scholarly journals Mapping Resistance to Argentinean Fusarium (Graminearum) Head Blight Isolates in Wheat

2021 ◽  
Vol 22 (24) ◽  
pp. 13653
Author(s):  
Carolina Sgarbi ◽  
Ismael Malbrán ◽  
Luciana Saldúa ◽  
Gladys Albina Lori ◽  
Ulrike Lohwasser ◽  
...  
Keyword(s):  
Fusarium Graminearum ◽  
Wheat Yield ◽  
Kernel Weight ◽  
Type I ◽  
Type Ii ◽  
Head Blight ◽  
Yield And Quality ◽  
Type I Resistance ◽  
Additive Qtls ◽  
Type Ii Resistance

Fusarium head blight (FHB) of wheat, caused by Fusarium graminearum (Schwabe), is a destructive disease worldwide, reducing wheat yield and quality. To accelerate the improvement of scab tolerance in wheat, we assessed the International Triticeae Mapping Initiative mapping population (ITMI/MP) for Type I and II resistance against a wide population of Argentinean isolates of F. graminearum. We discovered a total of 27 additive QTLs on ten different (2A, 2D, 3B, 3D, 4B, 4D, 5A, 5B, 5D and 6D) wheat chromosomes for Type I and Type II resistances explaining a maximum of 15.99% variation. Another four and two QTLs for thousand kernel weight in control and for Type II resistance, respectively, involved five different chromosomes (1B, 2D, 6A, 6D and 7D). Furthermore, three, three and five QTLs for kernel weight per spike in control, for Type I resistance and for Type II resistance, correspondingly, involved ten chromosomes (2A, 2D, 3B, 4A, 5A, 5B, 6B, 7A, 7B, 7D). We were also able to detect five and two epistasis pairs of QTLs for Type I and Type II resistance, respectively, in addition to additive QTLs that evidenced that FHB resistance in wheat is controlled by a complex network of additive and epistasis QTLs.

Genetic characterization of QTL associated with resistance to Fusarium head blight in a doubled-haploid spring wheat population

Genome ◽  
2005 ◽  
Vol 48 (2) ◽  
pp. 187-196 ◽  
Author(s):  
Zhuping Yang ◽  
Jeannie Gilbert ◽  
George Fedak ◽  
Daryl J Somers
Keyword(s):  
Spring Wheat ◽  
Resistance Genes ◽  
Type I ◽  
Type Ii ◽  
Head Blight ◽  
Kernel Infection ◽  
Wheat Population ◽  
Fhb Resistance ◽  
Type I Resistance ◽  
Type Ii Resistance

Fusarium head blight (FHB) is one of the most important fungal wheat diseases worldwide. Understanding the genetics of FHB resistance is the key to facilitating the introgression of different FHB resistance genes into adapted wheat. The objectives of the present study were to detect and map quantitative trait loci (QTL) associated with FHB resistance genes and characterize the genetic components of the QTL in a doubled-haploid (DH) spring wheat population using both single-locus and two-locus analysis. A mapping population, consisting of 174 DH lines from the cross between DH181 (resistant) and AC Foremost (susceptible), was evaluated for type I resistance to initial infection during a 2-year period in spray-inoculated field trials, for Type II resistance to fungal spread within the spike in 3 greenhouse experiments using single-floret inoculation, and for resistance to kernel infection in a 2001 field trial. One-locus QTL analysis revealed 7 QTL for type I resistance on chromosome arms 2DS, 3AS, 3BS, 3BC (centromeric), 4DL, 5AS, and 6BS, 4 QTL for type II resistance on chromosomes 2DS, 3BS, 6BS, and 7BL, and 6 QTL for resistance to kernel infection on chromosomes 1DL, 2DS, 3BS, 3BC, 4DL, and 6BS. Two-locus QTL analysis detected 8 QTL with main effects and 4 additive by additive epistatic interactions for FHB resistance and identified novel FHB resistance genes for the first time on chromosomes 1DL, 4AL, and 4DL. Neither significant QTL by environment interactions nor epistatic QTL by environment interactions were found for either type I or type II resistance. The additive effects of QTL explained most of the phenotypic variance for FHB resistance. Marker-assisted selection for the favored alleles at multiple genomic regions appears to be a promising tool to accelerate the introgression and pyramiding of different FHB resistance genes into adapted wheat genetic backgrounds.Key words: Triticum aestivum, Fusarium graminearum, microsatellite, additive effect, additive by additive epistatic effect.

