scholarly journals Quantitative Trait Locus Mapping of Increased Fusarium Head Blight Susceptibility Associated with a Wild Emmer Wheat Chromosome

2009 ◽  
Vol 99 (4) ◽  
pp. 447-452 ◽  
Author(s):  
David F. Garvin ◽  
Robert W. Stack ◽  
Jana M. Hansen

Chromosome 2A of wild emmer wheat (Triticum turgidum var. dicoccoides) genotype Israel A increases Fusarium head blight (FHB) severity when present in durum wheat (T. turgidum var. durum) cv. Langdon (LDN). The goal of this study was to identify regions of Israel A chromosome 2A associated with this difference in resistance. A recombinant inbred chromosome line population (RICL) from a cross between LDN and the LDN-Israel A chromosome 2A substitution line [LDN(DIC-2A)] was employed for analysis. Three greenhouse FHB evaluations were completed on the RICL to obtain phenotypic data on variation for FHB resistance, and a simple sequence repeat (SSR)-based molecular map of chromosome 2A was developed. Quantitative trait locus (QTL) mapping identified a region on the long arm of chromosome 2A that was associated with FHB resistance in each independent FHB evaluation. Depending on the evaluation, the single best SSR marker in this region accounted for between 21 and 26% of the variation for FHB resistance, with the Israel A marker alleles associated with increased FHB susceptibility. The single best markers from each evaluation reside within an interval of approximately 22 cM. This study identifies one or more new QTL on chromosome 2A in tetraploid wheat that can contribute to significant variation in FHB resistance.

2007 ◽  
Vol 97 (5) ◽  
pp. 592-597 ◽  
Author(s):  
S. Kumar ◽  
R. W. Stack ◽  
T. L. Friesen ◽  
J. D. Faris

Fusarium head blight (FHB) caused by Fusarium graminearum is one of the most destructive diseases of durum (Triticum turgidum sp. durum) and common wheat (T. aestivum). Promising sources of FHB resistance have been identified among common (hexaploid) wheats, but the same is not true for durum (tetraploid) wheats. A previous study indicated that chromosome 7A from T. turgidum sp. dicoccoides accession PI478742 contributed significant levels of resistance to FHB. The objectives of this research were to develop a genetic linkage map of chromosome 7A in a population of 118 recombinant inbred lines derived from a cross between the durum cv. Langdon (LDN) and a disomic LDN-T. turgidum sp. dicoccoides PI478742 chromosome 7A substitution line [LDN-DIC 7A(742)], and identify a putative FHB resistance quantitative trait locus (QTL) on chromosome 7A derived from LDN-DIC 7A(742). The population was evaluated for type II FHB resistance in three greenhouse environments. Interval regression analysis indicated that a single QTL designated Qfhs.fcu-7AL explained 19% of the phenotypic variation and spanned an interval of 39.6 cM. Comparisons between the genetic map and a previously constructed physical map of chromosome 7A indicated that Qfhs.fcu-7AL is located in the proximal region of the long arm. This is only the second FHB QTL to be identified in a tetraploid source, and it may be useful to combine it with the QTL Qfhs.ndsu-3AS in order to develop durum wheat germ plasm and cultivars with higher levels of FHB resistance.


2005 ◽  
Vol 18 (12) ◽  
pp. 1318-1324 ◽  
Author(s):  
Marc Lemmens ◽  
Uwe Scholz ◽  
Franz Berthiller ◽  
Chiara Dall'Asta ◽  
Andrea Koutnik ◽  
...  

