2.2.28
EXPLORING DIFFERENTIAL INTERACTION BETWEEN RHIZOCTONIA SOLANI ISOLATES AND HOST GENOTYPES IN THREE PATHOSYSTEMS

JHM SCHNEIDER1,2, PHJF VAN DEN BOOGERT2 and W HEIJBROEK1

1Institute of Sugar Beet Research (IRS), PO Box 32, NL-4600 AA, Bergen op Zoom, The Netherlands; 2DLO-Research Institute for Plant Protection (IPO-DLO), PO Box 9060, NL-6700 GW Wageningen, The Netherlands

Background and objectives
Rhizoctonia solani is a severe soil-borne pathogen in tulip, sugar beet and potato - three important crops in the Netherlands. A environmentally friendly management strategy may include detection of specific AG and AG subgroups and, if possible, host-resistant genotypes. A specific detection method and a breeding programme should take into account any variability for aggressiveness within a group of field isolates for each AG. Aggressiveness is quantifiable as the degree of attack and is usually assessed on a range of host genotypes. We consider differential interaction when the ranking of aggressiveness of isolates differs according to genotypes.

The aim of our study was to assess whether a reported statistically significant interaction between AG 2-t isolates and tulip genotypes in greenhouse experiments [1] indicated an isolate by genotype interaction, with the possible implication of physiological races within AG 2-t, or an interaction induced by environmental factors. In addition, interactions between AG 2-2 isolates and sugar beet genotypes and between AG 3 isolates and potato genotypes were explored statistically.

Results and conclusions
A significant interaction between R. solani AG 2-t isolates and tulip genotypes, found by ANOVA (P=0.001), was statistically further explored by an additive main effects and multiplicative interaction effects model, AMMI. The statistical significance of four AMMI-axes indicated complex interactions. Quantitative differential interactions were found for leaf infection between AG 2-t isolates and tulip genotypes. Differential interaction may suggest a gradual evolution towards physiological specialization. The genetic background, if any, is unknown. In the biplot derived after AMMI-analysis over isolates by year and genotypes, isolates tended to occur in year clusters indicating a differential influence of year on disease expression. Two isolates occurred in isolate clusters, thus accounting for a significant year-isolate-genotype interaction. Three isolates were very aggressive on all tulip genotypes tested and occurred in one cluster. Three contrasting isolates, low in aggressiveness, were also clustered. Quantitative differential interaction patterns were found but were significantly influenced by greenhouse conditions and type of inoculum carrier.

A statistically significant interaction between five R. solani AG 2-2 isolates and five sugar beet genotypes in one greenhouse experiment was found (ANOVA, P=0.001). Further analysis of the isolate by host genotype table showed differential interactions. However, reciprocal interactions did not occur in this experiment. A statistically significant interaction was also found (ANOVA, P=0.001) for five R. solani AG 3 isolates and six potato genotypes and reciprocal differential interactions occurred. Isolate 3R3, for example, had a DI of 54 for one potato genotype V and 72 for another genotype D on a scale of 0 to 100, whereas isolate 3R9 had a DI of 79 for genotype V and 54 for genotype D.

In conclusion, differential interaction of AG isolates to genotypes does occur in the three pathosystems studied, although it cannot yet be completely elucidated. The most aggressive isolates can be used for breeding purposes. Extremes in aggressiveness between isolates can be used for the study of mechanisms of interactions. In all three pathosystems partial resistance of some host genotypes was found. Partial resistance is often polygenically determined and sensitive to environmental conditions. Differential interaction of isolates has its implications for the development of detection methods for these specific isolates.

References
1. Schneider JHM, Schilder MT, Dijst G, 1997. European Journal of Plant Pathology 103, 265-269.