scholarly journals Quantitative Trait Loci for Fusarium Head Blight Resistance in a Recombinant Inbred Population of Wangshuibai/Wheaton

2008 ◽  
Vol 98 (1) ◽  
pp. 87-94 ◽  
Author(s):  
J.-B. Yu ◽  
G.-H. Bai ◽  
W.-C. Zhou ◽  
Y.-H. Dong ◽  
F. L. Kolb
Keyword(s):  
Quantitative Trait Loci ◽  
Quantitative Trait ◽  
Recombinant Inbred ◽  
Type I ◽  
Type Ii ◽  
Head Blight ◽  
Type Iii ◽  
Fhb Resistance ◽  
Type I Resistance ◽  
Type Ii Resistance

Use of diverse sources of Fusarium head blight (FHB)-resistant germplasm in breeding may significantly improve wheat resistance to FHB. Wangshuibai is an FHB-resistant Chinese landrace unrelated to cv. Sumai 3, the most commonly used FHB-resistant source. In all, 139 F6 recombinant inbred lines were developed from a cross between Wangshuibai and an FHB-susceptible cultivar, Wheaton, to map quantitative trait loci (QTL) for wheat resistance to initial infection (type I resistance), spread of FHB symptoms within a spike (type II resistance), and deoxynivalenol (DON) accumulation (type III resistance) in infected grain. The experiments were conducted in a greenhouse at Manhattan, KS from 2003 to 2005. More than 1,300 simple-sequence repeat and amplified fragment length polymorphism markers were analyzed in this population. Five QTL for type I resistance were detected on chromosomes 3AS, 3BS, 4B, 5AS, and 5DL after spray inoculation; seven QTL for type II resistance were identified on chromosomes 1A, 3BS, 3DL, 5AS, 5DL, and 7AL after point inoculation; and seven QTL for type III resistance were detected on chromosomes 1A, 1BL, 3BS, 5AS, 5DL, and 7AL with the data from both inoculation methods. These QTL jointly explained up to 31.7, 64, and 52.8% of the phenotypic variation for the three types of FHB resistance, respectively. The narrow-sense heritabilities were low for type I resistance (0.37 to 0.41) but moderately high for type II resistance (0.45 to 0.61) and type III resistance (0.44 to 0.67). The QTL on the distal end of 3BS, 5AS, and 5DL contributed to all three types of resistance. Two QTL, on 7AL and 1A, as well as one QTL near the centromere of 3BS (3BSc), showed effects on both type II and type III resistance. Selection for type II resistance may simultaneously improve type I and type III resistance as well. The QTL for FHB resistance identified in Wangshuibai have potential to be used to pyramid FHB-resistance QTL from different sources.

scholarly journals Molecular Characterization of Two Types of Resistance in Sunflower to Plasmopara halstedii, the Causal Agent of Downy Mildew

2011 ◽  
Vol 101 (8) ◽  
pp. 970-979 ◽  
Author(s):  
Osman Radwan ◽  
Mohamed Fouad Bouzidi ◽  
Said Mouzeyar
Keyword(s):  
Downy Mildew ◽  
Interleukin 1 ◽  
Coiled Coil ◽  
Hypersensitive Reaction ◽  
Type I ◽  
Basal Region ◽  
Type Ii ◽  
Plasmopara Halstedii ◽  
Type I Resistance ◽  
Type Ii Resistance

