Co-infection of wheat by Pyrenophora tritici-repentis and Parastagonospora nodorum in the wheatbelt of Western Australia

2020 ◽  
Vol 71 (2) ◽  
pp. 119
Author(s):  
Araz S. Abdullah ◽  
Mark R. Gibberd ◽  
John Hamblin
Keyword(s):  
Empirical Studies ◽  
Triticum Aestivum L ◽  
Fungal Species ◽  
Tan Spot ◽  
Robust Methods ◽  
Pyrenophora Tritici Repentis ◽  
Septoria Nodorum Blotch ◽  
Fungal Abundance ◽  
Wheat Leaves ◽  
Parastagonospora Nodorum

The pathogenic fungal species Pyrenophora tritici-repentis (Ptr) and Parastagonospora nodorum (Pan) are common in many wheat-producing parts of the world. These two fungi cause tan spot and septoria nodorum blotch, respectively, frequently co-infecting wheat leaves. Empirical studies of this and other co-infections are rare because of the visual similarity of symptoms and the lack of robust methods for quantifying the abundance of pathogens associated with the co-infection. Here, we use a recently developed molecular method that simultaneously distinguishes and quantifies, in DNA equivalent, the abundance of Ptr and Pan, thereby allowing the prevalence of co-infection to be determined. The study examines the prevalence of co-infection under field conditions, at three widely spaced sites and on three wheat (Triticum aestivum L.) cultivars varying in disease resistance. Co-infection by Ptr and Pan was almost ubiquitous (overall prevalence 94%), and Pan DNA was detected only in association with Ptr. Although Ptr and Pan commonly co-infected, Ptr was more abundant during early and mid-season, at 80% of total fungal abundance when crops were tillering and 67% at booting stage. Pan became as abundant as Ptr when crops reached flowering. Variability in total fungal abundance and disease severity was primarily determined by cultivar; however, Ptr was the more abundant despite differences in cultivar resistance to this pathogen.

scholarly journals New Insights into the Roles of Host Gene-Necrotrophic Effector Interactions in Governing Susceptibility of Durum Wheat to Tan Spot and Septoria nodorum Blotch

2016 ◽  
Vol 6 (12) ◽  
pp. 4139-4150 ◽  
Author(s):  
Simerjot K Virdi ◽  
Zhaohui Liu ◽  
Megan E Overlander ◽  
Zengcui Zhang ◽  
Steven S Xu ◽  
...  
Keyword(s):  
Durum Wheat ◽  
Common Wheat ◽  
Tan Spot ◽  
Septoria Nodorum ◽  
Pyrenophora Tritici Repentis ◽  
Septoria Nodorum Blotch ◽  
Necrotrophic Fungi ◽  
Host Genetic ◽  
Parastagonospora Nodorum ◽  
Necrotrophic Effector

Abstract Tan spot and Septoria nodorum blotch (SNB) are important diseases of wheat caused by the necrotrophic fungi Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively. The P. tritici-repentis necrotrophic effector (NE) Ptr ToxB causes tan spot when recognized by the Tsc2 gene. The NE ToxA is produced by both pathogens and has been associated with the development of both tan spot and SNB when recognized by the wheat Tsn1 gene. Most work to study these interactions has been conducted in common wheat, but little has been done in durum wheat. Here, quantitative trait loci (QTL) analysis of a segregating biparental population indicated that the Tsc2-Ptr ToxB interaction plays a prominent role in the development of tan spot in durum. However, analysis of two biparental populations indicated that the Tsn1-ToxA interaction was not associated with the development of tan spot, but was strongly associated with the development of SNB. Pa. nodorum expressed ToxA at high levels in infected Tsn1 plants, whereas ToxA expression in P. tritici-repentis was barely detectable, suggesting that the differences in disease levels associated with the Tsn1-ToxA interaction were due to differences in pathogen expression of ToxA. These and previous results together indicate that: (1) the effects of Tsn1-ToxA on tan spot in common wheat can range from nonsignificant to highly significant depending on the host genetic background; (2) Tsn1-ToxA is not a significant factor for tan spot development in durum wheat; and (3) Tsn1-ToxA plays a major role in SNB development in both common and durum wheat. Durum and common wheat breeders alike should strive to remove both Tsc2 and Tsn1 from their materials to achieve disease resistance.

