Disease resistance. Fusarium head blight (FHB)
References
1. DNA markers for Fusarium head blight resistance QTLs its two wheat populations. Anderson, J.A.; Stack, R.W.; Liu, S.; Waldron, B.L.; Fjeld, A.D.; Coyne, C.; Moreno-Sevilla, B.; Fetch J.M.; Song, Q.J.; Cregan, P.B.; Frohberg, R.C. In:Theoretical and Applied Genetics, 2001, 102(8):1164-1168.
Genetic resistance to Fusarium head blight (FHB), caused by Fusarium graminearum, is necessary to reduce the wheat grain yield and quality losses caused by this disease. Development of resistant cultivars has been slowed by poorly adapted and incomplete resistance sources and confounding environmental effects that make screening of germplasm difficult. DNA markers for FHB resistance QTLs have been identified and may be used to speed the introgression of resistance genes into adapted germplasm. This study was conduct ed to identify and map additional DNA markers linked to genes controlling FHB resistance in two spring wheat recombinant inbred populations, both segregating for genes from the widely used resistance source 'Sumai 3'.
2. Molecular genetic diversity and variation for aggressiveness in populations of Fusarium graminearum and Fusarium culmorum sampled from wheat fields in different countries. Miedaner, T.; Schilling, A.G.; Geiger, H.H. In: Journal of Phytopathology, 2001, 149(11-12):641-648.
Fusarium graminearum and Fusarium culmorum are the major pathogenic organisms causing head blight in small-grain cereals. Natural epidemics may result in severe yield losses, reduction in quality, and contamination of the grain by mycotoxins. The genetic diversity of four field populations of F. graminearum from Germany, Hungary, and Canada. and one population of F. culmorum from Russia was investigated by polymerase chain reaction (PCR)-based fingerprinting. Additionally, a world-wide collection and two of the F. graminearum populations were analysed for their aggressiveness on young plants of winter rye in the greenhouse. The number of isolates analysed per population varied from 25 to 70. Significant quantitative variation for aggressiveness was observed within each of the individual field populations amounting to the same range as the world-wide collection. Abundant variation within populations was also revealed by DNA markers. The F. graminearum populations from Hungary and Winnipeg displayed the least genotypic diversity, the two German F. graminearum populations and the Russian F. culmorum population were highly diverse. Population diversity., however, followed no spatial pattern among samples within a German field for aggressiveness or molecular markers. For F. graminearum, sexual recombination is the most likely explanation for the large genetic diversity within field populations. Asexual and/ or parasexual recombination, and balancing selection caused by the periodic alternation between the saprophytic and parasitic phase might play an additional role and account for the variation within the F. culmorum population. For improving Fusarium resistance, several resistance genes of different sources should be combined to avoid an unspecific adaptation of the genetically variable pathogen to an increased resistance level.
3. Genetic dissection of a major Fusarium head blight QTL in tetraploid wheat. Otto, C.D.; Kianian, S.F.; Elias, E.M.; Stack, R.W.; Joppa, L.R. In:Plant Molecular Biology, 2002, 48(5):625-632.
The devastating effect of Fusarium head blight (FHB) caused by Fusarium graminearum has led to significant financial losses across the Upper Midwest of the USA. These losses have spurred the need for research in biological, chemical, and genetic control methods for this disease. To date, most of the research on FHB resistance has concentrated on hexaploid wheat (Triticum aestivum L.) lines originating from China. Other sources of resistance to FHB would be desirable. One other source of resistance for both hexaploid wheat and tetraploid durum wheat (T. turgidum L. var. durum) is the wild tetraploid, T. turgidum L. var. dicoccoides (T. dicoccoides). Previous analysis of the `Langdon'-T. dicoccoides chromosome substitution lines, LDN(Dic), indicated that the chromosome 3A substitution line expresses moderate levels of resistance to FHB. LDN(Dic-3A) recombinant inbred chromosome lines (RICL) were used to generate a linkage map of chromosome 3A with 19 molecular markers spanning a distance of 155.2 cM. The individual RICL and controls were screened for their FHB phenotype in two greenhouse seasons. Analysis of 83 RICL identified a single major quantitative trait locus, Qfhs.ndsu-3AS, that explains 37% of the phenotypic or 55% of the genetic variation for FHB resistance. A microsatellite locus, Xgwm2, is tightly linked to the highest point of the QTL peak. A region of the LDN (Dic-3A) chromosome associated with the QTL for FHB resistance encompasses a 29.3 cM region from Xmwg14 to Xbcd828.
4. Present strategies in resistance breeding against scab (Fusarium spp.). Ruckenbauer, P.; Buerstmayr, H.; Lemmens, M. In: Euphytica, 2001, 119(1-2):121-127
Recent epidemics of fusarium head blight (FHB), caused by Fusarium graminearum Schwabe (telomorph: Gibberella zeae), in the USA and Canada have caused severe yield and quality losses in wheat (Triticum aestivum L.). Development of resistant cultivars has been difficult because of the complex inheritance of resistance and con founding environmental effects. This study was conducted to identify and map DNA markers linked to genes associated with FHB resistance. A population of 112 F-5-derived recombinant inbred (RI) wheat lines from the cross 'Sumai 3' (resistant)/'Stoa' (moderately susceptible) was evaluated in two greenhouse experiments for Type II resistance (spread within the spike). On the basis of restriction fragment length polymorphism (RFLP) marker analyses, five genomic regions were significantly (P < 0.01) associated with FHB resistance, three derived from Sumai 3 and two from Stoa. Regions on Chromosomes 3BS (from Sumai 3) and 2AL (from Stoa) were identified by interval analysis using a LOD threshold of 3.0. These two quantitative trait loci (QTL) have been assigned the gene designations QFhs.ndsu-3B and QFhs.ndsu-2A, respectively. Recombinant inbred lines with these two QTL had a median severity of 20.9%, compared with 36.2% for all RI lines. The best RFLP marker in the 3BS region explained 15.4% of the variation and a multiple regression model consisting of three QTL explained 29.5% of the variation. These results indicate that resistance to FHB is inherited in a quantitative manner and that marker-assisted selection may aid the development of FHB-resistant cultivars.
