Tritici-repentis Race Research Articles

Changes in Phenolic Acid Levels in Wheat Cultivars Inoculated with Pyrenophora tritici-repentis race 1

Changes in Phenolic Acid Levels in Wheat Cultivars Inoculated with Pyrenophora tritici-repentis race 1

Characterization of Pyrenophora tritici-repentis (tan spot of wheat) races in Kazakhstan

Tan spot, caused by Pyrenophora tritici-repentis, is an economically important foliar disease of wheat in Kazakhstan. Population structure of the pathogen changes every year due to climate change. This study aimed to characterize the race structure of P. tritici-repentis isolates recovered from wheat in south and north Kazakhstan, and identify tan spot resistance in host genotypes based on disease phenotypes and molecular screening. Virulence profiles were determined within 40 isolates of the pathogen from wheat crops during the 2020 growing season. Seven races, (1, 3, 4, 5, 6, 7 and 8) were identified. A collection of 80 wheat accessions, including promising lines and cultivars from Kazakhstan and Russia, were evaluated for their reactions to races 1 and 5 of the pathogen, and to Ptr ToxA and Ptr ToxB, using greenhouse assessments and molecular markers diagnostic for the Tsn1 and Tsc2 genes. From a practical viewpoint, 18 wheat genotypes were insensitive to the two races and the two Ptr toxins. This resistant germplasm can be used in breeding programmes aiming to develop wheat varieties resistant to P. tritici-repentis.

Identification of a Novel ToxA Haplotype of Pyrenophora tritici-repentis from Japan.

Pyrenophora tritici-repentis was described first as a pathogen of wheat (tan spot) in Japan in the 1920s, but, since then, no reports on P. tritici-repentis race structure or its effectors in Japan have been published. In this study, 10 single-spore isolates of P. tritici-repentis were collected from bread wheat in Japan. These isolates were evaluated for virulence on four differential wheat genotypes and tested for the presence/absence of the effector-encoding genes, ToxA and ToxB, in multiplex PCR assays. These isolates were identified as ToxA producers, of which eight were designated as race 2 (ToxA producers) and two were classified as race 1 (ToxA and ToxC producers) based on their virulence patterns. Sequence analysis of the ToxA amplicons from these 10 isolates indicated the presence of a novel ToxA haplotype (denoted PtrA2). A comparative sequence analysis and resequencing of ToxA from reference P. tritici-repentis isolates showed that all previously published ToxA haplotypes in P. tritici-repentis were identical, and are hence denoted PtrA1 in this study. A total of 163 PtrToxA sequences from global origins were already deposited in GenBank and were confirmed identical to PtrA1. Sequence variation in PtrA1 and PtrA2 open reading frames were found at three positions: one synonymous mutation at position 412 (C/G) and two nonsynonymous mutations at positions 342 and 362 that alter amino acid sequence. These mutations did not seem to affect the necrosis development on a ToxA-sensitive wheat genotype when rated for symptoms 5 to 7 days after inoculation. This is the first report correctly confirming the presence of an additional novel ToxA haplotype in P. tritici-repentis for which we have predicted its isoform and updated the ToxA haplotype evolutionary network.

Pyrenophora tritici-repentis population structure in the Republic of Kazakhstan and identification of wheat germplasm resistant to tan spot.

Pyrenophora tritici-repentis is a causative agent of tan spot in wheat. In recent years, there has been an increasing spread and harmfulness of wheat tan spot. The aim of the research was to study the racial composition of the P. tritici-repentis population in the Republic of Kazakhstan. A collection of 30 common wheat accessions, including promising lines and cultivars from Kazakhstan and CIMMYT–ICARDA, was assessed for resistance to P. tritici- repentis in a greenhouse and characterized using the Xfcp623 molecular marker, diagnostic for the Tsn1 gene. Monosporic isolates of P. tritici-repentis isolated from the southeastern region were assigned to certain races based on the manifestation of symptoms of necrosis/chlorosis on standard differentials (Glenlea, 6B662, 6B365). Five races of P. tritici-repentis have been identified, including races 1, 2, 3, 7 and 8. It has been shown that races 1 and 8 of P. tritici-repentis are dominant. As a result of the analysis of the frequency of occurrence of the P. tritici-repentis races, it was found that race 1 (50 %) producing Ptr ToxA and Ptr ToxB and race 8 (35 %) producing Ptr ToxA, Ptr ToxB and Ptr ToxC turned out to be dominant. From a practical point of view, of greatest interest are 16 wheat samples, which demonstrated resistance to race 1 and confirmed insensitivity to Ptr ToxA in a molecular screening. These include eight Kazakhstani (4_PSI, 10204_2_KSI, 10204_3_KSI, 10205_2_KSI, 10205_3_KSI, 605_SP2, 632_SP2, Dana) and seven foreign lines (KR11-20, KR11-03, KR11-9014, 11KR-13, KR11-9025, KR12-07, GN-68/2003). The results of this study are of interest in wheat breeding programs for tan spot resistance.