scholarly journals Characterizing Virulence of the Pyrenophora tritici-repentis Isolates Lacking Both ToxA and ToxB Genes

Pathogens ◽  
2018 ◽  
Vol 7 (3) ◽  
pp. 74 ◽  
Author(s):  
Jingwei Guo ◽  
Gongjun Shi ◽  
Zhaohui Liu
Keyword(s):  
Triticum Aestivum L ◽  
Tan Spot ◽  
Pyrenophora Tritici Repentis ◽  
Tan Spot Disease ◽  
Hard Red Winter Wheat ◽  
Winter Wheat Cultivars ◽  
Race 2 ◽  
Genomic Regions ◽  
Race 4 ◽  
Necrotrophic Effectors

The fungus Pyrenophora tritici-repentis (Ptr) causes tan spot of wheat crops, which is an important disease worldwide. Based on the production of the three known necrotrophic effectors (NEs), the fungal isolates are classified into eight races with race 4 producing no known NEs. From a laboratory cross between 86–124 (race 2 carrying the ToxA gene for the production of Ptr ToxA) and DW5 (race 5 carrying the ToxB gene for the production of Ptr ToxB), we have obtained some Ptr isolates lacking both the ToxA and ToxB genes, which, by definition, should be classified as race 4. In this work, we characterized virulence of two of these isolates called B16 and B17 by inoculating them onto various common wheat (Triticum aestivum L.) and durum (T. turgidum L.) genotypes. It was found that the two isolates still caused disease on some genotypes of both common and durum wheat. Disease evaluations were also conducted in recombinant inbred line populations derived from two hard red winter wheat cultivars: Harry and Wesley. QTL mapping in this population revealed that three genomic regions were significantly associated with disease, which are different from the three known NE sensitivity loci. This result further indicates the existence of other NE-host sensitivity gene interactions in the wheat tan spot disease system.

scholarly journals Parastagonospora nodorum and Related Species in Western Canada: Genetic Variability and Effector Genes

2020 ◽  
Vol 110 (12) ◽  
pp. 1946-1958
Author(s):  
Mohamed Hafez ◽  
Ryan Gourlie ◽  
Therese Despins ◽  
Thomas K. Turkington ◽  
Timothy L. Friesen ◽  
...  
Keyword(s):  
Evolutionary Relationship ◽  
Haplotype Network ◽  
Bipolaris Sorokiniana ◽  
Western Canada ◽  
Pyrenophora Tritici Repentis ◽  
Septoria Nodorum Blotch ◽  
Effector Genes ◽  
Parastagonospora Nodorum ◽  
Almost All ◽  
Necrotrophic Effectors

Parastagonospora nodorum is an important fungal pathogen that causes Septoria nodorum blotch (SNB) in wheat. This pathogen produces several necrotrophic effectors that act as virulence factors; three have been cloned, SnToxA, SnTox1, and SnTox3. In this study, P. nodorum and its sister species P. avenaria f. tritici (Pat1) were isolated from wheat node and grain samples collected from distanced sites in western Canada during 2018. The presence of effector genes and associated haplotypes were determined by PCR and sequence analysis. An internal transcribed spacer-restriction fragment length polymorphism test was developed to distinguish between leaf spotting pathogens (P. nodorum, Pat1, Pyrenophora tritici-repentis, and Bipolaris sorokiniana). P. nodorum was mainly recovered from wheat nodes and to a lesser extent from the grains, while Pat1 was exclusively isolated from grain samples. The effector genes were present in almost all P. nodorum isolates, with the ToxA haplotype 5 (H5) being most prevalent, while a novel ToxA haplotype (denoted here H21) is reported for the first time. In Pat1, only combinations of SnTox1 and SnTox3 genes were present. A ToxA haplotype network was also constructed to assess the evolutionary relationship among globally found haplotypes to date. Finally, cultivars representing wheat development in Canada for the last century were tested for sensitivity to Sn-effectors and to the presence of Tsn1, the ToxA sensitivity gene. Of tested cultivars, 32.9 and 56.9% were sensitive to SnTox1 and SnTox3, respectively, and Tsn1 was present in 59% of the cultivars. In conclusion, P. nodorum and Pat1 were prevalent wheat pathogens in Canada with a potential tissue-specific colonization capacity, while producing necrotrophic effectors to which wheat is sensitive.

