Browsing by Subject "Nivalenol"

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Genetische und physiologische Einflußfaktoren sowie deren Wechselwirkungen auf die Trichothecenbildung bei Roggen, Triticale und Weizen nach Inokulation mit Fusarium culmorum (W. G. Sm.) Sacc.
(2002) Reinbrecht, Carsten; Geiger, Hartwig H.
Fusarium culmorum causes specific hazards of cereal quality by the producion of trichothecenes. Prophylaxis by plant breeding can be highly effective. The aim of this study was to investigate the accumulation of trichothecenes in cereals with regard to host and fungal genotype, to physiological factors and the resulting interactions. To determine the effects of 6 environments (E), 2 inoculation dates (ID), 2 fungal isolates (I), and 5 conidia concentrations (C) and their interactions, field trials with up to 12 rye, 6 triticale, and 8 wheat genotypes (G) were conducted in 1995-1997. Kinetics of trichothecene in the heads were described with 6 harvest dates (H) in 2 host genotypes each. In a growth chamber, 2 levels of temperature (T) and 2 of relative humidity (R) were investigated by using 2 host genotypes each. Average deoxynivalenol (DON) accumulation of rye, triticale, and wheat was 41, 46, and 82 mg kg-1, respectively. Genotypes differed significantly in rye and wheat. In all cereal species, GxE interactions were important. In wheat, DON content was highly correlated to all resistance traits, whereas in rye only a tight correlation existed to the relative specific grain weight. In triticale and wheat, inoculation at full anthesis resulted in higher DON contents than inoculation at heading. In rye, no effect of inoculation date was found. In contrast, GxID interaction was significant in rye. The nivalenol (NIV) producing isolate led to lower trichothecene contents than the DON producing isolate. This effect was found to be significant only in rye and triticale. Significant GxI interactions occurred in wheat only. Even one week after inoculation, considerable DON concentrations could be obtained in harvested heads, especially in wheat. Maximum DON contents were observed between 3 and 6 weeks after inoculation (in wheat: partially above 300 mg kg-1). NIV contents were always lower than DON contents. Until full ripening, DON contents slightly decreased, whereas NIV contents increased continuously. HxE and HxI interactions were most important. Trichothecene content in chaff and spindles was 2-4 fold higher than in the respective kernels at 6 and 8 weeks after inoculation. With higher conidia concentrations, increasing contents of DON+3-Acetyl-DON were measured. GxC interactions were highly significant. Highest heritabilities were found in the upper concentration levels. When the relative humidity was high, trichothecene concentrations of kernels were superior. With the temperature, an inverse effect was obtained. It seems that GxT interaction contributed most to GxE in rye and wheat, in triticale also the GxR interaction. In conclusion, assisting resistance traits may replace an expensive quantification of trichothecenes in early generations. In advanced generations, tests should be conducted in several environments with high conidia concentrations, and a toxin analysis should be carried out directly.
Molecular and phenotypic analyses of pathogenicity, aggressiveness, mycotoxin production, and colonization in the wheat-Gibberella zeae pathosystem
(2004) Cumagun, Christian Joseph R.; Miedaner, Thomas
Fusarium head blight (FHB), caused by Gibberella zeae (Schwein.) Petch (anamorph: Fusarium graminearum Schwabe), is one of the principal diseases responsible for extensive damage in wheat fields and contamination of grain with the mycotoxins deoxynivalenol (DON) and nivalenol (NIV), rendering the harvest unsafe for human and animal consumption. Control of FHB is difficult because of the complex nature of host-pathogen-environment interaction and the nonavailability of highly effective fungicides. Agronomic practices and resistance breeding, therefore, offer the best strategies for disease management. Mapping by molecular markers provides an accurate approach for genetic analyses of simple and complex traits particularly pathogenicity, aggressiveness, and mycotoxin production. Pathogenicity, as defined here, is the ability to cause disease whereas aggressiveness is the quantity of disease induced by a pathogenic isolate on a susceptible host in which isolates do not interact differentially with host cultivars. The project aims to (1) map pathogenicity and aggressiveness of G. zeae based on a published genetic map (2) estimate genetic diversity of four parent isolates by PCR-based markers (3) examine the inheritance of pathogenicity, aggressiveness, mycotoxin type (DON/NIV), and DON production on a phenotypic basis, (4) analyse genetic covariation among aggressiveness, DON, and