Association Mapping of Seedling Resistance to Tan Spot (Pyrenophora tritici-repentis Race 1) in CIMMYT and South Asian Wheat Germplasm

Tan spot caused by Pyrenophora tritici-repentis (Ptr) is an important disease of wheat in many wheat producing areas of the world. A genome wide association study (GWAS) was conducted using 11,401 SNP markers of the Illumina Infinium 15K Bead Chip with whole genome coverage to identify genomic regions associated with resistance to tan spot in a diverse panel of 184 wheat genotypes originating from South Asia and CIMMYT. The GWAS panel was phenotyped for seedling resistance to tan spot with Ptr race 1 in two greenhouse experiments. Besides CIMMYT germplasm, several lines from South Asia (India, Bangladesh and Nepal) showed good degree of resistance to tan spot. Association mapping was conducted separately for individual experiments and for pooled data using mixed linear model (MLM) and Fixed and random model Circulating Probability Unification (FarmCPU) model; no significant MTAs were recorded through the MLM model, whereas FarmCPU model reported nine significant MTAs located on chromosomes 1B, 2A, 2B, 3B, 4A, 5A, 5B, 6A, and 7D. The long arms of chromosomes 5A and 5B were consistent across both environments, in which the Vrn-A1 locus was found in identified region of chromosome 5A, and MTA at IACX9261 on 5BL appears to represent the resistance gene tsn 1. MTAs observed on chromosomes 1B, 2A, 2B, 3B, 4A, 6A, and 7D have not been reported previously and are likely novel.

Assessing the genetic diversity and characterizing genomic regions conferring Tan Spot resistance in cultivated rye.

Rye (Secale cereale L.) is known for its wide adaptation due to its ability to tolerate harsh environments in semiarid areas. To assess the diversity in rye we genotyped a panel of 178 geographically diverse accessions of four Secale sp. from U.S. National Small Grains Collection using 4,037 high-quality SNPs (single nucleotide polymorphisms) developed by genotyping-by-sequencing (GBS). PCA and STRUCTURE analysis revealed three major clusters that separate S. cereale L. from S. strictum and S. sylvestre, however, genetic clusters did not correlate with geographic origins and growth habit (spring/winter). The panel was evaluated for response to Pyrenophora tritici-repentis race 5 (PTR race 5) and nearly 59% accessions showed resistance or moderate resistance. Genome-wide association study (GWAS) was performed on S. cereale subsp. cereale using the 4,037 high-quality SNPs. Two QTLs (QTs.sdsu-5R and QTs.sdsu-2R) on chromosomes 5R and 2R were identified conferring resistance to PTR race 5 (p < 0.001) that explained 13.1% and 11.6% of the phenotypic variation, respectively. Comparative analysis showed a high degree of synteny between rye and wheat with known rearrangements as expected. QTs.sdsu-2R was mapped in the genomic region corresponding to wheat chromosome group 2 and QTs.sdsu-5R was mapped to a small terminal region on chromosome 4BL. Based on the genetic diversity, a set of 32 accessions was identified to represents more than 99% of the allelic diversity with polymorphic information content (PIC) of 0.25. This set can be utilized for genetic characterization of useful traits and genetic improvement of rye, triticale, and wheat.

Phenotypical and genotypical characterization of Pyrenophora tritici-repentis races in Brazil

Tan spot, caused by Pyrenophora tritici-repentis, is one of the major wheat diseases in southern Brazil as well as in the wheat production areas of several other countries. The fungal isolates have been classified into eight races according to the production of three fungal necrotrophic effectors. The knowledge about the pathogen population structure is essential for disease control strategies, but such information is lacking in Brazil. The aim of this study was to determine the P. tritici-repentis race structure of Brazilian isolates using, for the first time, biological and molecular techniques. P. tritici-repentis isolates were characterized for their virulence on a set of wheat genotypes, and for the presence of ToxA and ToxB gene. The results from the PCR amplification with the gene specific primers showed that all Brazilian P. tritici-repentis isolates carried ToxA, but no ToxB is present. Race typing on the set of wheat genotypes indicate 65% of the isolates were race 2 while 35% were race 1. This is the first study on the P. tritici-repentis race structure in Brazil and the information will be useful to the local wheat breeders who aim to improve tan spot resistance in wheat cultivars.