Depending on host–pathotype combination, two types of sunflower–Plasmopara halstedii incompatibility reactions have previously been identified. Type I resistance can restrict the growth of the pathogen in the basal region of the hypocotyls, whereas type II cannot, thus allowing the pathogen to reach the cotyledons. In type II resistance, a large portion of the hypocotyls is invaded by the pathogen and, subsequently, a hypersensitive reaction (HR) is activated over a long portion of the hypocotyls. Thus, the HR in type II resistance coincides with a higher induction of hsr203j sunflower homologue in comparison with type I resistance, where the HR is activated only in the basal part of hypocotyls. Although the pathogen was not detected in cotyledons of type I resistant plants, semiquantitative polymerase chain reaction confirmed the early abundant growth of the pathogen in cotyledons of susceptible plants by 6 days postinfection (dpi). This was in contrast to scarce growth of the pathogen in cotyledons of type II-resistant plants at a later time point (12 dpi). This suggests that pathogen growth differs according to the host–pathogen combination. To get more information about sunflower downy mildew resistance genes, the full-length cDNAs of RGC151 and RGC203, which segregated with the PlARG gene (resistance type I) and Pl14 gene (resistance type II), were cloned and sequenced. Sequence analyses revealed that RGC151 belongs to the Toll/interleukin-1 receptor (TIR) nucleotide-binding site leucine-rich repeat (NBS-LRR) class whereas RGC203 belongs to class coiled-coil (CC)-NBS-LRR. This study suggests that type II resistance may be controlled by CC-NBS-LRR gene transcripts which are enhanced upon infection by P. halstedii, rather than by the TIR-NBS-LRR genes that might control type I resistance.

scholarly journals Effects of plant height on type I and type II resistance to fusarium head blight in wheat

2011 ◽  
Vol 60 (3) ◽  
pp. 506-512 ◽  
Author(s):  
W. Yan ◽  
H. B. Li ◽  
S. B. Cai ◽  
H. X. Ma ◽  
G. J. Rebetzke ◽  
...  
Keyword(s):  
Fusarium Head Blight ◽  
Plant Height ◽  
Type I ◽  
Type Ii ◽  
Head Blight ◽  
Type Ii Resistance

scholarly journals Transgenic Wheat Expressing a Barley UDP-Glucosyltransferase Detoxifies Deoxynivalenol and Provides High Levels of Resistance to Fusarium graminearum

2015 ◽  
Vol 28 (11) ◽  
pp. 1237-1246 ◽  
Author(s):  
Xin Li ◽  
Sanghyun Shin ◽  
Shane Heinen ◽  
Ruth Dill-Macky ◽  
Franz Berthiller ◽  
...  
Keyword(s):  
Fusarium Graminearum ◽  
Severe Disease ◽  
Transgenic Wheat ◽  
Disease Spread ◽  
Economic Losses ◽  
Complete Suppression ◽  
Type Ii ◽  
Head Blight ◽  
Fungal Virulence ◽  
Type Ii Resistance

Fusarium head blight (FHB), mainly caused by Fusarium graminearum, is a devastating disease of wheat that results in economic losses worldwide. During infection, F. graminearum produces trichothecene mycotoxins, including deoxynivalenol (DON), that increase fungal virulence and reduce grain quality. Transgenic wheat expressing a barley UDP-glucosyltransferase (HvUGT13248) were developed and evaluated for FHB resistance, DON accumulation, and the ability to metabolize DON to the less toxic DON-3-O-glucoside (D3G). Point-inoculation tests in the greenhouse showed that transgenic wheat carrying HvUGT13248 exhibited significantly higher resistance to disease spread in the spike (type II resistance) compared with nontransformed controls. Two transgenic events displayed complete suppression of disease spread in the spikes. Expression of HvUGT13248 in transgenic wheat rapidly and efficiently conjugated DON to D3G, suggesting that the enzymatic rate of DON detoxification translates to type II resistance. Under field conditions, FHB severity was variable; nonetheless, transgenic events showed significantly less-severe disease phenotypes compared with the nontransformed controls. In addition, a seedling assay demonstrated that the transformed plants had a higher tolerance to DON-inhibited root growth than nontransformed plants. These results demonstrate the utility of detoxifying DON as a FHB control strategy in wheat.

