Evaluation of type I fusarium head blight resistance of wheat using non-deoxynivalenol-producing fungi

A series of experiments was conducted to determine whether type I resistance (resistance to initial infection) to fusarium head blight (FHB) in wheat could be assessed using fungal species/isolates that do not produce deoxynivalenol (DON), a mycotoxin critical to the spread of Fusarium graminearum in the wheat spike. It was shown that, while the non-toxin-producing species Microdochium nivale and M. majus could infect following spray inoculation of wheat spikes, they were unable to spread within the spike following point inoculation. However, although these species might reveal type I resistance, they are not highly pathogenic towards wheat. A nivalenol (NIV)-producing isolate of F. graminearum caused high levels of disease following spray inoculation, but spread only very slowly within the spike and rarely induced bleaching above the point of inoculation. It is proposed that spray inoculation with an appropriate, aggressive, non-DON-producing FHB pathogen may be used to characterize type I resistance to complement point inoculation with a DON-producing isolate to assess type II resistance (resistance to spread within the spike).     

Resistance to rice sheath blight (<Emphasis Type="Italic">Rhizoctonia solani</Emphasis> Kühn) [(teleomorph: <Emphasis Type="Italic">Thanatephorus cucumeris</Emphasis> (A.B. Frank) Donk.] disease: current status and perspectives

Sheath blight (ShB) disease, caused by Rhizoctonia solani, is an economically important rice disease worldwide, especially in intensive production systems. Several studies have been conducted to identify sources for ShB resistance in different species of rice, including local accessions and landraces. To date, none of the genotypes screened are immune to ShB, although variation in levels of resistance have been reported. Several quantitative trait loci (QTL) for ShB resistance have been identified using mapping populations derived from indica or japonica rice. A total of 33 QTL associated with ShB resistance located on all 12 rice chromosomes have been reported, with ten of these co-localizing with QTL for morphological attributes, especially plant height, or for heading date. Sixteen QTL, from the same or differing genetic backgrounds, have been mapped at least twice. Of these, nine QTL were independent of morphological traits and heading date. We hypothesize that two main, distinct, mechanisms contribute to ShB resistance: physiological resistance and disease escape. Strategies to improve our understanding of the genetics of resistance to ShB are discussed.     

A strategy to identify sources of quantitative resistance in pathosystems involving disease escape and physiological resistance: the case study of rice sheath blight

An epidemiology‐based strategy using rice sheath blight (ShB) as a biological model was developed that enables identification of sources of resistance. A set of 163 cultivated rice genotypes, including genotypes which had been reported to express partial resistance to ShB, and a few genotypes reported as very susceptible, were assessed using two complementary methods. First, microfield experiments allowed measurement of disease intensification at, and spread from, inoculated sources, along with morphological traits of each genotype. Secondly, detached tiller tests allowed measurement of the physiological resistance to the disease under conditions where morphology does not come into play. Multivariate analysis involving hierarchical cluster analysis, followed by multiple correspondence analysis, indicated that levels of physiological resistance, groups of plant morphology and disease levels in microfields were associated. Results from logistic regressions further indicated that a decreased number of lesions measured on detached tillers increased the odds of a rice genotype belonging to the group with low disease intensity in microfields. The combined results from microfield and detached tiller tests allowed identification of 23 genotypes with low level of disease intensity, which may be used as sources of resistance to ShB in breeding programmes. The results suggest that this strategy, which combines the crop stand and the individual tiller scales, may be applied to the identification of sources of resistance to a range of diseases with similar life cycle traits.