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

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.

2001 ◽  
Vol 81 (3) ◽  
pp. 527-533 ◽  
Author(s):  
S. D. Duguid ◽  
A. L. Brûlé-Babel

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


2020 ◽  
Vol 110 (11) ◽  
pp. 1781-1790
Author(s):  
Jingwei Guo ◽  
Gongjun Shi ◽  
Audrey Kalil ◽  
Andrew Friskop ◽  
Elias Elias ◽  
...  

The ascomycete fungus Pyrenophora tritici-repentis is the causal agent of tan spot of wheat. The disease can occur on both common wheat (Triticum aestivum) and durum wheat (T. turgidum ssp. durum) and has potential to cause significant yield and quality losses. The fungal pathogen is known to produce necrotrophic effectors (NEs) that act as important virulence factors. Based on the NE production and virulence on a set of four differentials, P. tritici-repentis isolates have been classified into eight races. Race 4 produces no known NEs and is avirulent on the differentials. From a fungal collection in North Dakota, we identified several isolates that were classified as race 4. These isolates caused no or little disease on all common wheat lines including the differentials; however, they were virulent on some durum cultivars and tetraploid wheat accessions. Using two segregating tetraploid wheat populations and quantitative trait locus mapping, we identified several genomic regions significantly associated with disease caused by two of these isolates, some of which have not been previously reported. This is the first report that race 4 is virulent on tetraploid wheat, likely utilizing unidentified NEs. Our findings further highlight the insufficiency of the current race classification system for P. tritici-repentis.


Agriculture ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 417
Author(s):  
Pao Theen See ◽  
Nikki Schultz ◽  
Caroline S. Moffat

The incidence of wheat head infection by Pyrenophora tritici-repentis (Ptr), the etiological agent of tan spot disease, was evaluated during grain development in a glasshouse experiment. Heads artificially inoculated with a Ptr spore suspension developed widespread brown spots across the spikelets, and mycelia and conidophores were observed on glumes and awns. Seeds of heavily infected heads were darkened and shrivelled, but no red smudge symptoms were apparent. The recovery rate of Ptr isolates from the inoculated wheat heads was low, and colonies that were re-isolated displayed an irregular morphology with reddish mycelia when grown on agar plates. The presence of Ptr on inoculated wheat heads was assessed directly via PCR detection, and a limitation of Ptr hyphae to proliferate beyond the point of contact of spore inoculum on floret tissues was observed. The systemic transmission of Ptr from infected seeds was minimal; however, saprophytic growth of the pathogen occurred on the senescing leaves of wheat plants grown from inoculated seeds. Thus, even though Ptr seed infection is not as common as foliar infection, infected seeds are still a source of disease inoculum and screening for pathogen contamination is advisable.


2005 ◽  
Vol 95 (2) ◽  
pp. 172-177 ◽  
Author(s):  
P. K. Singh ◽  
G. R. Hughes

The symptoms of tan spot of wheat, caused by Pyrenophora triticirepentis, include a tan necrosis component and an extensive chlorosis component. Since tan spot has become the major component of the leafspotting disease complex of wheat in western Canada, the need for resistant cultivars has increased. This study was conducted to determine whether the resistance to tan spot found in a diverse set of spring and winter wheat genotypes was due to resistance genes not previously reported. The genetic control of resistance to necrosis induced by P. triticirepentis race 1 and race 2 was determined, under controlled environmental conditions, for spring wheat genotypes Erik and 86ISMN 2137 and winter wheat genotypes Hadden, Red Chief, and 6B-365. Plants were inoculated at the two-leaf stage and disease reaction was assessed based on lesion type. Tests of the F1 and F2 generations, and of F2:3 and F2:8 families, indicated that one recessive gene controlled resistance to the necrosis component of tan spot caused by both race 1 and race 2 in each cross studied. Lack of segregation in crosses between the resistant cultivars indicated that the resistance gene was the same in all of the cultivars.


Genome ◽  
1996 ◽  
Vol 39 (3) ◽  
pp. 598-604 ◽  
Author(s):  
W. S. Stock ◽  
A. L. Brûlé-Babel ◽  
G. A. Penner

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.


2003 ◽  
Vol 93 (4) ◽  
pp. 397-401 ◽  
Author(s):  
T. L. Friesen ◽  
S. Ali ◽  
S. Kianian ◽  
L. J. Francl ◽  
J. B. Rasmussen

Pyrenophora tritici-repentis race 2 produces Ptr ToxA, a host-selective toxin previously described as a pathogenicity factor for tan spot on wheat. The objective of this research was to evaluate the role of host sensitivity to toxin, conditioned by a single dominant gene on chromosome 5BL, in the disease development by race 2. An F2-derived F6 recombinant inbred population of 108 wheat lines, produced from crosses of toxin-sensitive, disease-susceptible cv. Kulm with the toxin-insensitive, disease-resistant cv. Erik segregated 1:1 for toxin reaction. However, the population was skewed toward resistance to race 2 of the fungus. Toxin reaction accounted for 24.4% of the genetic variance for disease. Heritability estimates suggested the presence of four to five genes that influence disease reaction in the population. Toxin-insensitive mutants, previously derived Kulm, were susceptible to race 2, although disease developed more slowly on the mutants than it did on the wild-type Kulm. The data indicate that sensitivity to Ptr ToxA influences disease severity in some host genotypes without defining susceptibility.


1998 ◽  
Vol 78 (3) ◽  
pp. 489-496 ◽  
Author(s):  
M. R. Fernandez ◽  
R. P. Zentner ◽  
B. G. McConkey ◽  
C. A. Campbell

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


Plant Disease ◽  
2003 ◽  
Vol 87 (2) ◽  
pp. 203-203
Author(s):  
T. L. Peever ◽  
T. D. Murray

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.


2012 ◽  
Vol 58 (1) ◽  
pp. 73-78 ◽  
Author(s):  
J. Šárová ◽  
A. Hanzalová ◽  
P. Bartoš

<i>Pyrenophora tritici</i>-<i>repentis</i>, causal agent of tan spot, is one of the most important wheat leaf spot pathogens worldwide. The race structure of <i>P. tritici</i>-<i>repentis</i> isolates obtained from wheat (except one from noncereal grass species) in the Czech Republic was studied. The 86 monosporic isolates of <i>P. tritici</i>-<i>repentis</i> originated from different parts of the Czech Republic were grouped into five known races based on necrosis/chlorosis induction on standard differentials (Katepwa, Glenlea, 6B365, Salamouni). The isolates recovered from wheat were races 1, 2 and 4. Race 1 was the most frequent (50%), races 2 and 4 were found rarely (3% and 5% respectively). The isolate of <i>P. tritici</i>-<i>repentis</i> recovered from noncereal grass species was determined as race 4 which seems to be typical for noncereal hosts. The reaction of 30 isolates (42%) was difficult to be compared to reactions of so far identified <i>P. tritici</i>-<i>repentis</i> races. They have to be tested again on additional wheat genotypes.


2019 ◽  
Vol 133 (2) ◽  
pp. 433-442 ◽  
Author(s):  
Yuan Liu ◽  
Qijun Zhang ◽  
Evan Salsman ◽  
Jason D. Fiedler ◽  
Justin B. Hegstad ◽  
...  

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