Reaction of Global Collection of Rye (Secale cereale L.) to Tan Spot and Pyrenophora tritici-repentis Races in South Dakota.

Rye (Secale cereale L.) serves as an alternative host of Pyrenophora tritici-repentis (PTR) the cause of tan spot on wheat. Rye is cultivated as a forage or cover crop and overlaps with a significant portion of wheat acreage in the U.S. northern Great Plains; however, it is not known whether the rye crop influences the evolution of PTR races. We evaluated a global collection of 211 rye accessions against tan spot and assessed the diversity in PTR population on rye in South Dakota. All the rye genotypes were inoculated with PTR races 1 and 5, and infiltrated with Ptr ToxA and Ptr ToxB, at seedling stage. We observed 21% of the genotypes exhibited susceptibility to race 1, whereas, 39% were susceptible to race 5. All 211 accessions were insensitive to both the Ptr toxins. It indicates that though rye exhibits diversity in reaction to tan spot, it lacks Ptr ToxA and ToxB sensitivity genes. This suggests that unknown toxins or other factors can lead to PTR establishment in rye. We characterized the race structure of 103 PTR isolates recovered from rye in South Dakota. Only 22% of the isolates amplified Ptr ToxA gene and were identified as race 1 based on their phenotypic reaction on the differential set. The remaining 80 isolates were noted to be race 4. Our results show that races 1 and 4 are prevalent on rye in South Dakota with a higher frequency of race 4, suggesting a minimal role of rye in the disease epidemiology.

Insights into Tan Spot and Stem Rust Resistance and Susceptibility by Studying the Pre-Green Revolution Global Collection of Wheat.

Tan spot (TS), caused by the fungus Pyrenophora tritici-repentis (Died) Drechs, is an important foliar disease of wheat and has become a threat to world wheat production since the 1970s. In this study a globally diverse pre-1940s collection of 247 wheat genotypes was evaluated against Ptr ToxA, P. tritici-repentis race 1, and stem rust to determine if; (i) acquisition of Ptr ToxA by the P. tritici-repentis from Stagonospora nodorum led to increased pathogen virulence or (ii) incorporation of TS susceptibility during development stem rust resistant cultivars led to an increase in TS epidemics globally. Most genotypes were susceptible to stem rust; however, a range of reactions to TS and Ptr ToxA were observed. Four combinations of disease-toxin reactions were observed among the genotypes; TS susceptible-Ptr ToxA sensitive, TS susceptible-Ptr ToxA insensitive, TS resistant-Ptr ToxA insensitive, and TS resistant-Ptr ToxA toxin sensitive. A weak correlation (r = 0.14 for bread wheat and −0.082 for durum) was observed between stem rust susceptibility and TS resistance. Even though there were no reported epidemics in the pre-1940s, TS sensitive genotypes were widely grown in that period, suggesting that Ptr ToxA may not be an important factor responsible for enhanced prevalence of TS.

Characterization of Pyrenophora tritici-repentis (Tan Spot of Wheat) Races in Baltic States and Romania.

Tan spot, caused by the fungus Pyrenophora triticirepentis, is economically important foliar disease in Latvia, Lithuania, and Romania; however, race structure from Baltic States and Romania is not known. In this study, we performed genotypic and phenotypic race characterization of a large collection of P. triticirepentis isolates from these countries to determine race structure and utilize this information for better disease management and breeding wheat for tan spot resistance. We characterized 231 single spore isolates from Latvia (n = 15), Lithuania (n = 107), and Romania (n = 109) for Ptr ToxA and Ptr ToxB genes using two genes specific primers. A subset (139) of 231 isolates were further characterized for their race structure by inoculating them individually on tan spot wheat differentials set. Majority (83%) of the 231 isolates amplified Ptr ToxA gene suggesting prevalence of race 1 and 2. Further, phenotypic characterization of 139 isolates also showed wide prevalence of races 1 (68%), 2 (8%), 3 (11%), and 4 (5%) were also identified from Baltic States as well as Romania. Eighteen of the isolates (13%) did not seem to be of any of the eight known races as they lacked Ptr ToxA gene but they behaved like either race 1 or race 2, suggesting possibility of novel toxins in these isolates as their virulence tools.

