-transgenic plants. The results suggest that the quaternary structure of the TMV CP regulates the mechanism(s) of heterologous CP-mediated resistance. Similarly, transgenic protoplasts that produced PVX CP conferred transient protection against infection by TMV RNA. Transgenic plants that accumulated PVX CP reduced the cell-to-cell spread of infection and resulted in a delay in systemic infection following inoculation with TMV or TMV RNA. Heterologous CP-mediated resistance was characterized by a brief delay in systemic infection, whilst homologous CP-mediated resistance conferred reduced or no systemic infection.

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