fungal colonization, (5) and compare aggressiveness of 42 isolates in greenhouse and field environments. Two crosses of G. zeae using nit (nitrate nonutilizing) marker technique were performed: (1) pathogenic DON-producing Z-3639 (Kansas, USA) x nonpathogenic NIV-producing R-5470 (Japan) belonging to lineage 7 and 6, respectively, and (2) DON-producing FG24 (Hungary) x FG3211 (Germany), both aggressive lineage 7 isolates. For the first cross, 99 progeny segregated in a consistent 61:38 for pathogenicity: nonpathogenicity in a two-year greenhouse experiment. Among the 61 pathogenic progeny, disease severity, measured as percentage infected spikelets, varied significantly (P = 0.01). Heritability for aggressiveness was high. Pathogenicity locus was mapped on linkage group IV near loci PIG1 (red pigment production), TOX1 (trichothecene toxin amount), and PER1 (perithecial production) explaining 60%, 43%, and 51% of the phenotypic variation, respectively. Two large aggressiveness QTLs were mapped on linkage group I linked to the locus TRI5 (trichodiene synthase in the trichothecene gene cluster) and an amplified fragment length polymorphism (AFLP) marker (EAAMTG0655K), explaining 51% and 29% of the observed phenotypic variation, respectively. These unlinked loci suggest that genetic basis between pathogenicity and aggressiveness were different. TRI5 is located in the same gene cluster as a previously identified gene known as TRI13, which determines whether DON or NIV will be produced. DON-producing progeny were, on average, twice as aggressive as were those producing NIV. Loci were only detected in the two linkage groups mentioned from the nine linkage groups present in the map. For the second cross FG24 x FG3211 with 153 progeny, head blight rating and relative plot yield were used as aggressiveness traits. DON production was measured by a commercial kit enzyme immunoassay. These three traits were quantitatively inherited among 153 progeny across three environments. Repeatabilities within each environment were medium to high but heritabilities across environments were medium only due to high progeny-environment interaction. DON was a less environmentally stable trait than aggressiveness. Transgressive segregants were detected frequently. This implies that even a cross within a lineage could lead to an increase in aggressiveness. Mapping of this cross was not initiated because the parents were not polymorphic enough to construct a genetic map. Instead, the parents were analysed for polymorphism in comparison to the parents of the first cross using 31 AFLP primer combinations and 56 random amplified polymorphic DNA (RAPD) primers. Polymorphism between Z-3639 and R-5470 was about three to four times higher than between FG24 and FG3211. Cluster analysis revealed that R-5470 was genetically separated from the other three parents, thus confirming the lineage assignments. Among preselected 50 progeny from the same field experiments that showed normal distribution for aggressiveness - head blight rating, fungal colonization, and DON production were correlated (r = 0.7, P = 0.01). Fungal colonization measured as Fusarium exoantigen (ExAg) content using enzyme-linked immunosorbent assay (ELISA) varied also quantitatively, but heritability was lower due to high progeny-environment interaction and error. Strong correlations among all traits indicate control by similar genes or gene complexes. No significant variation was observed for DON/ExAg ratio. Aggressiveness traits and DON production were more environmentally stable compared to Fusarium ExAg content. Our findings imply that aggressiveness may have other components apart from mycotoxin production. Genotypic variation for aggressiveness among the 42 progeny in one greenhouse and three field environments was significant and their correlation was moderate (r = 0.7, P = 0.01). High heritability in both environments again indicates that aggressiveness was a relatively stable trait, although methods of inoculation differed, i.e., injection for greenhouse and spraying for field experiments. Greenhouse aggressiveness could predict aggressiveness in the field, and thereby should reduce costs for resistance and phytopathological studies. In conclusion, we consider G. zeae as medium-risk pathogen with the potential to evolve to a higher level of aggressiveness due to sexual recombination. Erosion of quantitative resistance in FHB cannot be ignored, especially if host resistances with oligogenic inheritance, e.g. Sumai 3 from China, are used on a large acreage. Consequently, the rather simple inheritance of pathogenicity and aggressiveness in G. zeae could lead to a gradual increase of aggressiveness. These results should enhance efforts of plant breeders to use several, genetic distinct sources of resistance in order to avoid possible FHB outbreaks in the future.