Resistance to Infection

Bruening, George

doi:10.1007/1-4020-3780-5_10

Cited by 10 publications

(5 citation statements)

References 176 publications

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“…Most plants in the host panel used in this study recovered from virus infection after infection was initially established in inoculated leaves. Recovery from virus infection can be controlled by simple or complex host plant genetics, and can be countered by effective pathogen virulence factors [ 30 , 52 , 53 ]. Host plant and pathogen genotype determined the level of plant recovery to GFLV (Figure 2 ).…”

Section: Discussionmentioning

confidence: 99%

Allopolyploidy and the evolution of plant virus resistance

et al. 2014

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BackgroundThe relationship between allopolyploidy and plant virus resistance is poorly understood. To determine the relationship of plant evolutionary history and basal virus resistance, a panel of Nicotiana species from diverse geographic regions and ploidy levels was assessed for resistance to non-coevolved viruses from the genus Nepovirus, family Secoviridae. The heritability of resistance was tested in a panel of synthetic allopolyploids. Leaves of different positions on each inoculated plant were tested for virus presence and a subset of plants was re-inoculated and assessed for systemic recovery.ResultsDepending on the host-virus combination, plants displayed immunity, susceptibility or intermediate levels of resistance. Synthetic allopolyploids showed an incompletely dominant resistance phenotype and manifested systemic recovery. Plant ploidy was weakly negatively correlated with virus resistance in Nicotiana species, but this trend did not hold when synthetic allopolyploids were taken into account. Furthermore, a relationship between resistance and geographical origin was observed.ConclusionThe gradients of resistance and virulence corresponded to a modified matching allele model of resistance. Intermediate resistance responses of allopolyploids corresponded with a model of multi-allelic additive resistance. The variable virus resistance of extant allopolyploids suggested that selection-based mechanisms surpass ploidy with respect to evolution of basal resistance to viruses.

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Section: Discussionmentioning

confidence: 99%

Allopolyploidy and the evolution of plant virus resistance

et al. 2014

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“…Whether or not the ‘subliminal infection’ mode of NHR is in fact the most common remains to be established. Several instances of complete immunity (extreme resistance) to virus infection have been described in specific cultivars or variants of otherwise virus‐susceptible plant species (Bruening, ). In these combinations, no virus replication, accumulation or movement can be detected at all.…”

Section: Introductionmentioning

confidence: 99%

The apparent non‐host resistance of Ethiopian mustard to a radish‐infecting strain of Turnip mosaic virus is largely determined by the C‐terminal region of the P3 viral protein

Sardaru

Sinausía

López‐González

et al. 2018

Molecular Plant Pathology

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Two different isolates of Turnip mosaic virus (TuMV: UK 1 and JPN 1) belonging to different virus strains were tested on three different Brassica species, namely turnip (Brassica rapa L.), Indian mustard (Brassica juncea L.) and Ethiopian mustard (Brassica carinata A. Braun). Although all three hosts were readily infected by isolate UK 1, isolate JPN 1 was able to establish a visible systemic infection only in the first two. Ethiopian mustard plants showed no local or systemic symptoms, and no virus antigens could be detected by enzyme-linked immunosorbent assay (ELISA). Thus, this species looks like a non-host for JPN 1, an apparent situation of non-host resistance (NHR). Through an experimental approach involving chimeric viruses made by gene interchange between two infectious clones of both virus isolates, the genomic region encoding the C-terminal domain of viral protein P3 was found to bear the resistance determinant, excluding any involvement of the viral fusion proteins P3N-PIPO and P3N-ALT in the resistance. A further determinant refinement identified two adjacent positions (1099 and 1100 of the viral polyprotein) as the main determinants of resistance. Green fluorescent protein (GFP)-tagged viruses showed that the resistance of Ethiopian mustard to isolate JPN 1 is only apparent, as virus-induced fluorescence could be found in discrete areas of both inoculated and non-inoculated leaves. In comparison with other plant-virus combinations of extreme resistance, we propose that Ethiopian mustard shows an apparent NHR to TuMV JPN 1, but not complete immunity or extreme resistance.

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“…To control virus diseases, introduction of resistance genes has been the most useful approach because viruses are difficult to control with chemicals and cultural methods. A number of single, dominant or recessive genes that induce complete resistance to viruses have been identified [1]. One of the issues with using such resistance genes is how to maintain the durability of the resistance because resistance controlled by single major genes is often broken by viral mutation [9].…”

Section: Introductionmentioning

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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Resistance to Infection

Cited by 10 publications

References 176 publications

Allopolyploidy and the evolution of plant virus resistance

Allopolyploidy and the evolution of plant virus resistance

The apparent non‐host resistance of Ethiopian mustard to a radish‐infecting strain of Turnip mosaic virus is largely determined by the C‐terminal region of the P3 viral protein

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

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