scholarly journals The Pressure of Fusarium Disease and Its Relation with Mycotoxins in The Wheat Grain and Malt

Toxins ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 198 ◽  
Author(s):  
Valentina Spanic ◽  
Zvonimir Zdunic ◽  
Georg Drezner ◽  
Bojan Sarkanj
Keyword(s):  
De Novo ◽  
Disease Incidence ◽  
Type I ◽  
Head Blight ◽  
Wheat Varieties ◽  
Progress Curve ◽  
Resistant Varieties ◽  
Type I Resistance ◽  
One Year ◽  
Moderately Resistant

Fusarium head blight (FHB) is one of the most destructive wheat fungal diseases, causing yield loss, quality reduction, and accumulation of mycotoxins. The aim of this research was to summarize the occurrence of major Fusarium mycotoxins: deoxynivalenol (DON), 3-acetyldeoxynivalenol (3-AcDON), nivalenol (NIV), and zearalenone (ZEN) in two consecutive years to search the relationship between disease incidence and severity with mycotoxins found in control and inoculated grains and corresponding malt. In addition, deoxynivalenol-3-glucoside (D3G) in one-year research was measured. Tested wheat varieties showed infection scores of 3% (‘U1’ and ‘Sirban Prolifik’) to 79% (‘Golubica’) for Type I resistance evaluation. There were few moderately resistant varieties in view of their areas under the disease progress curve, which can be considered Type III resistance (‘Sirban Prolifik’ and ‘U1’). According to the data quantified by LC–MS/MS, DON decreased in infected malt in comparison to corresponding grain, while ZEN occurred only in infected malt samples. Both 3-AcDON and NIV increased in inoculated malt in comparison to corresponding grain, due to a combination of plant metabolism and de novo synthesis by molds during malting. Based on the results, we can draw a few conclusions: the resistance to Fusarium decreased quantified concentrations of DON; ZEN gets synthetized during malting; unregulated 3-AcDON and NIV increase during malting; more resistant varieties have converted DON to D3G more successfully. Modified mycotoxins should be also included to legislation, since they could be transformed back to the corresponding mycotoxins under food processing conditions or during digestion.

scholarly journals Cross-Resistance of the Codling Moth against Different Isolates of Cydia pomonella Granulovirus Is Caused by Two Different but Genetically Linked Resistance Mechanisms

Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 1952
Author(s):  
Annette J. Sauer ◽  
Eva Fritsch ◽  
Karin Undorf-Spahn ◽  
Kento Iwata ◽  
Regina G. Kleespies ◽  
...  
Keyword(s):  
Biological Control Agent ◽  
Cydia Pomonella ◽  
Codling Moth ◽  
Resistance Mechanisms ◽  
Cross Resistance ◽  
Viral Gene ◽  
Type I ◽  
Type Ii ◽  
Cydia Pomonella Granulovirus ◽  
Type Ii Resistance

Cydia pomonella granulovirus (CpGV) is a widely used biological control agent of the codling moth. Recently, however, the codling moth has developed different types of field resistance against CpGV isolates. Whereas type I resistance is Z chromosomal inherited and targeted at the viral gene pe38 of isolate CpGV-M, type II resistance is autosomal inherited and targeted against isolates CpGV-M and CpGV-S. Here, we report that mixtures of CpGV-M and CpGV-S fail to break type II resistance and is expressed at all larval stages. Budded virus (BV) injection experiments circumventing initial midgut infection provided evidence that resistance against CpGV-S is midgut-related, though fluorescence dequenching assay using rhodamine-18 labeled occlusion derived viruses (ODV) could not fully elucidate whether the receptor binding or an intracellular midgut factor is involved. From our peroral and intra-hemocoel infection experiments, we conclude that two different (but genetically linked) resistance mechanisms are responsible for type II resistance in the codling moth: resistance against CpGV-M is systemic whereas a second and/or additional resistance mechanism against CpGV-S is located in the midgut of CpR5M larvae.

