Resistance to Turnip mosaic virus in the Brassicaceae

Walsh, John A.; Jenner, Carol E.

doi:10.1007/1-4020-3780-5_19

Cited by 9 publications

(13 citation statements)

References 56 publications

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“…Because both Rnt1-1 and TuRB01b (the TuMV resistance gene previously reported [14,16]) were identified using the same TuMV strain UK1 and mapped on the chromosome R6, and because the avirulence gene in TuMV that corresponded to the two resistance genes was the viral CI gene [15, (Fig. 1).…”

Section: Resultsmentioning

confidence: 99%

Combinations of a host resistance gene and the CI gene of turnip mosaic virus differentially regulate symptom expression in Brassica rapa cultivars

et al. 2011

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In the pathosystem of Brassica rapa and Turnip mosaic virus (TuMV), the type of symptoms expressed by susceptible plants are determined by the gene combinations between the host cultivar and virus strain. In this study, we found that the resistant reaction and symptoms such as systemic lethal necrosis, leaf malformation and mosaic were differentially determined, depending on the combinations of the genotypes for a host locus or two closely linked host loci and the viral CI gene. Systemic necrosis caused by TuMV-UK1 on some B. rapa subsp. pekinensis cultivars is induced in conjunction with a recessive gene rnt1-2 (resistance and necrosis to tumv 1-2), which is allelic or closely linked to TuMV resistance gene Rnt1-1 on chromosome R6. rnt1-2 is incompletely recessive to rnt1-3, which does not cause any necrotic responses. The genotype rnt1-2/rnt1-3 caused a mild necrosis along leaf veins of severely malformed leaves. A spontaneous mutant TuMV-UK1 (UK1m) with the amino acid substitution (V1827E) in CI broke Rnt1-1 resistance and altered the systemic necrosis and leaf malformation induced by rnt1-2. This single amino acid in the CI protein of UK1 was also associated with severe mosaic and abnormal leaf development, perhaps interacting with a host unknown factor(s). To clarify the relationship of Rnt1-1 with TuRB01b, which was previously reported as a TuMV-UK1 resistance gene on chromosome R6, the B. rapa cultivar Tropical Delight carrying TuRB01b was inoculated with UK1m or the infectious UK1 clone with the CI V1827E mutation. Because Tropical Delight showed resistance to both mutants, Rnt1-1 might be different from TuRB01b.3

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Section: Resultsmentioning

confidence: 99%

Combinations of a host resistance gene and the CI gene of turnip mosaic virus differentially regulate symptom expression in Brassica rapa cultivars

et al. 2011

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“…pekinesis). Several workers have found resistance in Chinese cabbage and these have been examined by Hughes et al (2002) and Walsh et al (2002). The most promising resistances appear to be those obtained by Liu et al (1996).…”

Section: Turnip Mosaic Virusmentioning

confidence: 99%

Swedes and Turnips

Gowers

2010

Root and Tuber Crops

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“…Turnip mosaic virus (TuMV; family Potyviridae , genus Potyvirus ) occurs worldwide and causes severe yield and quality losses in many economically important plants (Tomlinson, ). Use of virus‐resistant cultivars, when available, can provide an important approach to managing TuMV spread in Brassica crops (Walsh & Jenner, , ). A range of TuMV resistance phenotypes occur in vegetable and oilseed Brassica species, including extreme resistance, HR, SHR and localization associated with chlorotic lesions (Jenner & Walsh, ; Walsh & Jenner, , ; Coutts et al ., ; Nyalugwe et al ., , , ,b).…”

Section: Introductionmentioning

confidence: 99%

“…Use of virus‐resistant cultivars, when available, can provide an important approach to managing TuMV spread in Brassica crops (Walsh & Jenner, , ). A range of TuMV resistance phenotypes occur in vegetable and oilseed Brassica species, including extreme resistance, HR, SHR and localization associated with chlorotic lesions (Jenner & Walsh, ; Walsh & Jenner, , ; Coutts et al ., ; Nyalugwe et al ., , , ,b). R genes have been associated with extreme resistance, HR and SHR phenotypes in Brassica species (Walsh & Jenner, ; Nyalugwe et al ., , ), but not as yet with virus localization associated with chlorotic lesions.…”

Section: Introductionmentioning

confidence: 99%

“…A range of TuMV resistance phenotypes occur in vegetable and oilseed Brassica species, including extreme resistance, HR, SHR and localization associated with chlorotic lesions (Jenner & Walsh, ; Walsh & Jenner, , ; Coutts et al ., ; Nyalugwe et al ., , , ,b). R genes have been associated with extreme resistance, HR and SHR phenotypes in Brassica species (Walsh & Jenner, ; Nyalugwe et al ., , ), but not as yet with virus localization associated with chlorotic lesions. Most of these TuMV R genes are pathotype‐specific and often overcome in the field (Walsh & Jenner, ) as TuMV evolves readily by mutation and recombination (Ohshima et al ., ).…”

Section: Introductionmentioning

confidence: 99%

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Programmed cell death pathways induced by early plant‐virus infection are determined by isolate virulence and stage of infection

et al. 2016

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Programmed cell death (PCD) pathways caused by Turnip mosaic virus (TuMV) infection before symptom appearance were studied by light microscopy and electrolyte leakage following sap inoculation of Brassica carinata (Ethiopian mustard) TZ‐SMN‐44‐6 plants. Leaf responses to inoculation with avirulent (TuMV‐avir) and virulent (TuMV‐vir) isolates, and mock‐inoculation, were compared at 2, 20 and 52 h after inoculation (hai). The phenotypes induced were localized resistance (TuMV‐avir) and systemic susceptibility (TuMV‐vir). No visible TuMV symptoms were recorded in any inoculated plants during the 2–52 hai sampling period, but appeared as chlorotic spots in inoculated leaves at 5 days after inoculation. With TuMV‐vir alone, they were followed by systemic infection (mosaic). Dead cell number, deformation, percentage area and percentage integrated intensity, and conductivity of electrolyte leakage data, were analysed to examine their possible roles in stimulating cell death pathways. At 2 hai, dead cell number and percentage area were significantly greater for TuMV‐avir than TuMV‐vir infection or mock‐inoculation. Overall, isolate TuMV‐vir caused significantly greater cell deformation than TuMV‐avir, whereas wounding by mock‐inoculation had negligible effects. By 52 hai, isolate TuMV‐avir caused significantly greater electrolyte leakage than isolate TuMV‐vir or mock‐inoculation. This suggests both isolates triggered morphological changes consistent with apoptotic‐like PCD and necrosis‐like PCD that depended upon isolate virulence and stage of infection, respectively. These findings highlight how quantification of dead cell deformation and electrolyte leakage offer a new understanding of compatible and incompatible plant responses to early virus infection in plants.

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Resistance to Turnip mosaic virus in the Brassicaceae

Cited by 9 publications

References 56 publications

Combinations of a host resistance gene and the CI gene of turnip mosaic virus differentially regulate symptom expression in Brassica rapa cultivars

Combinations of a host resistance gene and the CI gene of turnip mosaic virus differentially regulate symptom expression in Brassica rapa cultivars

Swedes and Turnips

Programmed cell death pathways induced by early plant‐virus infection are determined by isolate virulence and stage of infection

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