Construction of Infectious cDNA Clones Derived from the Potyviruses Clover Yellow Vein Virus and Bean Yellow Mosaic Virus

Author(s):  
Kenji S. Nakahara ◽  
Kei Nishino ◽  
Ichiro Uyeda
1994 ◽  
Vol 45 (1) ◽  
pp. 183 ◽  
Author(s):  
SJ McKirdy ◽  
BA Coutts ◽  
RAC Jones

In 1990, infection with bean yellow mosaic virus (BYMV) was widespread in subterranean clover (Trifolium subterraneum) pastures in the south-west of Western Australia. When 100 leaves were sampled at random per pasture, the virus was detected by ELISA in 23 of 87 pastures and incidences of infection ranged from 1 to 64%. BYMV was present in all seven districts surveyed, but highest incidences of infection occurred in the Busselton district. In smaller surveys in 1989 and 1992, incidences of infection in pastures were higher than in 1990, and ranged up to 90%. In 1992, when petals from 1703 samples of 59 species of perennial native legumes from 117 sites were tested by ELISA, only 1% were found infected with BYMV. The infected samples came from 5/7 districts surveyed. Species found infected were Kennedia prostrata, K. coccinea, Hovea elliptica and H. pungens. Representative isolates of BYMV from subterranean clover and native legumes did not infect white clover systemically confirming that clover yellow vein virus (CYVV) was not involved. It was concluded that BYMV infection was present in many subterranean clover pastures, but normally at low incidences, except in epidemic years such as 1992. Also, perennial native legumes are unlikely to act as major reservoirs for reinfection of annual pastures each year. In areas of Australia with Mediterranean climates where perennial pastures are absent, persistence of the virus over summer is therefore by some other method than infection of perennials.


2009 ◽  
Vol 99 (3) ◽  
pp. 251-257 ◽  
Author(s):  
Eiko Nakazono-Nagaoka ◽  
Tsubasa Takahashi ◽  
Takumi Shimizu ◽  
Yoshitaka Kosaka ◽  
Tomohide Natsuaki ◽  
...  

Attenuated isolate M11 of Bean yellow mosaic virus (BYMV), obtained after exposing BYMV-infected plants to low temperature, and its efficacy in cross-protecting against infection by BYMV isolates from gladiolus, broad bean (Vicia faba) and white clover (Trifolium repens) was assessed with western blotting and reverse transcription-polymerase chain reaction. The level of cross-protection varied depending on the challenge virus isolates. Cross-protection was complete against BYMV isolates from gladiolus, but incomplete against BYMV isolates from other hosts. M11 also partially cross-protected against an isolate of Clover yellow vein virus. A comparison of the nucleotide sequence of M11 and those of BYMV isolates from gladiolus and from other hosts showed higher homology among gladiolus isolates than the homology between gladiolus isolates and nongladiolus isolates. In the phylogenetic trees, constructed using the nucleotide sequences of an overall polyprotein of the genomes, five gladiolus isolates clustered together, completely separated from the three BYMV isolates from other hosts. A comparison of the amino acid sequences between M11 and its parental isolate IbG, and analysis of recombinant infectious clones between M11 and IbG revealed that an amino acid at position 314 was involved in the attenuation of BYMV.


2009 ◽  
Vol 22 (2) ◽  
pp. 166-175 ◽  
Author(s):  
Go Atsumi ◽  
Uiko Kagaya ◽  
Hiroaki Kitazawa ◽  
Kenji Suto Nakahara ◽  
Ichiro Uyeda

The wild-type strain (Cl-WT) of Clover yellow vein virus (ClYVV) systemically induces cell death in pea cv. Plant introduction (PI) 118501 but not in PI 226564. A single incompletely dominant gene, Cyn1, controls systemic cell death in PI 118501. Here, we show that activation of the salicylic acid (SA) signaling pathway enhances ClYVV virulence in susceptible pea cultivars. The kinetics of virus accumulation was not significantly different between PI 118501 (Cyn1) and PI 226564 (cyn1); however, the SA-responsive chitinase gene (SA-CHI) and the hypersensitive response (HR)-related gene homologous to tobacco HSR203J were induced only in PI 118501 (Cyn1). Two mutant viruses with mutations in P1/HCPro, which is an RNA-silencing suppressor, reduced the ability to induce cell death and SA-CHI expression. The application of SA and of its analog benzo (1,2,3) thiadiazole-7-carbothioic acid S-methyl ester (BTH) partially complemented the reduced virulence of mutant viruses. These results suggest that high activation of the SA signaling pathway is required for ClYVV virulence. Interestingly, BTH could enhance Cl-WT symptoms in PI 226564 (cyn1). However, it could not enhance symptoms induced by White clover mosaic virus and Bean yellow mosaic virus. Our report suggests that the SA signaling pathway has opposing functions in compatible interactions, depending on the virus–host combination.


1996 ◽  
Vol 62 (5) ◽  
pp. 472-477 ◽  
Author(s):  
Shigeo NAKAMURA ◽  
Ryoso HONKURA ◽  
Takayoshi IWAI ◽  
Masashi UGAKI ◽  
Yuko OHASHI

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