A gene for resistance to a necrosis-inducing isolate of Pyrenophora tritici-repentis located on 5BL of Triticum aestivum cv. Chinese Spring

Genome ◽  
1996 ◽  
Vol 39 (3) ◽  
pp. 598-604 ◽  
Author(s):  
W. S. Stock ◽  
A. L. Brûlé-Babel ◽  
G. A. Penner
Keyword(s):  
Triticum Aestivum ◽  
Resistance Gene ◽  
Chinese Spring ◽  
Recessive Gene ◽  
Triticum Aestivum L ◽  
Tan Spot ◽  
Monosomic Analysis ◽  
Chromosome Location ◽  
Pyrenophora Tritici Repentis ◽  
Chromosome Arm

Several sources of high-level resistance to tan spot caused by Pyrenophora tritici-repentis have been identified in hexaploid wheat (Triticum aestivum L.). This study was conducted to determine the number and chromosome location of a gene(s) in the cultivar Chinese Spring (CS) that confers resistance to a tan necrosis inducing isolate (nec+chl−) of P. tritici-repentis, 86-124, and insensitivity to Ptr necrosis toxin. Reciprocal crosses were made between CS (resistant–insensitive) and 'Kenya Farmer' (KF) (susceptible–sensitive). Analysis of the CS/KF F1and F2 populations and F2-derived F3 families identified a single nuclear recessive gene governing resistance to isolate 86-124 and Ptr necrosis toxin. Evaluation of the CS(KF) substitution series, F2 monosomic analysis, and screening of a series of 19 CS compensating nullitetrasomic and two ditelosomic lines (2AS and 5BL) indicated that the resistance gene was located on chromosome arm 5BL. No linkage exists between Lr18 and the tan necrosis resistance gene on chromosome arm 5BL. It is proposed that the gene for resistance to the tan necrosis inducing isolate 86-124 (nec+chl−) of P. tritici-repentis and Ptr necrosis toxin be named tsn1. Key words : wheat, Triticum aestivum L., tan spot resistance, Pyrenophora tritici-repentis (Died.) Drechs., chromosome location, Ptr necrosis toxin.

Effects of crop rotations and fertilizer management on leaf spotting diseases of spring wheat in southwestern Saskatchewan

1998 ◽  
Vol 78 (3) ◽  
pp. 489-496 ◽  
Author(s):  
M. R. Fernandez ◽  
R. P. Zentner ◽  
B. G. McConkey ◽  
C. A. Campbell
Keyword(s):  
Spring Wheat ◽  
Leaf Spot ◽  
Leaf Tissue ◽  
Triticum Aestivum L ◽  
Fertilizer Application ◽  
Tan Spot ◽  
P Deficiency ◽  
Pyrenophora Tritici Repentis ◽  
Leaf Spots ◽  
Phaeosphaeria Nodorum

The objective of this study was to determine the effect of crop sequence, summerfallow frequency, and fertilizer application, on the severity of leaf spotting diseases of spring wheat (Triticum aestivum L.). In the field experiment examined, Pyrenophora tritici-repentis (Died.) Drechs. was the pathogen most commonly isolated from lesioned leaf tissue, followed by stagonospora blotch (Phaeosphaeria nodorum [E. Müller] Hedjaroude). The severity of leaf spots in wheat after fallow was greater than in monoculture continuous wheat, or in wheat after a noncereal crop. Percent area with leaf spots in wheat grown after wheat was higher than in wheat grown after flax (Linum usitatissimum L.) or lentil (Lens culinaris Medikus) in years with high disease pressure (1995 and 1996), but not in 1993 or 1994 when overall disease levels were low. Under soil N-deficient conditions, leaf spot levels increased in years with dry summers (1994 and 1996), whereas a P deficiency decreased leaf spot severity in years that had cool and wet springs (1995 and 1996). A survey of producers' fields confirmed the observations made in the research plots, in particular, wheat after wheat was not more severely diseased than wheat grown in rotation with a noncereal crop. We concluded that the use of fallow, or 1 yr of rotation with a noncereal crop, will not reduce leaf spotting diseases of spring wheat in southwestern Saskatchewan. The best rotation aimed at reducing the levels of disease appeared to be 2 consecutive years of spring wheat, followed by at least 2 yr of a noncereal crop, or by a noncereal crop and summerfallow. Key words: Leaf spot, tan spot, Pyrenophora tritici-repentis, stagonospora blotch, Phaeosphaeria nodorum, septoria blotch, Mycosphaerella graminicola, crop rotation, tillage, fertility

