Reaction of Ptr ToxA-Insensitive Wheat Mutants to Pyrenophora tritici-repentis Race 1

ABSTRACT The host-selective toxin Ptr ToxA is produced by races 1 and 2 of Pyrenophora tritici-repentis, causal agent of tan spot of wheat. Ptr ToxA has been causally associated with pathogenicity by the race 2 phenotype in this system. However, the role of toxin in disease caused by race 1, the most prevalent form of the fungus in the central and northern Great Plains of North America, has not been rigorously investigated. Three independent wheat lines harboring mutations for insensitivity to Ptr ToxA were derived from ethylmethane sulfonate treatment of the hard red spring wheat cv. Kulm, possessing the single dominant gene for toxin sensitivity. Each of the three mutants was insensitive to Ptr ToxA in bioassays based on necrosis development and electrolyte leakage. Each mutant was crossed to each of the other mutants and to the wild-type Kulm. Segregation data indicate that each mutant line harbors a single recessive mutation for toxin insensitivity that maps to or near the same locus, possibly the toxin-sensitivity gene. Each toxin-insensitive mutant line was susceptible to two isolates of race 1 of P. tritici-repentis. F(2) and F(3) generations derived from crosses between Kulm and each mutant segregated for toxin reaction. However, segregation for fungal reaction was not evident, and all F(3) families were tan spot susceptible regardless of toxin reaction. Host insensitivity to Ptr ToxA is not necessarily equivalent to resistance to race 1. Ptr ToxA should not be used alone as a proxy for fungal inoculations by breeding programs aimed at developing tan spot-resistant wheat.     

The Identification of Two New Races of Pyrenophora tritici-repentis from the Host Center of Diversity Confirms a One-to-One Relationship in Tan Spot of Wheat

ABSTRACT Pyrenophora tritici-repentis, causal agent of tan spot, induces necrosis and chlorosis in its wheat host. The tan spot system conforms to the toxin model and three host-specific toxins have been identified (Ptr ToxA, Ptr ToxB, and putative Ptr ToxC). Processing of a collection of isolates, obtained in the Fertile Crescent and Caucasus regions, yielded two new virulence patterns. Isolate Az35-5 combined the virulences of races 2 and 5 and was classified in the new race 7. Isolates TS93-71B and TS93-71F had a virulence pattern that combined those of races 2, 3, and 5 and were grouped in the new race 8. Southern analysis revealed that all three isolates possessed copies of the ToxA and ToxB genes, the first time the genes were found in a common background. The production of Ptr ToxA and Ptr ToxB by the isolates was confirmed by western blotting. Virulence patterns suggested that TS93-71B and TS93-71F may also produce Ptr ToxC, even though it was not present at detectable levels in culture filtrates. The identification of races 7 and 8 complete the theoretical maximum number of races that can be differentiated by three loci in the host (2(3) = 8), assuming a one-to-one relationship. It appears that the wheat/P. tritici-repentis system is a mirror image of the classical gene-for-gene relationship.     

Genetic Analysis of Sensitivity to a Pyrenophora tritici-repentis Necrosis-Inducing Toxin in Durum and Common Wheat

ABSTRACT The fungus Pyrenophora tritici-repentis produces a toxin (Ptr ToxA) that causes rapid cell necrosis in sensitive wheat genotypes. A single recessive gene (tsn1) on chromosome 5BL in common wheat confers insensitivity to this toxin. Our objectives were to analyze the allelic relationships of genotypes that have shown insensitivity to a P. tritici-repentis necrosis-inducing toxin, map the gene for insensitivity to the necrosis-inducing factor produced by P. tritici-repentis in a durum wheat population, and determine the reaction to P. tritici-repentis of aneuploid genotypes that do not contain the gene. Greenhouse-grown plants of seven populations from crosses of insensitive genotypes; an F(2) population of durum wheat; and 'Chinese Spring' aneuploid, substitution, and deletion lines were infiltrated with Ptr ToxA. All crosses involving insensitive genotypes failed to produce sensitive progeny, indicating that the same gene is present in these genotypes. The gene for insensitivity in the durum population was mapped to the same region on 5BL as in common wheat using restriction fragment length polymorphism markers. 'Chinese Spring', its homoeologous group 5 nullisomic-tetrasomic stocks, and 5BL deletion lines were insensitive to the toxin. Substitution of a 5B chromosome from sensitive genotypes into 'Chinese Spring' resulted in sensitivity. Therefore, insensitivity is not conferred by a gene product per se, but rather conferred by absence of a gene for sensitivity.     

