scholarly journals Genes Associated with Foliar Resistance to Septoria Nodorum Blotch of Hexaploid Wheat (Triticum aestivum L.)

2021 ◽  
Vol 22 (11) ◽  
pp. 5580
Author(s):  
Dora Li ◽  
Esther Walker ◽  
Michael Francki
Keyword(s):  
Host Response ◽  
Molecular Mechanisms ◽  
Triticum Aestivum L ◽  
Reference Sequence ◽  
Septoria Nodorum ◽  
R Genes ◽  
Dh Population ◽  
Septoria Nodorum Blotch ◽  
Foliar Resistance ◽  
Full Complement

The genetic control of host response to the fungal necrotrophic disease Septoria nodorum blotch (SNB) in bread wheat is complex, involving many minor genes. Quantitative trait loci (QTL) controlling SNB response were previously identified on chromosomes 1BS and 5BL. The aim of this study, therefore, was to align and compare the genetic map representing QTL interval on 1BS and 5BS with the reference sequence of wheat and identify resistance genes (R-genes) associated with SNB response. Alignment of QTL intervals identified significant genome rearrangements on 1BS between parents of the DH population EGA Blanco, Millewa and the reference sequence of Chinese Spring with subtle rearrangements on 5BL. Nevertheless, annotation of genomic intervals in the reference sequence were able to identify and map 13 and 12 R-genes on 1BS and 5BL, respectively. R-genes discriminated co-located QTL on 1BS into two distinct but linked loci. NRC1a and TFIID mapped in one QTL on 1BS whereas RGA and Snn1 mapped in the linked locus and all were associated with SNB resistance but in one environment only. Similarly, Tsn1 and WK35 were mapped in one QTL on 5BL with NETWORKED 1A and RGA genes mapped in the linked QTL interval. This study provided new insights on possible biochemical, cellular and molecular mechanisms responding to SNB infection in different environments and also addressed limitations of using the reference sequence to identify the full complement of functional R-genes in modern varieties.

scholarly journals Evaluation of Septoria Nodorum Blotch (SNB) Resistance in Glumes of Wheat (Triticum aestivum L.) and the Genetic Relationship With Foliar Disease Response

2021 ◽  
Vol 12 ◽  
Author(s):  
Michael G. Francki ◽  
Esther Walker ◽  
Christopher J. McMullan ◽  
W. George Morris
Keyword(s):  
Physical Map ◽  
Phenotypic Selection ◽  
Triticum Aestivum L ◽  
Phenotypic Correlation ◽  
Septoria Nodorum ◽  
Genotype By Environment Interactions ◽  
Genotype By Environment ◽  
Septoria Nodorum Blotch ◽  
Foliar Resistance ◽  
Genetic Mechanisms

Septoria nodorum blotch (SNB) is a necrotrophic disease of wheat prominent in some parts of the world, including Western Australia (WA) causing significant losses in grain yield. The genetic mechanisms for resistance are complex involving multiple quantitative trait loci. In order to decipher comparable or independent regulation, this study identified the genetic control for glume compared to foliar resistance across four environments in WA against 37 different isolates. High proportion of the phenotypic variation across environments was contributed by genotype (84.0% for glume response and 82.7% for foliar response) with genotype-by-environment interactions accounting for a proportion of the variation for both glume and foliar response (14.7 and 16.2%, respectively). Despite high phenotypic correlation across environments, most of the eight and 14 QTL detected for glume and foliar resistance using genome wide association analysis (GWAS), respectively, were identified as environment-specific. QTL for glume and foliar resistance neither co-located nor were in LD in any particular environment indicating autonomous genetic mechanisms control SNB response in adult plants, regulated by independent biological mechanisms and influenced by significant genotype-by- environment interactions. Known Snn and Tsn loci and QTL were compared with 22 environment-specific QTL. None of the eight QTL for glume or the 14 for foliar response were co-located or in linkage disequilibrium with Snn and only one foliar QTL was in LD with Tsn loci on the physical map. Therefore, glume and foliar response to SNB in wheat is regulated by multiple environment-specific loci which function independently, with limited influence of known NE-Snn interactions for disease progression in Western Australian environments. Breeding for stable resistance would consequently rely on recurrent phenotypic selection to capture and retain favorable alleles for both glume and foliar resistance relevant to a particular environment.