We investigated the hypothesis that resistance to deoxynivalenol (DON) is a major resistance factor in the Fusarium head blight (FHB) resistance complex of wheat. Ninety-six double haploid lines from a cross between ‘CM-82036’ and ‘Remus’ were examined. The lines were tested for DON resistance after application of the toxin in the ear, and for resistances to initial infection and spread of FHB after artificial inoculation with Fusarium spp. Toxin application to flowering ears induced typical FHB symptoms. Quantitative trait locus (QTL) analyses detected one locus with a major effect on DON resistance (logarithm of odds = 53.1, R2 = 92.6). The DON resistance phenotype was closely associated with an important FHB resistance QTL, Qfhs.ndsu-3BS, which previously was identified as governing resistance to spread of symptoms in the ear. Resistance to the toxin was correlated with resistance to spread of FHB (r = 0.74, P < 0.001). In resistant wheat lines, the applied toxin was converted to DON-3-O-glucoside as the detoxification product. There was a close relation between the DON-3-glucoside/DON ratio and DON resistance in the toxintreated ears (R2 = 0.84). We conclude that resistance to DON is important in the FHB resistance complex and hypothesize that Qfhs.ndsu-3BS either encodes a DON-glucosyltransferase or regulates the expression of such an enzyme.


Crop Science ◽  
2007 ◽  
Vol 47 (2) ◽  
pp. 893-897 ◽  
Author(s):  
R. E. Oliver ◽  
R. W. Stack ◽  
J. D. Miller ◽  
X. Cai

Pathogens ◽  
2018 ◽  
Vol 7 (3) ◽  
pp. 58 ◽  
Author(s):  
Moustafa Eldakak ◽  
Aayudh Das ◽  
Yongbin Zhuang ◽  
Jai Rohila ◽  
Karl Glover ◽  
...  

Fusarium head blight (FHB) is a highly detrimental disease of wheat. A quantitative trait locus for FHB resistance, Qfhb1, is the most utilized source of resistance in wheat-breeding programs, but very little is known about its resistance mechanism. In this study, we elucidated a prospective FHB resistance mechanism by investigating the proteomic signatures of Qfhb1 in a pair of contrasting wheat near-isogenic lines (NIL) after 24 h of inoculation of wheat florets by Fusarium graminearum. Statistical comparisons of the abundances of protein spots on the 2D-DIGE gels of contrasting NILs (fhb1+ NIL = Qfhb1 present; fhb1- NIL = Qfhb1 absent) enabled us to select 80 high-ranking differentially accumulated protein (DAP) spots. An additional evaluation confirmed that the DAP spots were specific to the spikelet from fhb1- NIL (50 spots), and fhb1+ NIL (seven spots). The proteomic data also suggest that the absence of Qfhb1 makes the fhb1- NIL vulnerable to Fusarium attack by constitutively impairing several mechanisms including sucrose homeostasis by enhancing starch synthesis from sucrose. In the absence of Qfhb1, Fusarium inoculations severely damaged photosynthetic machinery; altered the metabolism of carbohydrates, nitrogen and phenylpropanoids; disrupted the balance of proton gradients across relevant membranes; disturbed the homeostasis of many important signaling molecules induced the mobility of cellular repair; and reduced translational activities. These changes in the fhb1- NIL led to strong defense responses centered on the hypersensitive response (HSR), resulting in infected cells suicide and the consequent initiation of FHB development. Therefore, the results of this study suggest that Qfhb1 largely functions to either alleviate HSR or to manipulate the host cells to not respond to Fusarium infection.


2019 ◽  
Vol 109 (10) ◽  
pp. 1664-1675 ◽  
Author(s):  
Jemanesh K. Haile ◽  
Amidou N’Diaye ◽  
Sean Walkowiak ◽  
Kirby T. Nilsen ◽  
John M. Clarke ◽  
...  

