scholarly journals The Ability to Detoxify the Mycotoxin Deoxynivalenol Colocalizes With a Major Quantitative Trait Locus for Fusarium Head Blight Resistance in Wheat

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.

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.


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.


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.


2017 ◽  
Vol 38 (SI 2 - 6th Conf EFPP 2002) ◽  
pp. 580-582 ◽  
Author(s):  
A. Steed ◽  
E. Chandler ◽  
M. Thomsett ◽  
J. Carter ◽  
S. Faure ◽  
...  

Chromosome 4A of Triticum macha carries resistance to Fusarium head blight (FHB). Double haploid lines (DH) of T. macha 4A were used to determine the type of resistance and location of the gene(s). FHB resistance and yield trait data collected over two seasons following spray and point inoculation, indicate that the resistance is of type I and is probably conferred by a single gene. The resistance was mapped with microsatellite markers to a small area of the T. macha 4A chromosome flanked by markers gwm 610 and gwm 165. This could greatly facilitate future marker assisted selection work aimed at increasing resistance to FHB in other winter wheat lines.


2013 ◽  
Vol 26 (4) ◽  
pp. 442-450 ◽  
Author(s):  
Yongbin Zhuang ◽  
Aravind Gala ◽  
Yang Yen

Fusarium head blight (FHB) is a devastating disease worldwide, affecting wheat and other small grains. To identify key wheat genes involved in FHB pathogenesis, 406 FHB-related wheat expressed sequence tags functionally identified in Sumai 3 were investigated for their association with FHB-resistance quantitative trait loci (QTL) Fhb1 and Fhb_6BL in 2010 and 2011. A total of 47 candidate genes were identified by bulk analysis, near-isogenic screening and expression QTL mapping, and were finally mapped to their carrier chromosomes with Chinese Spring nulli-tetra deficiency lines. One gene, designated WFhb1_c1 (wheat Fhb1 candidate gene 1), was both functionally associated with and physically located within Fhb1 and was found to be weakly similar (E = 5e+0) to an Arabidopsis gene encoding pectin methyl esterase inhibitor. Two other genes, designated WFI_6BL1 and WFI_6BL2 (wheat-Fusarium interaction genes 6BL1 and 6BL2), were functionally associated with Fhb_6BL but physically mapped on chromosomes 7D and 5A, respectively. WFI_6BL1 was annotated as a 13- lipoxygenase gene and WFI_6BL2 might encode a PR-4-like protein. Our data suggested that i) Fhb1 seems to contribute to FHB resistance by reducing susceptibility in the first 60 h, ii) Fhb_6BL makes its contribution via the jasmonate-mediated pathways, and iii) wheat seems to activate its defense mechanism in the biotrophic phase of FHB pathogenesis.


2021 ◽  
Author(s):  
Xianrui Guo ◽  
Qinghua Shi ◽  
Jing Yuan ◽  
Mian Wang ◽  
Jing Wang ◽  
...  

AbstractFusarium head blight (FHB), caused by Fusarium species, seriously threaten global wheat production. Three wheat-Th.elongatum FHB resistant translocation lines have been developed and used for breeding. Transcriptomic analysis identified a derivative glutathione S-transferase transcript T26102, which was homologous to Fhb7 and induced dramatically by Fusarium graminearum. Homologs of Fhb7 were detected in several genera in Triticeae, including Thinopyrum, Elymus, Leymus, Pseudoroegeria and Roegeria. Several wheat-Thinopyrum translocation lines carrying Fhb7 remain susceptible to FHB, and transgenic plants overexpressing the T26102 on different backgrounds did not improve the FHB resistance. Taken as a whole, we show the application of the chromatin derived from diploid Thinopyrum elongatum successfully conferring wheat with high level FHB resistance independent of the Fhb7.One Sentence SummaryThinopyrum elongatum chromatin from 7EL was successfully applied to wheat FHB resistance breeding, but the resistant gene other than the reported Fhb7 remained unknown.


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