scholarly journals The 3' untranslated region of cucumber mosaic virus (CMV) subgroup II RNA3 arose by interspecific recombination between CMV and tomato aspermy virus

2009 ◽  
Vol 90 (9) ◽  
pp. 2293-2298 ◽  
Author(s):  
J. R. Thompson ◽  
M. Tepfer
Plant Disease ◽  
2006 ◽  
Vol 90 (11) ◽  
pp. 1457-1457 ◽  
Author(s):  
N. Sudhakar ◽  
D. Nagendra-Prasad ◽  
N. Mohan ◽  
K. Murugesan

During a survey in January 2006 near Salem in Tamil Nadu (south India), Cucumber mosaic virus was observed infecting tomatoes with an incidence of more than 70%. Plants exhibiting severe mosaic, leaf puckering, and stunted growth were collected, and the virus was identified using diagnostic hosts, evaluation of physical properties of the virus, compound enzyme-linked immunosorbent assay (ELISA) (ELISA Lab, Washington State University, Prosser), reverse-transcription polymerase chain reaction (RT-PCR), and restriction fragment length polymorphism analysis (DSMZ, S. Winter, Germany). To determine the specific CMV subgroup, total RNA was extracted from 50 infected leaf samples using the RNeasy plant RNA isolation kit (Qiagen, Hilden, Germany) and tested for the presence of the complete CMV coat protein gene using specific primers as described by Rizos et al. (1). A fragment of the coat protein was amplified and subsequently digested with MspI to reveal a pattern of two fragments (336 and 538 bp), indicating CMV subgroup II. No evidence of mixed infection with CMV subgroup I was obtained when CMV isolates representing subgroups I (PV-0419) and II (PV-0420), available at the DSMZ Plant Virus Collection, were used as controls. Only CMV subgroup I has been found to predominantly infect tomato in the Indian subcontinent, although Verma et al. (2) identified CMV subgroup II infecting Pelargonium spp., an ornamental plant. To our knowledge, this is the first report of CMV subgroup II infecting tomato crops in India. References: (1) H. Rizos et al. J. Gen. Virol. 73:2099, 1992. (2) N. Verma et al. J. Biol. Sci. 31:47, 2006.


Plant Disease ◽  
2015 ◽  
Vol 99 (8) ◽  
pp. 1191 ◽  
Author(s):  
M. S. Wei ◽  
J. Kong ◽  
G. F. Li ◽  
J. Ma

Virology ◽  
1992 ◽  
Vol 186 (2) ◽  
pp. 475-480 ◽  
Author(s):  
Enrique Moriones ◽  
Isabel Diaz ◽  
Emilio Rodriguez-Cerezo ◽  
Aurora Fraile ◽  
Fernando Garcia-Arenal

HortScience ◽  
1998 ◽  
Vol 33 (6) ◽  
pp. 1032-1035 ◽  
Author(s):  
John F. Murphy ◽  
Edward J. Sikora ◽  
Bernard Sammons ◽  
Wojciech K. Kaniewski

Three processing tomato (Lycopersicon esculentum Mill.) lines engineered to express the cucumber mosaic virus (CMV) capsid protein (CP) gene were evaluated in the summers of 1995 and 1996 under high levels of naturally occurring CMV disease pressure. One tomato line expressed the capsid protein gene from a subgroup II isolate of CMV (line 11527), whereas two lines (12261 and 12295) expressed the capsid protein genes from a CMV subgroup I and a subgroup II isolate. Evaluation of CMV incidence based on symptomatic plants revealed that only 9% and 8% of the plants in line 11527 were infected in 1995 and 1996, respectively, 5 weeks after being transplanted. None of the plants in line 12261 developed symptoms in 1995, whereas 26% were symptomatic in 1996. There were no symptomatic plants in line 12295 in either the 1995 or the 1996 trial. In contrast to the CMV transgenic lines, 96% and 95% of the susceptible control plants were symptomatic by the 5-week rating period. CMV incidence in the CMV transgenic lines was much higher when infection was based on detection of virus by enzyme-linked immunosorbent assay (ELISA). This was particularly true in the 1996 trial where no less than 97% of the plants within a treatment were determined to be infected. Though a relatively high percentage of the transgenic plants were infected, the amount of CMV that accumulated in these plants was significantly less than in the susceptible controls, which may explain the occurrence of the attenuated symptoms. Despite CMV infection of the transgenic lines in the Alabama field trials, the performance of these lines could be of practical value to growers.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yingying Gao ◽  
Jinrui Yang ◽  
Xiaobei Zhang ◽  
Aizhong Chen ◽  
Zhouhang Gu ◽  
...  