Fusarium head blight (FHB) is a major fungal disease affecting wheat production worldwide. Since the early 1990s, FHB, caused primarily by Fusarium graminearum, has become one of the most significant diseases faced by wheat producers in Canada and the United States. The increasing FHB problem is likely due to the increased adoption of conservation tillage practices, expansion of maize production, use of susceptible wheat varieties in rotation, and climate variability. Durum wheat (Triticum turgidum sp. durum) is notorious for its extreme susceptibility to FHB and breeding for resistance is complicated because sources of FHB resistance are rare in the primary gene pool of tetraploid wheat. Losses due to this disease include yield, test weight, seed quality, food and feed quality, and when severe, market access. More importantly, it is the contamination with mycotoxins, such as deoxynivalenol, in Fusarium-infected durum kernels that causes the most serious economic as well as food and feed safety concerns. Several studies and thorough reviews have been published on germplasm development and breeding for FHB resistance and the genetics and genomics of FHB resistance in bread or common wheat (T. aestivum); however, similar reviews have not been conducted in durum wheat. Thus, the aim of this review is to summarize and discuss the recent research efforts to mitigate FHB in durum wheat, including quantitative trait locus mapping, genome-wide association studies, genomic prediction, mutagenesis and characterization of genes and pathways involved in FHB resistance. It also highlights future directions, FHB-resistant germplasm, and the potential role of morphological traits to enhance FHB resistance in durum wheat.


2017 ◽  
Vol 107 (1) ◽  
pp. 92-99 ◽  
Author(s):  
X. Li ◽  
Z. P. Xiang ◽  
W. Q. Chen ◽  
Q. L. Huang ◽  
T. G. Liu ◽  
...  

Fusarium head blight (FHB), mainly caused by Fusarium graminearum, is a destructive disease in wheat. A population consisting of 229 F2 and F2:3 plants derived from the cross PI 672538 × L661 was used to evaluate the reactions to FHB. The FHB resistance data distribution in the F2 population indicates that some quantitative trait loci (QTLs) were controlling the FHB resistance in PI 672538. We further detected two major QTLs (Qfhs-2B, Qfhs-3B) from analysis of the resistance data and the PCR-amplified results using WinQTLCart 2.5 software. Qfhs-2B, flanked by Xbarc55-2B and Xbarc1155-2B, explained more than 11.6% of the phenotypic variation of the percentage of diseased spikelets (PDS), and Qfhs-3B, flanked by Xwmc54-3B and Xgwm566-3B, explained more than 10% of the PDS phenotypic variation in the F2:3 population. In addition, Qfhs-3B was different from Fhb1 in terms of the pedigree, inheritance, resistance response, chromosomal location, and marker diagnosis. We also detected QTLs for other disease resistance indices, including the percentage of damaged kernels and 1,000-grain weight, in similar chromosomal regions. Therefore, the FHB resistance of PI 672538 was mainly controlled by two major QTLs, mapped on 2B (FhbL693a) and 3B (FhbL693b). PI 672538 could be a useful germplasm for improving wheat FHB resistance.


Genome ◽  
2012 ◽  
Vol 55 (12) ◽  
pp. 853-864 ◽  
Author(s):  
Yuefeng Ruan ◽  
André Comeau ◽  
François Langevin ◽  
Pierre Hucl ◽  
John M. Clarke ◽  
...  

Most tetraploid durum wheat (Triticum turgidum L var. durum) cultivars are susceptible to Fusarium head blight (FHB). This study reports novel quantitative trait loci (QTL) associated with FHB resistance. A backcross recombinant inbred line (BCRIL) population was developed from the cross BGRC3487/2*DT735, and 160 lines were evaluated for resistance to Fusarium graminearum Schwabe (teleomorph Gibberella zeae (Schwein. Petch) in field trials over 3 years (2008–2010) and to a F. graminearum 3-acetyl-deoxynivalenol (3-ADON) chemotype in greenhouse trials. The population was genotyped with 948 polymorphic loci using DArT and microsatellite markers. Eleven QTL were associated with FHB resistance under field conditions on chromosomes 2A, 3B, 5A, 5B, 7A, and 7B. Two of these, QFhb.usw-3B from BGRC3487 and QFhb.usw-7A2, were consistently detected over environments. The QFhb.usw-3B QTL was in a similar position to a resistance QTL in hexaploid wheat. The combination of the two QTL reduced field index by 53.5%–86.2%. Two QTL for resistance to the 3-ADON chemotype were detected on chromosomes 1B and 4B. Both BGRC3487 and DT735 could provide new sources of FHB resistance and the combination of QTL reported here could be valuable tools in breeding FHB-resistant durum wheat.


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