Subterranean clover red leaf virus and bean yellow mosaic virus in alsike clover

1976 ◽  
Vol 19 (3) ◽  
pp. 373-376 ◽  
Author(s):  
J. W. Ashby
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.


1999 ◽  
Vol 50 (4) ◽  
pp. 589 ◽  
Author(s):  
Y. Cheng ◽  
R. A. C. Jones

A new strain of bean yellow mosaic virus (BYMV), a non-necrotic strain, was found in south-west Western Australia. It differs from the original necrotic strain of BYMV in that it does not kill Lupinus angustifolius (narrow-leafed lupin) plants, but causes symptoms of mottle and stunting, or dead growing points, fleshy expanded leaves, and stunting. A survey of L. angustifolius crops during September and October 1997 compared the distribution and incidence of the necrotic strain with that of the non-necrotic strain. Based on 1000 plants inspected at the edge of each crop, the necrotic strain was found in 100 of 102 crops while the non-necrotic strain was found in 64 of them. Incidences ranged from 0.3 to 56% (necrotic strain) and 0.1 to 7% (non-necrotic strain) of plants counted. Both strains were present over the whole range of the survey. Wild L. angustifolius and L. luteus (yellow lupin) populations were also inspected. The necrotic and non-necrotic strains were found in 31 and 9 of the 34 L. angustifolius populations examined, respectively. Incidences ranged from 0.1 to 28% (necrotic strain) and 0.1 to 3% (non-necrotic strain) of plants counted. BYMV was found in 9 of 11 wild L. luteus populations with incidences ranging from 0.3 to 7% of plants counted. In a separate survey in which samples of L. angustifolius crops, with necrotic symptoms suspected of being caused by Colletotrichum gloeosporioides (lupin anthracnose disease), were examined, 37 of 130 samples had typical necrotic BYMV symptoms. Samples with these necrotic symptoms also came from northern and eastern wheatbelt areas not normally associated with BYMV infection. When 8 BYMV isolates cultured by sap inoculation in Trifolium subterraneum (subterranean clover) were tested by aphid transmission to L. angustifolius plants in 1994 and again in 1997, the isolates of the 2 strains behaved the same on both occasions causing only necrotic (3 isolates) or non-necrotic (5 isolates) symptoms. Thus, despite repeated subculture by sap inoculation over a 3.5-year period, the 2 BYMV strains still remained distinct. An isolate collected from wild L. luteus in 1997 produced only non-necrotic symptoms in L. angustifolius. The non-necrotic strain caused symptoms typical of BYMV in hosts other than L. angustifolius, reacted strongly with BYMV antiserum, and failed to react with antiserum to clover yellow vein virus. In a BYMV-infected lupin crop, grain yields of individual L. angustifolius plants infected early with the non-necrotic strain were decreased by 95%. Shoot weights, seed number, and seed size were also greatly decreased. Widespread occurrence of the non-necrotic strain of BYMV is cause for concern for the lupin industry.


Author(s):  
P.B. Teh

AMV was shown to be transmitted by sap, aphids and through lucerne seed, but not by Cuscuta. Virus source and test plant influenced transmission frequency. Sap-inoculation tests showed that 20 species of plants were susceptible to this virus. Thirteen species of plants from the fields where AMV had been detected were tested but only three were found to be infected with the virus.


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

2004 ◽  
Vol 78 (21) ◽  
pp. 11890-11903 ◽  
Author(s):  
Basavaraj Bagewadi ◽  
Shoajiang Chen ◽  
Sunil K. Lal ◽  
Nirupam Roy Choudhury ◽  
Sunil K. Mukherjee

ABSTRACT Proliferative cell nuclear antigen (PCNA), a conserved plant protein as well as an important replication factor, is induced in response to geminivirus infection in the resting cells of the phloem tissues. The biochemical role of PCNA in rolling circle replication (RCR) of geminivirus DNA has not been explored in detail. The initiation of RCR of the bipartite genome of a geminivirus, Indian mung bean yellow mosaic virus (IMYMV), is mainly controlled by viral protein Rep (or AL1 or AC1). The role of host PCNA in RCR of IMYMV was revealed by studying the physical and functional interactions between recombinant PCNA and recombinant IMYMV Rep. Pea nuclear PCNA as well as recombinant pea PCNA showed binding to recombinant Rep in experiments involving both affinity chromatography and yeast two-hybrid approaches. The contacting amino acid residues of PCNA seemed to be present throughout a wide region of the trimeric protein, while those of Rep appeared to be localized only in the middle part of the protein. The site-specific nicking-closing activity and the ATPase function of IMYMV Rep were impaired by PCNA. These observations lead to interesting speculations about the control of viral RCR and dynamic profiles of protein-protein interactions at the RCR origin of the geminiviruses.


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