scholarly journals Spike architecture traits associated with type II resistance to fusarium head blight in bread wheat

Euphytica ◽  
2021 ◽  
Vol 217 (12) ◽  
Author(s):  
M. F. Franco ◽  
G. A. Lori ◽  
G. Cendoya ◽  
M. P. Alonso ◽  
J. S. Panelo ◽  
...  
Keyword(s):  
Fusarium Head Blight ◽  
Bread Wheat ◽  
Type Ii ◽  
Head Blight ◽  
Type Ii Resistance

scholarly journals Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

2019 ◽  
Author(s):  
Wenjing Hu ◽  
Derong Gao ◽  
Hongya Wu ◽  
Jian Liu ◽  
Chunmei Zhang ◽  
...  
Keyword(s):  
Genome Wide Association Study ◽  
Resistance Breeding ◽  
Snp Markers ◽  
Genome Wide Association ◽  
Type Ii ◽  
Head Blight ◽  
Genome Wide ◽  
A Genome ◽  
Fhb Resistance ◽  
Type Ii Resistance

Abstract Background: Fusarium head blight (FHB), primarily caused by Fusarium graminearum, is a major threat to wheat production and food security worldwide. Breeding stably and durably resistant cultivars is the most effective approach for managing and controlling the disease. The success of FHB resistance breeding relies on identification of an effective resistant germplasm. We performed a genome-wide association study (GWAS) using the high-density wheat 90K single nucleotide polymorphism (SNP) assays to better understand the genetic basis of FHB resistance in natural population and identify associated molecular markers. Results: The resistance to FHB fungal spread along the rachis (Type II resistance) was evaluated on 171 wheat cultivars in the 2016-2017 (abbr. as 2017) and 2017-2018 (abbr. as 2018) growing seasons. Using Illumina Infinum iSelect 90K SNP genotyping data, a genome-wide association study (GWAS) identified 26 loci (88 marker-trait associations), which explained 6.65-14.18% of the phenotypic variances. The associated loci distributed across all chromosomes except 2D, 6A, 6D and 7D, with those on chromosomes 1B, 4A, 5D and 7A being detected in both years. New loci for Type II resistance were found on syntenic genomic regions of chromsome 4AL (QFhb-4AL, 621.85-622.24 Mb) and chromosome 5DL (QFhb-5DL, 546.09-547.27 Mb) which showed high collinearity in gene content and order. SNP markers wsnp_JD_c4438_5568170 and wsnp_CAP11_c209_198467 of 5D, reported previously linked to a soil-borne wheat mosaic virus (SBWMV) resistance gene, were also associated with FHB resistance in this study. Conclusion: The syntenic FHB resistant loci and associated SNP markers identified in this study are valuable for FHB resistance breeding via marker-assisted selection.

A New Form Of Therapeutic Resistance: Drug Glucuronidation Regulated By The Sonic Hedgehog Factor Gli1

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 821-821
Author(s):  
Hiba A Zahreddine ◽  
Biljana Culjkovic-Kraljacic ◽  
Sarit Assouline ◽  
Abdellatif Amri ◽  
Patrick Gendron ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cell Lines ◽  
Phase Ii ◽  
Resistant Cell ◽  
Type I ◽  
Type Ii ◽  
Protein Levels ◽  
Gli 1 ◽  
Type Ii Resistance ◽  
Resistant Cells