Advances in the Characterization of the Pyrenophora tritici-repentis-Wheat Interaction

ABSTRACT Tan spot of wheat, caused by the fungus Pyrenophora tritici-repentis, is a destructive disease found in wheat-growing regions worldwide that can lead to serious yield losses. Changes in cultural practices have led to an increase in the severity and incidence of tan spot. Following infection, compatible races of the fungus elicit two distinct symptoms in differential wheat lines: tan necrosis and (extensive) chlorosis. Tan necrosis has been clearly demonstrated by several groups to result from the action of a protein toxin, Ptr ToxA. Wheat sensitivity to this toxin is conditioned by a single dominant gene. The chlorosis response may be more complex and appears to involve at least two other toxins, Ptr ToxB and Ptr ToxC, produced by different races of the fungus. Distinct genes apparently condition the reaction of wheat lines to each of these chlorosis-inducing toxins. This review concentrates on significant advances that have occurred during the past decade in the characterization of this disease interaction, ranging from the epidemiology and management of tan spot to molecular host-parasite interactions. Particular emphasis is placed on work describing fungal race differentiation, production of toxins and their importance in pathogenicity, and the genetics and physiology of host response to infection.     

Forensic pathology of canadian bread wheat: the case of tan spot

ABSTRACT Pyrenophora tritici-repentis causes necrosis and chlorosis in its wheat host. Susceptibility to races 2 (necrosis) and 5 (chlorosis) of the pathogen is known to be mediated by Ptr ToxA and Ptr ToxB, respectively. Sensitivity to each toxin is controlled by a single dominant and independently inherited gene. We used sensitivity to Ptr ToxA and Ptr ToxB as two genetic markers to investigate the origin and the state of tan spot susceptibility in Canadian Western Red Spring (CWRS) wheat over a period of more than a century. Sensitivity to Ptr ToxA, the toxin produced by nearly all isolates of the pathogen collected in the past 20 years in western Canada, appears to have been present in the first major cultivar, Red Fife, grown massively in the late 1800s. Sensitivity then was transmitted unknowingly into Canadian wheat lines through extensive use of backcrossing to maintain the Marquis-Thatcher breadmaking quality. Sensitivity to Ptr ToxA, which nearly disappeared from cultivars grown in western Canada in the 1950s, was reintroduced in the 1960s and unintentionally bred into many of the present-day cultivars. Sensitivity to Ptr ToxB, a toxin rarely found in isolates from western Canada, appeared with the release of Thatcher in 1934 and was transferred to many cultivars through backcross programs. In spite of large areas planted to Ptr ToxAand Ptr ToxB-sensitive cultivars over decades, tan spot epidemics remained sporadic until the 1970s. The results of this study raise the problem of the narrowing genetic base of CWRS wheat lines and the potential for unanticipated threats from plant pathogens. The intercrossing of genetically diverse material in one Canadian wheat breeding program resulted in the release of several modern cultivars with resistance to tan spot. The absence of wild-type Ptr ToxB-producing isolates in western Canada remains unexplained, given that sensitivity to Ptr ToxB was present continuously in western Canadian cultivars grown on vast areas for more than 70 years.     