The 2b proteins encoded by cucumber mosaic virus (CMV) subgroup I strains suppress RNA silencing primarily by competitively binding small RNAs (sRNAs) in the host cell cytoplasm. Interestingly, 2b proteins encoded by CMV subgroup II strains accumulate predominantly in nuclei. Here we determined that whereas the 2b protein (Fny2b) of subgroup IA strain Fny-CMV is highly effective in suppressing both sense RNA-induced and inverted repeat-induced posttranscriptional gene silencing, the 2b protein (LS2b) of the subgroup II strain LS-CMV was not as effective. Reducing nuclear accumulation of LS2b by mutating a residue in its nuclear localization sequence had no effect on RNA silencing suppressor activity, while attenuated viral symptoms. Electrophoretic mobility shift assays showed that the sRNA binding of LS2b was weaker and more selective than that of Fny2b. The domain determining the differential sRNA-binding ability was delimited to the putative helix α1 region. Moreover, LS2b mutants that completely lost suppressor activity still retained their weak sRNA-binding ability, suggesting that sRNA binding is not sufficient for LS2b to suppress RNA silencing. Considering the subgroup I strain-encoded 2b proteins that require sRNA-binding ability for the suppression of RNA silencing, we suggest that in addition to binding sRNA, the 2b proteins of subgroup II CMV strains would require extra biological activities to achieve RNA silencing inhibition.


1998 ◽  
Vol 38 (4) ◽  
pp. 375 ◽  
Author(s):  
Z. Singh ◽  
M. G. K. Jones ◽  
R. A. C. Jones

Summary. Transgenic tobacco (Nicotiana tabacum) plants of (i) cv. Samsun NN containing the cauliflower mosaic virus 35S constitutive promoter linked to a defective replicase (DR) gene derived from cucumber mosaic virus (CMV) subgroup I isolate Fny, and (ii) cv. Xanthi containing the CaMV 35S promoter linked to the coat protein (CP) gene of CMV subgroup I isolate C were tested for resistance to various Australian isolates of CMV. The tobacco plants were challenged with 3 CMV subgroup 1 isolates (BNRR, BMR and B6) using sap inoculation. When used to challenge non-transgenic tobacco plants with 5 subgroup II CMV isolates from lupins (LY, LCH, LAcc, LGu and LD), this inoculation method did not result in systemic infection so graft inoculation was used instead to challenge transgenic plants with these 5 isolates. When plants of the line with the DR gene were challenged with the 3 subgroup I isolates, extreme resistance was revealed as none showed symptoms and CMV was not detectable by ELISA. When the same 3 isolates were inoculated to the 3 lines with the CP gene, resistance was characterised by fewer plants becoming virus infected, delayed systemic movement and, in the plants that were infected, partial remission of symptoms plus somewhat decreased virus concentration. Challenge of transgenic plants with DR or CP with the 5 subgroup II isolates resulted in fewer plants becoming infected. Actual numbers of plants infected varied with line and subgroup II isolate and the DR gene was as effective as the CP gene at decreasing infection. With subgroup II isolate LY, infection was associated with remission of symptoms and with the other 4 isolates with delayed systemic movement. Thus the DR gene approach was more effective than the CP approach in obtaining extreme resistance against Australian subgroup I isolates of CMV. These results suggest that introducing a similar DR gene construct made from a subgroup II isolate from lupins into commercial lupin cultivars may be a suitable strategy for obtaining extreme resistance to subgroup II isolates from lupins.


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