scholarly journals Evaluation of Septoria nodorum blotch (SNB) resistance in glumes of wheat (Triticum aestivum L.) in multiple field environments and the genetic relationship with foliar disease response

2021 ◽  
Author(s):  
Michael Francki ◽  
Esther Walker ◽  
Christopher J. McMullan ◽  
W. George Morris
Keyword(s):  
Physical Map ◽  
Triticum Aestivum L ◽  
Phenotypic Correlation ◽  
Septoria Nodorum ◽  
Biological Mechanisms ◽  
Disease Response ◽  
Septoria Nodorum Blotch ◽  
Foliar Resistance ◽  
Genetic Mechanisms ◽  
Multiple Field

Abstract Septoria nodorum blotch (SNB) is a necrotrophic disease of wheat prominent in some parts of the world, including Western Australia (WA) causing significant losses in grain yield. The genetic mechanisms for resistance are complex involving multiple quantitative trait loci. In order to decipher comparable or independent regulation, this study identified the genetic control for glume compared to foliar resistance across four environments in WA against 37 different isolates. High proportion of the phenotypic variation across environments was contributed by genotype (84.0% for glume response and 82.7% for foliar response) with genotype-by-environment interactions accounting for a proportion of the variation for both glume and foliar response (14.7% and 16.2%, respectively). Despite high phenotypic correlation across environments, most of the eight and 14 QTL detected for glume and foliar resistance, respectively, were identified as environment-specific. QTL for glume and foliar resistance neither co-located nor were in LD in any particular environment indicating autonomous genetic mechanisms control SNB response in adult plants, regulated by independent biological mechanisms and influenced by significant genotype-by-isolate-by environment interactions. Known Snn and Tsn loci and QTL were compared with 22 environment-specific QTL. None of the eight QTL for glume or the 14 for foliar response were co-located or in linkage disequilibrium with Snn and only one foliar QTL was in LD with Tsn loci on the physical map. Therefore, known NE-Snn interactions are of limited relevance to glume and foliar SNB response in WA environments and other biological mechanisms are likely to prevail for host resistance and susceptibility.

scholarly journals A wheat chromosome 5AL region confers seedling resistance to both tan spot and Septoria nodorum blotch in two mapping populations

2019 ◽  
Vol 7 (6) ◽  
pp. 809-818 ◽  
Author(s):  
Wenjing Hu ◽  
Xinyao He ◽  
Susanne Dreisigacker ◽  
Carolina P. Sansaloni ◽  
Philomin Juliana ◽  
...  
Keyword(s):  
Wheat Chromosome ◽  
Tan Spot ◽  
Septoria Nodorum ◽  
Seedling Resistance ◽  
Septoria Nodorum Blotch ◽  
Mapping Populations

Karat winter wheat

1991 ◽  
Vol 71 (1) ◽  
pp. 207-210
Author(s):  
H. G. Nass ◽  
H. W. Johnston ◽  
E. Hansel ◽  
R. Blatt ◽  
C. Caldwell ◽  
...  
Keyword(s):  
Triticum Aestivum ◽  
Powdery Mildew ◽  
Winter Wheat ◽  
Triticum Aestivum L ◽  
Septoria Nodorum ◽  
Bread Making ◽  
Eastern Canada ◽  
Key Words Wheat ◽  
Glume Blotch ◽  
Cultivar Description

Karat is a winter wheat (Triticum aestivum L. em. Thell.) with bread making quality, high grain yield, and adequate straw strength. It is moderately susceptible to powdery mildew (caused by Erysiphe graminis D.C. ex. Merat f. sp. tritici Marchal) and septoria leaf and glume blotch (caused by Septoria nodorum Berk.) and is suited for production in areas of Eastern Canada where winter survival is not a problem. Key words: Wheat (winter), cultivar description

AC Winsloe winter wheat

1995 ◽  
Vol 75 (4) ◽  
pp. 905-907 ◽  
Author(s):  
H. G. Nass ◽  
H. W. Johnston ◽  
C. R. Blatt ◽  
G. Atlin ◽  
R. B. Walton
Keyword(s):  
Triticum Aestivum L ◽  
Septoria Nodorum ◽  
Head Blight ◽  
Fusarium Spp ◽  
Eastern Canada ◽  
Atlantic Region ◽  
Lodging Resistance ◽  
Glume Blotch ◽  
Cultivar Description ◽  
Moderately Resistant

