The integrated concept of disease resistance; a new view including horizontal and vertical resistance in plants

Horizontal, uniform, race-non-specific or stable resistance can be discerned according to Van der Plank, from vertical, differential, race-specific or unstable resistance by a test in which a number of host genotypes (cultivars or clones) are tested against a number of pathogen genetypes traces of isolatest. If the total non-environmental variance in levels of resistance is due to main effects only differences between cultivars and differences between isolates) the resistance and the pathogen many (in the broad sense) are horizontal in nature. Vertical resistance and pathogenicity are characterized by the interaction between host and pathogen showing up as a variance compenent in this test due to interaction between cultivars and isolates. A host and pathogen model was made in which resistance and pathogenicity are governed by live polygenic loci. Within the host the resistance genes show additivity. Two models were investigated in model I resistance and pathogenicity genes operate in an additive way as envisaged by Van der Plank in his horizontal resistance. Model II is characterized by a gene-for-gene action between the polygenes of the host and those of the pathogen. The cultivar isolate test in model I showed only main effect variance. Surprisingly, the variance in model II was also largely due to main effects. The contribution of the interaction to the variance uppeared so small, that it would be difficult to discern it from a normal error variance. So-called horizontal resistance can therefore be explained by a polygenic resistance, where the individual genes are vertical and operating on a gene-for-gene basis with virulence genes in the pathogen. The data reported so far support the idea that model II rather than model I is the realistic one. The two models also revealed that populations with a polygenic resistance based on the gene-for-gene action have an increased level of resistance compared with the addition model, while its stability as far as mutability of the pathogen is concerned, is higher compared to those with an additive gene action. Mathematical studies of Mode too support the gene-for-gene concept. The operation of all resistance and virulence genes in a natural population is therefore seen as one integrated system. All genes for true resistance in the host population, whether they are major or minor genes are considered to interact in a gene-for-gene way with virulence genes either major or minor, in the pathogen population. The models revealed other important aspects. Populations with a polygenic resistance based on a gene-for-gene action have an increased level of resistance compared to populations following the addition model. The stability, as far as mutability of the pathogen is concerned, is higher in the interaction model than in the addition model. The effect of a resistance gene on the level of resistance of the population consists of its effect on a single plant times its gene frequency in the population. Due to the adaptive forces in both the host and the pathogen population and the gene-for-gene nature of the gene action an equilibrium develops that allows all resistance genes to remain effective although their corresponding virulence genes are present. The frequencies of the resistance and virulence genes are such that the effective frequencies of resistance genes tend to be negatively related to the magnitude of the gene effect. This explains why major genes often occur at low frequencies, while minor genes appear to be frequent. It is in this way that the host and the pathogen, both as extremely variable and vigorous populations, can co-exist. Horizontal and vertical resistance as meant by Van der Plank therefore do not represent different kinds of resistances, they represent merely polygenic and oligogenic resistances resp. In both situations the individual host genes interact specifically with virulence genes in the pathogen. Van der Plank's test for horizontal resistance appears to be a simple and sound way to test for polygenic inheritance of resistance. The practical considerations have been discussed. The agro-ecosystems should be made as diverse as possible. Multilines, polygenic resistance, tolerance, gene deployment and other measures should be employed, if possible in combination

Durability of resistance against fungal, bacterial and viral pathogens; present situation

In evolutionary sense no resistance lasts forever. The durability of a resistance can be seen as a quantitative trait; resistances may range from not durable at all (ephemeral, or transient) to highly durable. Ephemeral resistance occurs against fungi and bacteria with a narrow host range, specialists. It is characterised by a hypersensitive reaction (HR), major gene inheritance and many resistance genes, which often occur in multiple allelic series and/or complex loci. These resistance genes (alleles) interact in a gene-for-gene way with a virulence genes (alleles) in the pathogen to give an incompatible reaction. The pathogen neutralises the effect of the resistance gene by a loss mutation in the corresponding avirulence allele. The incompatible reaction is not elicited any more and the pathogenicity is restored. The pathogens can afford the loss of many avirulences without loss of fitness. Durable resistance against specialised fungi and bacteria is often quantitative and based upon the additive effects of some to several genes, the resulting resistance being of another nature than the hypersensitive reaction. This quantitative resistance is present to nearly all pathogens at low to fair levels in most commercial cultivars. Durable resistance of a monogenic nature occurs too and is usually of a non-HR type. Resistance against fungi and bacteria with a wide host range, generalists, is usually quantitative and durable. Resistances against viruses are often fairly durable, even if these are based on monogenic, race-specific, HR resistances. The level of specialisation does not seem to be associated with the durability of resistance

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Rede Wageningen, 4 november 199

Characterization of the resistance to Phytophthora infestans in local potato cultivars in Bolivia

