The Full-Length Product of Cauliflower Mosaic Virus Open Reading Frame Ill Is Associated with the Viral Particle

Virology ◽  
1994 ◽  
Vol 202 (2) ◽  
pp. 1043-1045 ◽  
Author(s):  
Sandrine Dautel ◽  
Thierry Guidasci ◽  
Martin Pique ◽  
Jean-Luc Mougeot ◽  
Genevieve Lebeurier ◽  
...  
Virology ◽  
1990 ◽  
Vol 176 (2) ◽  
pp. 662-664 ◽  
Author(s):  
Michael Schultze ◽  
Josef Jiricny ◽  
Thomas Hohn

2005 ◽  
Vol 17 (3) ◽  
pp. 927-943 ◽  
Author(s):  
Muriel Haas ◽  
Angèle Geldreich ◽  
Marina Bureau ◽  
Laurence Dupuis ◽  
Véronique Leh ◽  
...  

2001 ◽  
Vol 75 (1) ◽  
pp. 100-106 ◽  
Author(s):  
Véronique Leh ◽  
Emmanuel Jacquot ◽  
Angèle Geldreich ◽  
Muriel Haas ◽  
Stéphane Blanc ◽  
...  

ABSTRACT Transmission of cauliflower mosaic virus (CaMV) by aphids requires two viral nonstructural proteins, the open reading frame (ORF) II and ORF III products (P2 and P3). An interaction between a C-terminal domain of P2 and an N-terminal domain of P3 is essential for transmission. Purified particles of CaMV are efficiently transmitted only if aphids, previously fed a P2-containing solution, are allowed to acquire a preincubated mixture of P3 and virions in a second feed, thus suggesting a direct interaction between P3 and coat protein. Herein we demonstrate that P3 directly interacts with purified viral particles and unassembled coat protein without the need for any other factor and that P3 mediates the association of P2 with purified virus particles. The interaction domain of P3 is located in its C-terminal half, downstream of the P3-P2 interaction domain but overlapping a region which binds nucleic acids. Mutagenesis of P3 which interferes with the interaction between P3 and virions is correlated with the loss of transmission by aphids. Taken together, our results demonstrate that P3 plays a crucial role in the formation of the CaMV transmissible complex by serving as a bridge between P2 and virus particles.


1998 ◽  
Vol 273 (44) ◽  
pp. 29015-29021 ◽  
Author(s):  
Denis Leclerc ◽  
Lena Burri ◽  
Andrey V. Kajava ◽  
Jean-Luc Mougeot ◽  
Daniel Hess ◽  
...  

1986 ◽  
Vol 6 (7) ◽  
pp. 2632-2637 ◽  
Author(s):  
J Schoelz ◽  
R J Shepherd ◽  
S Daubert

A domain of cauliflower mosaic virus (CaMV) which controls systemic spread in two solanaceous hosts (Datura stramonium and Nicotiana bigelovii) was mapped to the first half of open reading frame 6. Whereas ordinary strains of CaMV are unable to infect solanaceous species except to replicate locally in inoculated leaves, a new CaMV strain (D4) induces chlorotic local lesions and systemically infects both D. stramonium and N. bigelovii. To determine which portion of the CaMV genome controls systemic spread of the virus in solanaceous hosts, nine recombinant genomes constructed between D4 and two ordinary strains of the virus were tested for their ability to infect solanaceous hosts. A 496-base-pair DNA segment comprising the first half of open reading frame 6 specified the type of local lesions and systemic spread of the virus in solanaceous hosts. Exchange of this segment of the genome between strains of CaMV converted a compatible host reaction to an incompatible (hypersensitive) one in response to infection. This suggests that the gene VI protein interacts with the plant to suppress hypersensitivity, the normal response of solanaceous hosts to CaMV infection.


1986 ◽  
Vol 6 (7) ◽  
pp. 2632-2637
Author(s):  
J Schoelz ◽  
R J Shepherd ◽  
S Daubert

A domain of cauliflower mosaic virus (CaMV) which controls systemic spread in two solanaceous hosts (Datura stramonium and Nicotiana bigelovii) was mapped to the first half of open reading frame 6. Whereas ordinary strains of CaMV are unable to infect solanaceous species except to replicate locally in inoculated leaves, a new CaMV strain (D4) induces chlorotic local lesions and systemically infects both D. stramonium and N. bigelovii. To determine which portion of the CaMV genome controls systemic spread of the virus in solanaceous hosts, nine recombinant genomes constructed between D4 and two ordinary strains of the virus were tested for their ability to infect solanaceous hosts. A 496-base-pair DNA segment comprising the first half of open reading frame 6 specified the type of local lesions and systemic spread of the virus in solanaceous hosts. Exchange of this segment of the genome between strains of CaMV converted a compatible host reaction to an incompatible (hypersensitive) one in response to infection. This suggests that the gene VI protein interacts with the plant to suppress hypersensitivity, the normal response of solanaceous hosts to CaMV infection.


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