scholarly journals Pyrenophora tritici-repentis Race 4 Isolates Cause Disease on Tetraploid Wheat

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.

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.


2006 ◽  
Vol 96 (8) ◽  
pp. 885-889 ◽  
Author(s):  
P. K. Singh ◽  
J. L. Gonzalez-Hernandez ◽  
M. Mergoum ◽  
S. Ali ◽  
T. B. Adhikari ◽  
...  

Race 3 of the fungus Pyrenophora tritici-repentis, causal agent of tan spot, induces differential symptoms in tetraploid and hexaploid wheat, causing necrosis and chlorosis, respectively. This study was conducted to examine the genetic control of resistance to necrosis induced by P. tritici-repentis race 3 and to map resistance genes identified in tetraploid wheat (Triticum turgidum). A mapping population of recombinant inbred lines (RILs) was developed from a cross between the resistant genotype T. tur-gidum no. 283 (PI 352519) and the susceptible durum cv. Coulter. Based on the reactions of the Langdon-T. dicoccoides (LDN[DIC]) disomic substitution lines, chromosomal location of the resistance genes was determined and further molecular mapping of the resistance genes for race 3 was conducted in 80 RILs of the cross T. turgidum no. 283/Coulter. Plants were inoculated at the two-leaf stage and disease reaction was assessed 8 days after inoculation based on lesion type. Disease reaction of the LDN(DIC) lines and molecular mapping on the T. turgidum no. 283/Coulter population indicated that the gene, designated tsn2, conditioning resistance to race 3 is located on the long arm of chromosome 3B. Genetic analysis of the F2 generation and of the F4:5 and F6:7 families indicated that a single recessive gene controlled resistance to necrosis induced by race 3 in the cross studied.


2007 ◽  
Vol 114 (5) ◽  
pp. 855-862 ◽  
Author(s):  
W. Tadesse ◽  
M. Schmolke ◽  
S. L. K. Hsam ◽  
V. Mohler ◽  
G. Wenzel ◽  
...  

2008 ◽  
Vol 98 (5) ◽  
pp. 488-491 ◽  
Author(s):  
R. P. Oliver ◽  
M. Lord ◽  
K. Rybak ◽  
J. D. Faris ◽  
P. S. Solomon

The wheat disease tan (or yellow leaf) spot, caused by Pyrenophora tritici-repentis, was first described in the period 1934 to 1941 in Canada, India, and the United States. It was first noted in Australia in 1953 and only became a serious disease in the 1970s. The emergence of this disease has recently been linked to the acquisition by P. tritici-repentis of the ToxA gene from the wheat leaf and glume blotch pathogen, Stagonospora nodorum. ToxA encodes a host-specific toxin that interacts with the product of the wheat gene Tsn1. Interaction of ToxA with the dominant allele of Tsn1 causes host necrosis. P. tritici-repentis races lacking ToxA give minor indistinct lesions on wheat lines, whereas wheat lines expressing the recessive tsn1 are significantly less susceptible to the disease. Although the emergence and spread of tan spot had been attributed to the adoption of minimum tillage practices, we wished to test the alternative idea that the planting of Tsn1 wheat lines may have contributed to the establishment of the pathogen in Australia. To do this, wheat cultivars released in Australia from 1911 to 1986 were tested for their sensitivity to ToxA. Prior to 1941, 16% of wheat cultivars were ToxA-insensitive and hence, all other factors being equal, would be more resistant to the disease. Surprisingly, only one of the cultivars released since 1940 was ToxA insensitive, and the area planted to ToxA-insensitive cultivars varied from 0 to a maximum of only 14% in New South Wales. Thus, the majority of the cultivars were ToxA-sensitive both before and during the period of emergence and spread of the disease. We therefore conclude that the spread of P. tritici-repentis in Australia cannot be causally linked to the deployment of ToxA-sensitive cultivars.