This experiment was carried out to investigate whether and how much field resistance to late blight, caused by Phytophthora infestans, is present in the local cultivated potato germplasm. In total 36 entries were compared in a field experiment in an area highly conducive to late blight development. Of the 36 cultivars 32 were local cultivars belonging to five Solanum species, S. tuberosum (1 accession), S. andigena (18), S. juzepczukii (2), S. stenotomum (9) and S. ajanhuiri (2). The other four cultivars were derived from breeding programmes, one being the Dutch cultivar Alpha used as a highly susceptible control. The 36 cultivars were planted according to a simple 6 × 6 lattice design with three replicates. Each replicate was divided in six incomplete blocks each with six cultivars. The disease severity was assessed weekly during 9 weeks starting 48 days after planting. The area under the disease progress curve (AUDPC) was used as a measure of the field resistance. Nine isolates from surrounding potato fields were tested for their virulence to the resistance genes R1¿R11 using 22 differential cultivars. The components of the field resistance of 19 of these cultivars were compared in the greenhouse using a local isolate with virulence to all known R-genes, except to R9. The nine isolates represented seven races with a race complexity varying from 7 to 10 virulence factors. All isolates carried virulence against R1, R2, R3, R7, R10 and R11, while virulence against R9 was absent. The AUDPC among the 32 local cultivars ranged from very large, significantly larger than that of `Alpha¿ to very small. The AUDPC from S. stenotomum accessions ranged from very large to intermediate, those from S. andigena accessions from large to very small. Especially among the S. andigena accessions interesting levels of field resistance were found. Four components of field resistance were assessed, latency period (LP), lesion size (LS), lesion growth rate (LGR) and relative sporulation area (RSA). All four showed a considerable variation among the cultivars. The LP ranged from 3½ to 6 days. The LS ranged from 225 mm2 to 20 mm2. The LGR varied about six-fold, the RSA more than 10-fold. The components tended to vary in association with one another. LP and LGR were well associated with each other and had a significant correlation with the AUDPC

Genetic Relationships of Crown Rust Resistance, Grain Yield, Test Weight, and Seed Weight in Oat

Integrating selection for agronomic performance and quantitative resistance to crown rust, caused by Puccinia coronata Corda var. avenae W.P. Fraser & Ledingham, in oat (Avena sativa L.) requires an understanding of their genetic relationships. This study was conducted to investigate the genetic relationships of crown rust resistance, grain yield, test weight, and seed weight under both inoculated and fungicide-treated conditions. A Design II mating was performed between 10 oat lines with putative partial resistance to crown rust and nine lines with superior grain yield and grain quality potential. Progenies from this mating were evaluated in both crown rust-inoculated and fungicide-treated plots in four Iowa environments to estimate genetic effects and phenotypic correlations between crown rust resistance and grain yield, seed weight, and test weight under either infection or fungicide-treated conditions. Lines from a random-mated population derived from the same parents were evaluated in three Iowa environments to estimate heritabilities of, and genetic correlations between, these traits. Resistance to crown rust, as measured by area under the disease progress curve (AUDPC), was highly heritable (H = 0.89 on an entry-mean basis), and was favorably correlated with grain yield, seed weight, and test weight measured in crown rust-inoculated plots. AUDPC was unfavorably correlated or uncorrelated with grain yield, test weight, and seed weight measured in fungicide-treated plots. To improve simultaneously crown rust resistance, grain yield, and seed weight under both lower and higher levels of crown rust infection, an optimum selection index can be developed with the genetic parameters estimated in this stud

Quantitative resistance and its components in 16 barley cultivars to yellow rust, Puccinia striiformis f.sp. hordei

Sixteen barley cultivars with a susceptible infection type (IT = 7-8) in the seedling stage to an isolate of race 24 of Puccinia striiformis f. sp. hordei were planted at two locations in México. Disease severity (DS) parameters were assessed for the flag leaf and for the upper three leaves. The cultivars represented at least five levels of quantitative resistance ranging from very susceptible to quite resistant. ¿Granado¿, ¿Gloria/Copal¿ and ¿Calicuchima-92¿ represented the most resistant group and had an IT of 7 or 8. The cultivar × environment interaction variance, although significant, was very small compared with the cultivar variance. The disease severity parameters were highly correlated. The monocyclic parameter DSm, measured when the most susceptible cultivar had reached its maximum DS, was very highly correlated with the area under the disease progress curve (AUDPC), r being 0.98. Components of quantitative resistance were evaluated in two plant stages. In the seedling stage small cultivar effects for the latency period were observed, which were not correlated with the quantitative resistance measured in the field. In the adult plant stage the latency period (LP), infection frequency (IF) and colonization rate (CR) were measured in the upper two leaves. The LP was much longer than in the seedling stage and differed strongly between cultivars. The differences in IF were too large, those in CR varied much less. The components showed association with one another. The LP and IF were well correlated with the AUDPC (r = 0.7-0.8)