First Report of Pyrenophora tritici-repentis Race 5 From South Dakota

First Report of <i>Pyrenophora tritici-repentis</i> Race 5 From South Dakota

Association mapping for resistance to tan spot induced by Pyrenophora tritici-repentis race 1 in CIMMYTs historical bread wheat set

Tan spot, a major foliar disease of wheat, is caused by an ascomycete Pyrenophora tritici-repentis (PTR). Association mapping on germplasm collection is a novel approach for the discovery and validation of major genes/QTLs for a trait. Linkage disequilibrium, the genetic basis of association mapping, can be an important tool to identify genomic regions associated with tan spot resistance. Association analysis utilizing the population structure and additive genetic covariance between relatives was conducted for tan spot resistance on a set of historical bread wheat germplasm comprising of 170 lines developed at CIMMYT, Mexico with the genotypic data generated with 1644 molecular markers. Tan spot resistance data was obtained by screening the germplasm with PTR race 1 isolate Ptr-1. Two weeks old seedlings were inoculated and rated 8 days later on a lesion type disease scale. Three experiments were conducted in the greenhouse with each experiment as arranged in completely randomized design with two replicates. Over half of the entries were resistant to tan spot induced by PTR race 1. The genome-wide scan revealed significant marker-phenotype associations on the short arm of chromosomes 1A, 1B, and 6B and long arm of chromosomes 4A, 6A1, 6A2, 2B, 3B, 5B, and 7B that play an important role in conferring resistance to tan spot. Although some genomic regions contributing to tan spot resistance have been previously identified; novel regions on long arm of chromosomes 6A1, 6A2, and 7B, were identified in this study. Findings of this study reveal that a high proportion of CIMMYT wheat germplasm is resistant to tan spot caused by PTR race 1 and genetic base of CIMMYT germplasm resistance involves race specific and non-race specific resistance genes.

Evaluation of CIMMYT germplasm for resistance to leaf spotting diseases of wheat

The leaf spotting disease complex is a major biotic constrain in enhancing grain production in the major wheat growing regions. Two leaf spotting diseases, tan spot, caused by an ascomycete fungus Pyrenophora tritici-repentis, and Stagonospora nodorum blotch besides causing average yield losses of 5&amp;ndash;10%, cause significant losses in grain quality by red smudge, black point and grain shriveling. Conservation agriculture in combination with wheat monoculture involving cultivation of susceptible cultivars has resulted in frequent onset of leaf spots epidemics worldwide. Development of resistant wheat cultivars, in conjunction with crop rotation, will provide an effective, economical, and environmentally safe means of controlling leaf spot. International Maize and Wheat Improvement Center (CIMMYT), Mexico has initiated major efforts to mitigate the threat of tan spot. Efforts include screening of wheat germplasm, identification of new sources of resistance, characterization of new tan spot resistance genes through classical and molecular genetic analysis, incorporation of resistance into adapted cultivars, and assessing the variability in the tan spot fungus. Screening studies reveal that elite CIMMYT germplasm has high level of resistance to tan spot caused by P. tritici-repentis race 1. These germplasm have diverse genetic make-up and the resistance is likely broad based. Association mapping studies done with CIMMYT germplasm reconfirmed the presence of previously identified genomic regions for tan spot resistance; however, novel genomic regions on long arm of chromosomes 6A and 7B have also been identified. Studies done to date indicate that CIMMYT germplasm possess high level diverse genetic based resistance to tan spot of wheat. Efforts are in place to develop desired wheat cultivars with tan spot resistance. Virulence studies indicate presence of P. tritici-repentis race 1 only with some variability in level of toxin Ptr ToxA produced in each of the 76 isolates studied.