scholarly journals First Report of Tan Spot of Wheat Caused by Pyrenophora tritici-repentis in the Pacific Northwest

Plant Disease ◽  
2003 ◽  
Vol 87 (2) ◽  
pp. 203-203
Author(s):  
T. L. Peever ◽  
T. D. Murray
Keyword(s):  
New York ◽  
Pacific Northwest ◽  
Sequence Similarity ◽  
Triticum Aestivum L ◽  
Tan Spot ◽  
Morphological Description ◽  
Morphological Identification ◽  
First Report ◽  
Pyrenophora Tritici Repentis ◽  
The Pacific

In late May 2001, lesions resembling tan spot were observed on lower leaves of winter wheat (Triticum aestivum L.) in early boot stage in Nez Perce County, ID. Abundant sporulation was observed from tan lesions with chlorotic haloes after 2 days incubation in a moist chamber at room temperature. Conidia were multicelled, straw colored, approximately 100 × 15 µm, rounded at the apex, and borne singly on dark brown conidiophores. The fungus fit the morphological description of Drechslera tritici-repentis (Died.) Shoemaker, the anamorphic state of Pyrenophora tritici-repentis (Died.) Drechs. (2). Three single-conidial isolates were sampled from infected plants in a 5 × 1 m area of the affected field and induced to sporulate. Two of the isolates were used to spray-inoculate 3-week-old susceptible wheat (cv. Madsen) in the greenhouse (one plant per isolate, 1 × 105 conidia/ml), and tan spot lesions were apparent 3 to 5 days after inoculation with both isolates. DNA was extracted from all three isolates, and the entire nuclear ribosomal internal transcribed spacer (ITS) was amplified with ITS1 and ITS4 primers (4). Similarly, 610 bp of the 5′ end of the glyceraldehyde-3-phosphate-dehydrogenase gene (gpd) was amplified with gpd-1 and gpd-2 primers (1). ITS and gpd amplicons were direct-sequenced on both strands, and alignment revealed that all three isolates were identical for both regions. A BLAST search of the NCBI database with the ITS sequence revealed P. tritici-repentis accessions AY004808 and AF071348 and D. tritici-repentis accession AF163060 as the closest matches with 100, 99.8, and 98.8% sequence similarity, respectively. A similar search with the gpd sequence revealed P. tritici-repentis accessions AY004838 and AF081370 and P. bromi accession AY004839 as the closest matches with 100, 100, and 99.0% sequence similarity, respectively. These results, coupled with the morphological identification and inoculation results, confirm the identity of the fungus as P. tritici-repentis. Although reported on other grass hosts in the region (3), to our knowledge, this is the first report of tan spot of wheat in the Pacific Northwest. This disease has been of little concern to wheat producers in the Pacific Northwest due to low rainfall and relative humidity during the growing season. References: (1) M. L. Berbee et al. Mycologia 91:964, 1999. (2) M. B. Ellis, Dematiaceous Hyphomycetes. CMI, Kew, Surrey, UK. 1971. (3) R. Sprague. Diseases of Cereals and Grasses in North America (Fungi, Except Smuts and Rusts). Ronald Press Co. New York, 1950. (4) T. J. White et al. Pages 315–322 in: PCR Protocols: A Guide to Methods and Applications. Academic Press Inc., New York, 1990.

scholarly journals Volatile molecules secreted by the wheat pathogen Parastagonospora nodorum are involved in development and phytotoxicity