Three chromosomal regions associated with scab resistance were detected in a common cultivar, Ning7840, by microsatellite and AFLP analysis. Six microsatellites on chromosome 3BS, Xgwm389, Xgwm533, Xbarc147, Xgwm493, Xbarc102, and Xbarc131, were integrated into an amplified fragment length polymorphism (AFLP) linkage group containing a major quantitative trait locus (QTL) for scab resistance in a mapping population of 133 recombinant inbred lines (RILs) derived from 'Ning7840' x 'Clark'. Based on single-factor analysis of variance of scab infection data from four experiments, Xgwm533 and Xbarc147 were the two microsatellite markers most tightly associated with the major scab resistance QTL. Interval analysis based on the integrated map of AFLP and microsatellite markers showed that the major QTL was located in a chromosome region about 8 cM in length around Xgwm533 and Xbarc147. Based on mapping of six microsatellite markers on eight 3BS deletion lines, the major QTL was located distal to breakage point 3BS-8. In total, 18 microsatellites were physically located on different subarm regions on 3BS. Two microsatellites, Xgwm120 and Xgwm614, were significantly associated with QTL for scab resistance on chromosome 2BL and 2AS, respectively. The resistance alleles on 3BS, 2BL, and 2AS were all derived from 'Ning7840'. Significant interaction between the major QTL on 3BS and the QTL on 2BL was detected based on microsatellite markers linked to them. Using these microsatellite markers would facilitate marker-assisted selection to improve scab resistance in wheat.
7. AFLP and STS tagging of a major QTL for Fusarium head blight resistance in wheat. Guo, P.-G.; Bai, G.-H.; Shaner, G. E. In: Theoretical and Applied Genetics, 2003,106:1011-1017.
Large-scale field screening for Fusarium head blight (FHB) resistance in wheat is difficult because environmental factors strongly influences the expression of resistance genes. Marker-assisted selection (MAS) may provide a powerful alternative. Conversion of amplified fragment length polymorphism (AFLP) markers into sequence-tagged site (STS) markers can generate breeder-friendly markers for MAS. In a previous study, one major quantitative trait locus (QTL) on chromosome 3BS was identified by using EcoRI-AFLP and a recombinant inbred population derived from the cross Ning 7840/Clark. Further mapping with PstI-AFLPs identified five markers that were significantly associated with the QTL. Three of them individually explained 38% to 50% of the phenotypic variation for FHB resistance. Two of them (pAGT/mCTG57, pACT/mCTG136) were linked to the QTL in coupling, and another (pAG/mCAA244) was linked to the QTL in repulsion. Successful conversion of one AFLP marker (pAG/mCAA244) yielded a co-dominant STS marker that explains about 50% of the phenotypic variation for FHB resistance in the population. The STS was validated in 14 other cultivars and is the first STS marker for a FHB resistance QTL converted from an AFLP marker.
8. Mapping of quantitativetrait loci for field resistance to Fusarium head blight in an European winter wheat. Gervais, L.; Dedryver, F.; Morlais, J.-Y.; Bodusseau, V.; Negre, S.; Bilous, M.; Groos, C.; Trottet, M. In: Theoretical and Applied Genetics, 2003, 106:961-970.
Fusarium head blight (FHB) caused by Fusarium culmorum is an economically important disease of wheat that may cause serious yield and quality losses under favorable climate conditions. The development of disease-resistant cultivars is the most effective control strategy. Worldwide, there is heavy reliance on the resistance pool originating from Asian wheats, but excellent field resistance has also been observed among European winter wheats. The objective of this study was to map and characterize quantitative traits loci (QTL) of resistance to FHB among European winter wheats. A population of 194 recombinant inbred lines (RILs) was genotyped from a cross between two winter wheats Renan (resistant)/Récital (susceptible) with microsatellites, AFLP and RFLP markers. RILs were assessed under field conditions For 3 years in one location. Nine QTLs were detected, and together they explained 30–45% of the variance, depending on the year. Three of the QTLs were stable over the 3 years. One stable QTL, QFhs.inra.2b, was mapped to chromosome 2B and two QTLs QFhs.inra.5a2 and QFhs.inra5a3, to chromosome 5A; each of these QTLs explained 6.9–18.6% of the variance. Other QTLs were identified on chromosome 2A, 3A, 3B, 5D, and 6D, but these had a smaller effect on FHB resistance. One of the two QTLs on chromosome 5A was linked to gene B1 controlling the presence of awns. Overlapping QTLs for FHB resistance were those for plant height or/and flowering time. Our results confirm that wheat chromosomes 2A, 3A, 3B, and 5A carry FHB resistance genes, and new resistance factors were identified on chromosome arms 2BS and 5AL. Markers flanking these QTLs should be useful tools for combining the resistance to FHB of Asian and European wheats to increase the resistance level of cultivars.