Identification of novel genomic regions associated with resistance to Pyrenophora tritici-repentis races 1 and 5 in spring wheat landraces using association analysis

Tan spot, caused by Pyrenophora tritici-repentis, is a major foliar disease of wheat worldwide. Host plant resistance is the best strategy to manage this disease. Traditionally, bi-parental mapping populations have been used to identify and map quantitative trait loci (QTL) affecting tan spot resistance in wheat. The association mapping (AM) could be an alternative approach to identify QTL based on linkage disequilibrium (LD) within a diverse germplasm set. In this study, we assessed resistance to P. tritici-repentis races 1 and 5 in 567 spring wheat landraces from the USDA-ARS National Small Grains Collection (NSGC). Using 832 diversity array technology (DArT) markers, QTL for resistance to P. tritici-repentis races 1 and 5 were identified. A linear model with principal components suggests that at least seven and three DArT markers were significantly associated with resistance to P. tritici-repentis races 1 and 5, respectively. The DArT markers associated with resistance to race 1 were detected on chromosomes 1D, 2A, 2B, 2D, 4A, 5B, and 7D and explained 1.3-3.1% of the phenotypic variance, while markers associated with resistance to race 5 were distributed on 2D, 6A and 7D, and explained 2.2-5.9% of the phenotypic variance. Some of the genomic regions identified in this study correspond to previously identified loci responsible for resistance to P. tritici-repentis, offering validation for our AM approach. Other regions identified were novel and could possess genes useful for resistance breeding. Some DArT markers associated with resistance to race 1 also were localized in the same regions of wheat chromosomes where QTL for resistance to yellow rust, leaf rust and powdery mildew, have been mapped previously. This study demonstrates that AM can be a useful approach to identify and map novel genomic regions involved in resistance to P. tritici-repentis.

Genetics and mapping of resistance to spore inoculum and culture filtrate of Phaeosphaeria nodorum in spring wheat line ND 735

Stagonospora nodorum blotch (SNB), caused by Phaeosphaeria nodorum, is one of the most devastating foliar diseases on wheat ( Triticum aestivum L.) in the northern Great Plains of North America. This study was conducted, under controlled environmental conditions, to elucidate the genetics and map the resistance to SNB caused by spore inoculum and culture filtrate of P. nodorum isolate Sn2000. A hard red spring wheat population was developed from a cross between the susceptible cultivar Steele-ND and the resistant line ND 735 for this study. Two-leaf seedlings of the parents, F 1 and F 2 generations, and F 2:6 recombinant-inbred lines (RILs) were inoculated with spore suspensions while independent two week old seedlings of segregating generations were infiltrated with culture filtrate. Disease reaction was assessed 8 days after inoculation based on a lesion-type scale while plants were evaluated for culture filtrate response four days after infiltration for the presence or absence of necrosis. Genetic analysis revealed that a single recessive gene, Tsn1, in ND 735 confers resistance to both spore suspension and culture filtrate of P. nodorum isolate Sn2000. Mapping analysis using Diversity Arrays Technology (DArT) and simple sequence repeat (SSR) markers indicates the gene, Tsn1, is located on the long arm of chromosome 5B and is flanked by the DArt markers wPt-8285 and wPt-3049 at a distance of 7.0 cM and 2.9 cM, respectively. This gene also controls resistance to tan spot caused by Pyrenophora tritici-repentis race 2. Results of this study reveal that wheat- P. nodorum interaction follows the toxin model of gene-for-gene hypothesis. Additionally, the finding of single gene control in the line ND 735 for both tan spot and SNB enhances the utility of the line ND 735 in wheat breeding program as a source of multiple disease resistance.

Genetic and molecular analysis of wheat tan spot resistance effective against Pyrenophora tritici-repentis races 2 and 5

Tan spot, a major foliar disease of wheat (Triticum aestivum L.), is caused by an ascomycete Pyrenophora tritici-repentis. Both culture filtrates and conidiospore inocula induce disease symptoms in susceptible wheat genotypes. The objectives of this study were to determine and map the genetic control of resistance to spore inocula and culture filtrates of P. tritici-repentis races 2 and 5. The F1 and F2 generations and an F2:6 recombinant inbred lines (RIL) population were developed from a cross between the resistant ND 735 and the susceptible Steele-ND. Disease assessments of the segregating generations were done at the seedling stage using culture filtrates and spore inocula under controlled environmental conditions. Genetic and mapping analyses of the F1 and F2 generations and the RIL by both methods indicated that the same single recessive gene, Tsr1, located on chromosome 5BL, controlled resistance and insensitivity to necrosis induced by race 2. A second recessive gene, designated Tsr6, located on chromosome 2BS, conferred resistance/insensitivity to chlorosis induced by spore inocula or culture filtrates of race 5. Diversity Arrays Technology markers wPt-3049 (2.9 cM) and wPt-0289 (4.6 cM) were closely linked to Tsr1 and Tsr6, respectively. The results further indicated that culture filtrates can be used as surrogates for spore inoculation. Tsr1 and Tsr6 can be selected by marker-assisted selection in breeding for resistance to tan spot.