AC Winsloe is a winter feed wheat (Triticum aestivum L. em. Thell.) with high grain yield, lodging resistance, and good winter survival. It is resistant to powdery mildew (caused by Erisyphe graminis D.C. ex Merat f. sp. tritici Marchal), moderately resistant to septoria leaf and glume blotch [caused by Septoria nodorum (Berk.) Berk.] and moderately resistant to fusarium head blight (caused by Fusarium graminearum Schwab and other Fusarium spp.). AC Winsloe is suitable for production in Eastern Canada, particularly in the Atlantic region. Key words:Triticum aestivum, wheat (winter), cultivar description

scholarly journals The Host Response to West Nile Virus Infection Limits Viral Spread through the Activation of the Interferon Regulatory Factor 3 Pathway

2004 ◽  
Vol 78 (14) ◽  
pp. 7737-7747 ◽  
Author(s):  
Brenda L. Fredericksen ◽  
Maria Smith ◽  
Michael G. Katze ◽  
Pei-Yong Shi ◽  
Michael Gale
Keyword(s):  
West Nile Virus ◽  
Virus Replication ◽  
Host Response ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
West Nile Virus Infection ◽  
Null Mouse ◽  
Regulatory Factor ◽  
West Nile ◽  
Viral Spread

ABSTRACT Recent outbreaks of West Nile Virus (WNV) have been associated with an increase in morbidity and mortality in humans, birds, and many other species. We have initiated studies to define the molecular mechanisms by which a recent pathogenic isolate of WNV evades the host cell innate antiviral response. Biochemical and microarray analyses demonstrated that WNV induced the expression of beta interferon (IFN-β) and several IFN-stimulated genes late in infection of cultured human cells. The late expression of these antiviral genes was due to the delayed activation of the transcription factor IFN regulatory factor 3 (IRF-3). Despite this host response, WNV was still able to replicate efficiently. The effect of the IRF-3 pathway on WNV replication was assessed by examining virus replication and spread in cultures of wild-type or IRF-3-null mouse embryo fibroblasts. The absence of IRF-3 was marked by a significant increase in plaque size and a sustained production of infectious particles. Although the activation of the IRF-3 pathway was not sufficient to block virus replication, our results suggest that IRF-3 target genes function to constrain WNV infection and limit cell-to-cell virus spread.

scholarly journals Early Upregulation of Acute Respiratory Distress Syndrome-Associated Cytokines Promotes Lethal Disease in an Aged-Mouse Model of Severe Acute Respiratory Syndrome Coronavirus Infection

2009 ◽  
Vol 83 (14) ◽  
pp. 7062-7074 ◽  
Author(s):  
Barry Rockx ◽  
Tracey Baas ◽  
Gregory A. Zornetzer ◽  
Bart Haagmans ◽  
Timothy Sheahan ◽  
...  
Keyword(s):  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Severe Acute Respiratory Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Host Response ◽  
Molecular Mechanisms ◽  
Distress Syndrome ◽  
Aged Mice ◽  
Young Mice

ABSTRACT Several respiratory viruses, including influenza virus and severe acute respiratory syndrome coronavirus (SARS-CoV), produce more severe disease in the elderly, yet the molecular mechanisms governing age-related susceptibility remain poorly studied. Advanced age was significantly associated with increased SARS-related deaths, primarily due to the onset of early- and late-stage acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Infection of aged, but not young, mice with recombinant viruses bearing spike glycoproteins derived from early human or palm civet isolates resulted in death accompanied by pathological changes associated with ARDS. In aged mice, a greater number of differentially expressed genes were observed than in young mice, whose responses were significantly delayed. Differences between lethal and nonlethal virus phenotypes in aged mice could be attributed to differences in host response kinetics rather than virus kinetics. SARS-CoV infection induced a range of interferon, cytokine, and pulmonary wound-healing genes, as well as several genes associated with the onset of ARDS. Mice that died also showed unique transcriptional profiles of immune response, apoptosis, cell cycle control, and stress. Cytokines associated with ARDS were significantly upregulated in animals experiencing lung pathology and lethal disease, while the same animals experienced downregulation of the ACE2 receptor. These data suggest that the magnitude and kinetics of a disproportionately strong host innate immune response contributed to severe respiratory stress and lethality. Although the molecular mechanisms governing ARDS pathophysiology remain unknown in aged animals, these studies reveal a strategy for dissecting the genetic pathways by which SARS-CoV infection induces changes in the host response, leading to death.

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