Expression of Resistance to Barley Stripe Mosaic Virus in Barley and Oat Protoplasts

Zheng, Yuzhi; Edwards, Michael C.

doi:10.1099/0022-1317-71-8-1865

Cited by 11 publications

(5 citation statements)

References 22 publications

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“…The rsm1 resistance in Modjo-1, Moreval, CI 4197, and Morex barley, which constrains the BSMV CV42 strain, is observed in protoplasts in which virulent BSMV ND18, but not CV42 is able to establish infections. This result suggests that rsm1 resistance is due to the lack of a host factor required for BSMV replication [50]. However, a different result occurs with an uncharacterized gene in oat that imparts resistance to several BSMV strains [51], [52].…”

Section: Discussionmentioning

confidence: 99%

Fine Mapping of the Bsr1 Barley Stripe Mosaic Virus Resistance Gene in the Model Grass Brachypodium distachyon

et al. 2012

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The ND18 strain of Barley stripe mosaic virus (BSMV) infects several lines of Brachypodium distachyon, a recently developed model system for genomics research in cereals. Among the inbred lines tested, Bd3-1 is highly resistant at 20 to 25°C, whereas Bd21 is susceptible and infection results in an intense mosaic phenotype accompanied by high levels of replicating virus. We generated an F6∶7 recombinant inbred line (RIL) population from a cross between Bd3-1 and Bd21 and used the RILs, and an F2 population of a second Bd21 × Bd3-1 cross to evaluate the inheritance of resistance. The results indicate that resistance segregates as expected for a single dominant gene, which we have designated Barley stripe mosaic virus resistance 1 (Bsr1). We constructed a genetic linkage map of the RIL population using SNP markers to map this gene to within 705 Kb of the distal end of the top of chromosome 3. Additional CAPS and Indel markers were used to fine map Bsr1 to a 23 Kb interval containing five putative genes. Our study demonstrates the power of using RILs to rapidly map the genetic determinants of BSMV resistance in Brachypodium. Moreover, the RILs and their associated genetic map, when combined with the complete genomic sequence of Brachypodium, provide new resources for genetic analyses of many other traits.

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Section: Discussionmentioning

confidence: 99%

Fine Mapping of the Bsr1 Barley Stripe Mosaic Virus Resistance Gene in the Model Grass Brachypodium distachyon

et al. 2012

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“…After initial infection viruses need to spread locally, from cell-to-cell through plasmodesmata and then distantly through the vascular system (Hull, 1989). In 'Doublonʼ, the resistance to systemic infection may be the result of restriction of cell-to-cell movement, as reported in other incompatible virus-plant interactions, such as with barley stripe mosaic virus (BSMV) in oat plants (Zhen and Edwards, 1990), turnip crinkle virus (TCV) in Arabidopsis thaliana ecotype Dijon (Simon et al, 1992) or subterranean clover mottle virus (SCMoV) in highly Fig. 3.…”

Section: Discussionmentioning

confidence: 99%

A Resistance to Systemic Symptom Expression of Melon Necrotic Spot Virus in Melon

Mallor¹,

Álvarez²,

Luis-Arteaga³

2003

jashs

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Melon necrotic spot virus (MNSV) has been found affecting melon (Cucumis melo L.) crops. At present the only known resistance in melon is controlled by a single recessive gene, nsv. The presence of nsv in a melon genotype has been correlated with the lack of necrotic lesions on the mechanically inoculated cotyledons. Thus, in a screening program for MNSV resistance, melon genotypes that developed necrotic lesions in the inoculated cotyledons were discarded. However, in this paper we show that some melon accessions mechanically inoculated with MNSV do develop local necrotic lesions, therefore showing the absence of the gene nsv, but fail to develop the systemic symptoms typical of diseased plants under the screening conditions. In some of these accessions the influence of the temperature on the development of systemic symptoms was studied. The results showed that, depending on the accession, temperatures under 25 or 20 °C enhanced the systemic development of the disease. One of the tested varieties, `Doublon', did not develop systemic symptom at any of the tested temperatures (15, 17.5, 20, 22.5, 25, 27.5, and 30 °C). In this variety, the lack of systemic symptoms was correlated to the lack of virus infection of these tissues based upon ELISA results. MNSV was not detected in the uninoculated parts of the plant, and seems to remain confined to the local lesions produced on the cotyledons following the mechanical inoculation. Restriction of viral multiplication and/or cell-to-cell movement could explain the pattern of viral distribution in this variety. This reaction was observed in the `Doublon' plants mechanically inoculated with each of five isolates of MNSV tested, including an isolate that overcomes the nsv gene resistance.

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“…The centromeric location of rsm1 reduces the likelihood of finding markers for positional cloning because recombination is suppressed (Edwards 1995;Edwards and Steffenson 1996). Since the resistance is recessive, it may involve the loss of a functional host factor required for the replication or movement of BSMV (Zheng and Edwards 1990;Weiland and Edwards 1996). Another example is the resistance of pea (Pisum sativum) to seed transmission of Pea seedborne mosaic virus (PSbMV), a quantitative and polygenic characteristic (Wang and Maule 1994).…”

Section: Resistance To Plant-to-plant Transmissionmentioning

confidence: 98%

Genetic resistance for the sustainable control of plant virus diseases: breeding, mechanisms and durability

Gómez

Rodríguez-Hernández

Moury³

et al. 2009

Eur J Plant Pathol

102

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Plant viruses are important agricultural pathogens, and are responsible for a significant number of commercially relevant plant diseases. There are very few efficient control measures for viral diseases, but the use of genetic resistance appears to be the most promising strategy, often conferring effective protection without additional costs or labour during the growing season, and without damaging the environment. Sources of virus resistance have been identified for most crop species, and many resistant cultivars are already commercially available and of widespread cultivation; however, much remains to be learned about genetic resistance. This review article considers three main aspects that require intense investigation. First, we review the identification of sources of resistance and how plant breeders and pathologists have focused on aspects of the breeding process particularly relevant to viruses, such as germplasm screening and the dissection of resistance phenotypes. Second, we review how molecular mechanisms controlling resistance have been unravelled, looking at case studies where resistance mechanisms are now understood in detail for each stage of the infection cycle. Third, we turn to the durability of resistance in a global context, examining factors that influence durability and how this can be predicted. We conclude with a short discussion of the technological and scientific opportunities provided by recent advances in the field.

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Expression of Resistance to Barley Stripe Mosaic Virus in Barley and Oat Protoplasts

Cited by 11 publications

References 22 publications

Fine Mapping of the Bsr1 Barley Stripe Mosaic Virus Resistance Gene in the Model Grass Brachypodium distachyon

Fine Mapping of the Bsr1 Barley Stripe Mosaic Virus Resistance Gene in the Model Grass Brachypodium distachyon

A Resistance to Systemic Symptom Expression of Melon Necrotic Spot Virus in Melon

Genetic resistance for the sustainable control of plant virus diseases: breeding, mechanisms and durability

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