2019 ◽  
Author(s):  
M. Jordi Muria-Gonzalez ◽  
Hui Yeng Yeannie Yap ◽  
Susan Breen ◽  
Oliver Mead ◽  
Chen Wang ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Reverse Genetics ◽  
Mass Spectrometry Analysis ◽  
Synthetic Genes ◽  
Spectrometry Analysis ◽  
Septoria Nodorum Blotch ◽  
Volatile Organic ◽  
Wheat Leaves ◽  
Plant Assays ◽  
Parastagonospora Nodorum

AbstractSeptoria nodorum blotch is a major disease of wheat caused by the fungus Parastagonospora nodorum. Recent studies have demonstrated that secondary metabolites, including polyketides and non-ribosomal peptides, produced by the pathogen play important roles in disease and development. However, there is currently no knowledge on the composition or biological activity of the volatile organic compounds (VOCs) secreted by P. nodorum. To address this, we undertook a series of growth and phytotoxicity assays and demonstrated that P. nodorum VOCs inhibited bacterial growth, were phytotoxic and suppressed self-growth. Mass spectrometry analysis revealed that 3-methyl-1-butanol, 2-methyl-1-butanol, 2-methyl-1-propanol and 2-phenylethanol were dominant in the VOC mixture and phenotypic assays using these short chain alcohols confirmed that they were phytotoxic. Further analysis of the VOCs also identified the presence of multiple sesquiterpenes of which four were identified via mass spectrometry and nuclear magnetic resonance as β-elemene, α-cyperone, eudesma-4,11-diene and acora-4,9-diene. Subsequent reverse genetics studies were able to link these molecules to corresponding sesquiterpene synthases in the P. nodorum genome. However, despite extensive testing, these molecules were not involved in either of the growth inhibition or phytotoxicity phenotypes previously observed. Plant assays using mutants of the pathogen lacking the synthetic genes revealed that the identified sesquiterpenes were not required for disease formation on wheat leaves. Collectively, these data have significantly extended our knowledge of the VOCs in fungi and provided the basis for further dissecting the roles of sesquiterpenes in plant disease.

Inheritance and interaction of spring wheat (Triticum aestivum L.) resistance to Race 2 and Race 3 of Pyrenophora tritici-repentis (Died.) Drechs.

2001 ◽  
Vol 81 (3) ◽  
pp. 527-533 ◽  
Author(s):  
S. D. Duguid ◽  
A. L. Brûlé-Babel
Keyword(s):  
Triticum Aestivum ◽  
Fungal Pathogen ◽  
Nuclear Gene ◽  
Triticum Aestivum L ◽  
Tan Spot ◽  
Pyrenophora Tritici Repentis ◽  
Ptr Toxa ◽  
Recessive Genes ◽  
Race 2 ◽  
Dominant Genes

Tan spot is a residue-borne leaf spotting disease caused by the fungal pathogen Pyrenophora tritici-repentis. An understanding of the inheritance of resistance is required to build a strategy for incorporating tan spot resistance into commercial cultivars of wheat. The objectives of this study were to determine the inheritance of host resistance to isolates of races 2 (a necrosis-inducing race) and 3 (a chlorosis-inducing race) of P. tritici-repentis. Crosses were made between seven wheat (Triticum aestivum) genotypes (Katepwa, BH1146, ST15, ST6, Erik, 6B1043, 6B367). Parents, F1, F2and F2-derived F3 populations were inoculated with isolates 86-124 and D308 (races 2 and 3, respectively) of P. tritici-repentis and infiltrated with Ptr ToxA. Resistance to 86-124 and insensitivity to Ptr ToxA was controlled by a single recessive nuclear gene in all of the resistant/susceptible crosses. In contrast, resistance to D308 was controlled by a single dominant nuclear gene in five crosses and two genes in two crosses. In the BH1146/ST15 cross two dominant genes controlled resistance to D308, while in the Katepwa/ST15 cross two recessive genes controlled resistance. Reactions to race 2 were independent of reactions to race 3 and controlled by independent genetic systems. Key words: Triticum aestivum L., Pyrenophora tritici-repentis (Died.) Drechs., disease resistance, inheritance, Ptr necrosis toxin, tan spot

scholarly journals Interaction between the Bird Cherry-Oat Aphid (Rhopalosiphum padi) and Stagonospora Nodorum Blotch (Parastagonospora nodorum) on Wheat