2009 ◽  
Vol 99 (8) ◽  
pp. 906-912 ◽  
Author(s):  
Justin D. Faris ◽  
Timothy L. Friesen

The wheat Tsn1 gene on chromosome 5B confers sensitivity to a host-selective toxin produced by the pathogens that cause tan spot and Stagonospora nodorum blotch (SNB) known as Ptr ToxA and SnToxA, respectively (hereafter referred to as ToxA). A compatible Tsn1–ToxA interaction is known to play a major role in conferring susceptibility of hexaploid (common) wheat to SNB. However, a recent study by another group suggested that the Tsn1–ToxA interaction was not relevant in conferring susceptibility of the tetraploid (durum) wheat cv. Langdon (LDN). Here, we reevaluated the role of the Tsn1–ToxA interaction in governing SNB susceptibility using the same mapping population and Stagonospora nodorum isolate (Sn2000) as were used in the previous study. Results of our quantitative trait locus analysis showed that the Tsn1 locus accounted for 95% of the variation in SNB. In addition, inoculation of the mapping population with two ToxA-knockout strains of Sn2000 revealed that the entire population was resistant. Furthermore, several LDN Tsn1-disrupted mutants were evaluated and found to be resistant to SNB. Together, these results prove unequivocally that Tsn1 is the only factor present along chromosome 5B that governs response to SNB in this population and that a compatible Tsn1–ToxA interaction is necessary for the manifestation of disease. Therefore, the results from the previous study are refuted.


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.


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.


2015 ◽  
Vol 13 (1) ◽  
pp. 16 ◽  
Author(s):  
Ol’ga Aleksandrovna Orlovskaya ◽  
Irina Nikolaevna Leonova ◽  
Elena Artemovna Salina ◽  
Lyubov’ Vladimirovna Khotyleva

2019 ◽  
Vol 22 (8) ◽  
pp. 978-986 ◽  
Author(s):  
A. М. Kokhmetova ◽  
Sh. Ali ◽  
Z. Sapakhova ◽  
M. N. Atishova

Pyrenophora tritici-repentis(Ptr) is the causative agent of tan spot, one of the yield limiting diseases of wheat, rapidly increasing in wheat growing countries including Kazakhstan. The aim of this study was the identifcation of wheat genotypes with resistance to Ptr race 1 and race 5 and their host­selective effectors (toxins) Ptr ToxA and Ptr ToxB. A common wheat collection of 41 accessions (38 experimental and 3 controls) was characterized using the molecular markersXfcp623andXBE444541, diagnostic for theTsn1andTsc2genes conferring sensitivity to fungal toxins. The coincidence of the markerXBE444541with resistance to race 5 was 92.11 %, and with Ptr ToxB, 97.37 %. Genotyping results using the markerXfcp623confrmed the expected response to Ptr ToxA; the presence/absence of the markerXfcp623completely (100 %) coincided with sensitivity/resistance to race 1 and Ptr ToxA. This demonstrates the reliability of the diagnostic markerXfcp623for identifying wheat genotypes with resistance to the fungus and insensitivity to Ptr ToxA. The study of the reaction of wheat germplasm to the fungal inoculation and toxin infltration showed that out of 38 genotypes analyzed 30 (78 %) exhibited resistance to both race 1 and race 5, and insensitivity to toxins Ptr ToxA and ToxB. Of most signifcant interest are eight wheat genotypes that showed resistance/insensitivity both to the two races and two toxins. The results of phenotyping were reconfrmed by the molecular markers used in this study. Sensitivity to Ptr ToxB is not always correlated with susceptibility to race 5 and is dependent on the host’s genetic background of the wheat genotype, i. e. on a specifc wheat genotype. The results of the study are of interest for increasing the efciency of breeding based on the elimination of the genotypes with the dominant allelesTsn1andTsc2sensitive to the toxins Ptr ToxA and ToxB. The genotypes identifed will be used in wheat breeding for resistance to tan spot.


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