Abstract Despite many recent successes in the treatment of cancer, the development of chemoresistance in many of the initially responding patients, and primary resistance in others, remains a major impediment in therapy development. Our studies provide evidence for a novel mechanism underlying drug resistance: Gli1 dependent drug glucuronidation. While carrying out a Phase II clinical trial of targeting the eukaryotic translation initiation factor eIF4E with ribavirin in M4/M5 subtypes of AML, we observed that all responding patients eventually became clinically and molecularly resistant. To understand the cause of this resistance, we generated ribavirin resistant cell lines. In these models, ribavirin no longer targeted eIF4E activity or impaired growth, and importantly, the ability of ribavirin to bind eIF4E was severely impaired. However, the eIF4E gene was not mutated and its protein levels were not altered. The cell lines could be divided into two groups: type I with a defect in drug uptake and type II with a normal uptake. In type I resistant cells, we observed a substantial reduction in levels of Adenosine Kinase (ADK) an enzyme that catalyzes the rate limiting step in the metabolic activation of ribavirin allowing its retention in the cells. We used RNA Sequencing to examine the molecular underpinnings of type II resistance. Our data revealed a drastic increase in the levels of Gli1. In stably overexpressing cells, Gli1 was sufficient to produce the same resistance phenotype that we observed for type II cell models, both molecularly and at the level of cell growth. In addition, Gli1 overexpression correlated with the loss of drug-to-target interaction, as observed by our eIF4E immunoprecipitation studies using 3H-Ribavirin, similarly to the resistant cell lines. Conversely, Gli1 knockdown in type II cells or its pharmacological inhibition with the FDA approved Gli1 inhibitor GDC0449/Vismodegib, restored the eIF4E-ribavirin interaction and re-sensitized these cells to ribavirin. Our subsequent studies revealed a close correlation between Gli1 expression and the protein levels of the UGT1A glucuronosyl transferase enzymes involved in phase II drug metabolism whereby xenobiotics or metabolites are modified by the addition of a sugar, glucuronic acid. Given these findings, we examined whether the loss of the eIF4E interaction in resistant cells was due to the glucuronidation of ribavirin. Using 13C/12C ribavirin and mass spectrometry, we observed glucuronidated forms of ribavirin in resistant cells and cells overexpressing Gli1 but not in parental cells and that ribavirin is glucuronidated on its triazole ring which binds eIF4E. Treatment of cells with the Gli1 inhibitor GDC0449 reduces UGT1A levels, and correlates with reduced levels of ribavirin-glucuronides and the re-emergence of ribavirin-eIF4E complexes. We further hypothesized that the type II resistant cells could be resistant to other drugs. We observe that our ribavirin resistant cell lines are also resistant to the cornerstone of AML therapy, cytarabine. GDC0449/Vismodegib treatment reverts resistance to cytarabine in these cells. Preliminary studies indicate that these cells are also resistant to azacytidine and cisplatin. This is particularly striking as these cells were never exposed to these compounds. Thus, this could represent a novel form of multi-drug resistance. To establish the clinical relevance of our findings to patients in our AML ribavirin trial, we examined features of type I and type II resistance. Out of 10 patient samples available for evaluation, all six responding patient specimens showed elevated Gli-1 mRNA levels, up to 26 fold, upon relapse relative to levels during response. For most, the ratio of Gli1 during response relative to at relapse was about 2-4 fold with some patients up to 10 fold. For the two patients examined that did not respond, both had highly elevated Gli-1 levels prior to treatment relative to healthy individuals, and this was not lowered after 28 days of ribavirin treatment. We also noted elevated UGT1A protein levels upon relapse in our patient population. Type I resistance was observed in only two patients whereas Gli1 and UGT1A were dysregulated at relapse in all patients examined. In summary, we identified a novel form of drug resistance: Gli1 dependent drug glucuronidation. Treatment with Gli1 inhibitors appears to be a promising avenue for overcoming this form of drug resistance. Disclosures: No relevant conflicts of interest to declare.

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