A quantitative trait locus on chromosome 5B controls resistance of Triticum turgidum (L.) var. diccocoides to Stagonospora nodorum blotch

Stagonospora nodorum blotch (SNB) is an important foliar disease of durum wheat (Triticum turgidum var. durum) worldwide. The combined effects of SNB and tan spot, considered as components of the leaf spotting disease complex, result in significant damage to wheat production in the northern Great Plains of North America. The main objective of this study was the genetic analysis of resistance to SNB caused by Phaeosphaeria nodorum in tetraploid wheat, and its association with tan spot caused by Pyrenophora tritici-repentis race 2. The 133 recombinant inbred chromosome lines (RICL) developed from the cross LDN/LDN(Dic-5B) were evaluated for SNB reaction at the seedling stage under greenhouse conditions. Molecular markers were used to map a quantitative trait locus (QTL) on chromosome 5B, explaining 37.6% of the phenotypic variation in SNB reaction. The location of the QTL was 8.8 cM distal to the tsn1 locus coding for resistance to P. tritici-repentis race 2. The presence of genes for resistance to both SNB and tan spot in close proximity in tetraploid wheat and the identification of molecular markers linked to these genes or QTLs will be useful for incorporating resistance to these diseases in wheat breeding programs.

Seedling Resistance to Tan Spot and Stagonospora nodorum Leaf Blotch in Wild Emmer Wheat (Triticum dicoccoides).

Tan spot and Stagonospora nodorum blotch (SNB), caused by Pyrenophora tritici-repentis and Stagonospora nodorum, respectively, are two destructive foliar diseases of wheat, causing significant yield reduction worldwide. The objective of this study was to evaluate 172 accessions of wild emmer wheat (Triticum dicoccoides) for seedling resistance to tan spot and SNB. All accessions were inoculated with P. tritici-repentis race 1 and a mixture of three diverse isolates of S. nodorum, respectively. The accessions were also evaluated for sensitivity to host-selective toxins (HSTs), including ToxA produced by both S. nodorum and P. tritici-repentis and culture filtrate produced by S. nodorum. A total of 34 accessions were resistant to tan spot, and 136 accessions were resistant to SNB. Among these accessions, 31 were resistant to both diseases. Significant correlations between HST insensitivity and disease resistance were observed. Our results showed that T. dicoccoides is a good genetic source of resistance to tan spot and SNB in wheat.

Genetic Analysis of Resistance to Pyrenophora tritici-repentis Races 1 and 5 in Tetraploid and Hexaploid Wheat

Tan spot of wheat, caused by the fungus Pyrenophora tritici-repentis, is a destructive disease worldwide that can lead to serious losses in quality and quantity of wheat grain production. Resistance to multiple races of P. tritici-repentis was identified in a wide range of genetically diverse genotypes, including three different species Triticum aestivum (AABBDD), T. spelta (AABBDD), and T. turgidum (AABB). The major objectives of this study were to determine the genetic control of resistance to P. tritici-repentis races 1 and 5 in 12 newly identified sources of resistance. The parents, F(1), F(2), and F(2:3) or F(2:5) families of each cross were analyzed for the allelism tests and/or inheritance studies. Plants were inoculated at the two-leaf stage under controlled environmental conditions and disease reaction was assessed based on lesion-type rating scale. A single recessive gene controlled resistance to necrosis caused by P. tritici-repentis race 1 in both tetraploid and hexaploid resistant genotypes. The lack of segregation in the inter- and intra-specific crosses between the resistant tetraploid and hexaploid genotypes indicated that they possess the same genes for resistance to tan necrosis and chlorosis induced by P. tritici-repentis race 1. A single dominant gene for chlorosis in hexaploid wheat and a single recessive gene for necrosis in tetraploid wheat, controlled resistance to P. tritici-repentis race 5.

Emergence of Tan Spot Disease Caused by Toxigenic Pyrenophora tritici-repentis in Australia Is Not Associated with Increased Deployment of Toxin-Sensitive Cultivars

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.