Insects ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 35
Author(s):  
Belachew Asalf ◽  
Andrea Ficke ◽  
Ingeborg Klingen
Keyword(s):  
Pathogenic Fungus ◽  
Rhopalosiphum Padi ◽  
Stagonospora Nodorum ◽  
Controlled Experiments ◽  
Aphid Infestation ◽  
Pests And Diseases ◽  
Septoria Nodorum Blotch ◽  
Wheat Leaves ◽  
Parastagonospora Nodorum ◽  
New Strategies

Wheat plants are under constant attack by multiple pests and diseases. Until now, there are no studies on the interaction between the aphid Rhopalosiphum padi and the plant pathogenic fungus Parastagonospora nodorum causal agent of septoria nodorum blotch (SNB) on wheat. Controlled experiments were conducted to determine: (i) The preference and reproduction of aphids on P. nodorum inoculated and non-inoculated wheat plants and (ii) the effect of prior aphid infestation of wheat plants on SNB development. The preference and reproduction of aphids was determined by releasing female aphids on P. nodorum inoculated (SNB+) and non-inoculated (SNB−) wheat leaves. The effect of prior aphid infestation of wheat plants on SNB development was determined by inoculating P. nodorum on aphid-infested (Aphid+) and aphid free (Aphid−) wheat plants. Higher numbers of aphids moved to and settled on the healthy (SNB−) leaves than inoculated (SNB+) leaves, and reproduction was significantly higher on SNB− leaves than on SNB+ leaves. Aphid infestation of wheat plants predisposed the plants to P. nodorum infection and colonization. These results are important to understand the interactions between multiple pests in wheat and hence how to develop new strategies in future integrated pest management (IPM).

scholarly journals Variability in an effector gene promoter of a necrotrophic fungal pathogen dictates epistasis and effector-triggered susceptibility in wheat

2021 ◽  
Author(s):  
Evan John ◽  
Silke Jacques ◽  
Huyen Phan ◽  
Lifang Liu ◽  
Danilo Pereira ◽  
...  
Keyword(s):  
Regulatory Region ◽  
Gene Promoter ◽  
Epistatic Effect ◽  
Start Codon ◽  
Septoria Nodorum Blotch ◽  
Trait Locus ◽  
Repressor Molecule ◽  
Wheat Leaves ◽  
Parastagonospora Nodorum ◽  
Necrotrophic Effectors

The fungus Parastagonospora nodorum uses proteinaceous necrotrophic effectors (NEs) to induce tissue necrosis on wheat leaves during infection, leading to the symptoms of septoria nodorum blotch (SNB). The NEs Tox1 and Tox3 induce necrosis on wheat possessing the dominant susceptibility genes Snn1 and Snn3B1/Snn3D1, respectively. We previously observed that Tox1 is epistatic to the expression of Tox3 and a quantitative trait locus (QTL) on chromosome 2A that contributes to SNB resistance/susceptibility. The expression of Tox1 is significantly higher in the Australian strain SN15 compared to the American strain SN4. Inspection of the Tox1 promoter region revealed a 401 bp promoter genetic element in SN4 positioned 267 bp upstream of the start codon that is absent in SN15, called PE401. Analysis of the world-wide P. nodorum population revealed that a high proportion of Northern Hemisphere isolates possess PE401 whereas the opposite was observed in the Southern Hemisphere. The presence of PE401 ablates the epistatic effect of Tox1 on the contribution of the SNB 2A QTL but not Tox3. PE401 was introduced into the Tox1 promoter regulatory region in SN15 to test for direct regulatory roles. Tox1 expression was markedly reduced in the presence of PE401. This suggests a repressor molecule(s) binds PE401 and inhibits Tox1 transcription. Infection assays also demonstrated that P. nodorum which lacks PE401 is more pathogenic on Snn1 varieties than P. nodorum carrying PE401. An infection competition assay between P. nodorum isogenic strains with and without PE401 indicated that the higher Tox1-expressing strain rescued the reduced virulence of the lower Tox1-expressing strain on Snn1 wheat. Our study demonstrated that Tox1 exhibits both selfish and altruistic characteristics. This offers an insight into a NE arms race that is occurring within the P. nodorum population. The importance of PE401 in breeding for SNB resistance in wheat is discussed.

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