Crown rot (CR), caused by various Fusarium species, is a chronic wheat disease in Australia. As part of our objective of improving the efficiency of breeding CR resistant wheat varieties, we have been searching for novel sources of resistance. This paper reports on the genetic control of one of these newly identified resistant genotypes, 'CSCR6'. A population derived from a cross between CSCR6 and an Australian variety 'Lang' was analyzed using two Fusarium isolates belonging to two different species, one Fusarium pseudograminearum and the other Fusarium graminearum. The two isolates detected QTL with the same chromosomal locations and comparable magnitudes, indicating that CR resistance is not species-specific. The resistant allele of one of the QTL was derived from 'CSCR6'. This QTL, designated as Qcrs.cpi-3B, was located on the long arm of chromosome 3B and explains up to 48.8% of the phenotypic variance based on interval mapping analysis. Another QTL, with resistant allele from the variety 'Lang', was located on chromosome 4B. This QTL explained up to 22.8% of the phenotypic variance. A strong interaction between Qcsr.cpi-3B and Qcsr.cpi-4B was detected, reducing the maximum effect of Qcrs.cpi-3B to 43.1%. The effects of Qcrs.cpi-3B were further validated in four additional populations and the presence of this single QTL reduced CR severity by up to 42.1%. The fact that significant effects of Qcrs.cpi-3B were detected across all trials with different genetic backgrounds and with the use of isolates belonging to two different Fusarium species make it an ideal target for breeding programs as well as for further characterization of the gene(s) involved in its resistance.
Crown rot (CR) is one of the most destructive diseases of barley and wheat. Fusarium species causing CR survive in crop residue and a growing acceptance of stubble retention practices has exacerbated disease severity and yield loss. Growing resistant cultivars has long been recognised as the most effective way to reduce CR damage but these are not available in barley. In a routine screening of germplasm, a barley landrace from China gave the best CR resistance among the genotypes tested. Using a doubled haploid population derived from this landrace crossed to Franklin, we demonstrate that the CR resistance of TX9425 was conditioned by a major QTL. The QTL, designated as Qcrs.cpi-3H, was mapped near the centromere on the long arm of chromosome 3H. Its effect is highly significant, accounting for up to 63.3% of the phenotypic variation with a LOD value of 14.8. The location of Qcrs.cpi-3H was coincident with a major QTL conferring plant height (PH) and the effect of PH on CR reaction was also highly significant. When the effect of PH was accounted for by covariance analysis, the Qcrs.cpi-3H QTL remained highly significant, accounting for over 40% of the phenotypic variation. The existence of such a major QTL implies that breeding barley cultivars with enhanced CR resistance should be feasible.
By carefully separating type I and type II resistances, the possible effects of plant height on fusarium head blight (FHB) resistance in wheat were assessed using near-isogenic lines (NILs) for several different reduced-height (Rht) genes. Tall isolines all gave better type I resistance than their respective dwarf counterparts when assessed at their natural heights. These differences largely disappeared when the dwarf isolines were physically raised so that their spikes were positioned at the same height as those of their respective tall counterparts. The effects of plant height on type II resistance was less clear. For those NIL pairs which showed significant differences, it was the dwarf isolines which gave better resistance. As the Rht genes involved in these NILs locate at different genomic regions, the differences in FHB between the dwarf and tall isolines are unlikely to be the result of linkages between each of the different Rht loci with a beneficial or a deleterious gene affecting type I or type II resistance. Rather, the different FHB resistances are probably caused by direct or indirect effects of height difference per se, and microclimate may have contributed to the better type I resistance of the tall plants. Thus, caution should be exercised when attempting to exploit any of the FHB resistant loci co-located with Rht genes.
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