Evaluating the importance of the tan spot ToxA–Tsn1 interaction in Australian wheat varieties

The necrotrophic fungal pathogen Pyrenophora tritici‐repentis (Ptr) causes the major wheat disease tan spot, and produces multiple necrotrophic effectors that contribute to virulence. The proteinaceous effector ToxA induces necrosis in wheat genotypes possessing the Tsn1 gene, although the importance of the ToxA–Tsn1 interaction itself in varietal disease development has not been well studied. Here, 40 Australian spring wheat varieties were assessed for ToxA sensitivity and disease response to a race 1 wildtype Ptr isolate and ToxA‐deleted strain at both seedling and tillering growth stages. ToxA sensitivity was generally associated with disease susceptibility, but did not always predict spreading necrotic symptoms. Whilst the majority of Tsn1 varieties exhibited lower disease scores following toxa mutant infection, several exhibited no distinct differences between wildtype and toxa symptoms. This implies that ToxA is not the major determinant in tan spot disease development in some host backgrounds and indicates the presence of additional effectors. Unexpectedly, several tsn1 varieties exhibited a reduction in disease severity following toxa mutant inoculation, which may suggest an indirect role for ToxA in pathogen fitness. Additionally, increased chlorosis was observed following toxa mutant infection in three varieties, and further work is required to determine whether this is likely to be due to ToxA epistasis of ToxC symptoms. Taken together, these observations demonstrate that Ptr interacts with the host in a complex and intricate manner, leading to a variety of disease reactions that are dependent or independent of the ToxA–Tsn1 interaction.     

A Combination of Phenotypic and Genotypic Characterization Strengthens Pyrenophora tritici-repentis Race Identification

ABSTRACT Pyrenophora tritici-repentis, causal agent of tan spot of wheat, produces multiple host-selective toxins (HSTs), including Ptr ToxA, Ptr ToxB, and Ptr ToxC. The specific complement of HSTs produced by a particular isolate determines its host cultivar specificity. Each unique specificity profile, represented by the differential induction of necrosis or chlorosis on a standard set of wheat differentials, defines a unique race. Eight races of P. tritici-repentis have been formally published, although additional races are under investigation. Although visual assessment of disease phenotype is often used in race designation of P. tritici-repentis, our results suggest that it has the potential to be misleading. Inoculation of the P. tritici-repentis isolates SO3 and PT82 on the current wheat differential set indicated classification as race 2 and race 8, respectively; however, genetic characterization revealed that these isolates do not possess the associated HSTs expected for these race assignments. Despite sharing disease phenotypes similar to known races, SO3 and PT82 were genotypically distinct from these previously characterized races of P. tritici-repentis. To ensure detection of the breadth of physiological variation among the isolates of P. tritici-repentis, our results indicate that race classification, where possible, should include both phenotypic and genotypic analyses and eventual expansion of the differential set.     

Requirement of Host Signaling Mechanisms for the Action of Ptr ToxA in Wheat

Ptr ToxA, the host-selective toxin produced by Pyrenophora tritici-repentis, is genetically associated with the development of tan spot disease of wheat. The toxin was shown previously to cause a programmed cell death in the host that requires de novo mRNA and protein synthesis. In the present study, inhibitors of plant signaling mechanisms protected wheat leaves from toxin action, as determined by electrolyte leakage bioassays, when applied to leaves with toxin. Okadaic acid, calyculin A and phenylarsine oxide, all inhibitors of protein phosphatase activity, reduced toxin-induced electrolyte leakage by more than 90%. Inorganic calcium channel blockers (LaCl₃ and CoCl₂ reduced toxin-induced electrolyte leakage by 78–95%, depending on inhibitor and time of measurement. By comparison, about 50% protection was achieved by the application of the protein kinase inhibitors staurosporine and K-252A. Nonetheless, the reduction in toxin-induced electrolyte leakage by protein kinase inhibitors was reproduced in multiple trials and was statistically significant. The data indicate that host signaling mechanisms, including calcium fluxes and a protein phosphorylation cascade, are required for the Ptr ToxA-induced cell death in wheat. Our current model holds that the signaling events occur between toxin perception by the cell and the toxin-directed gene expression in the host associated with cell death. As an alternative, the toxin-induced mRNA synthesis required for cell death may be for protein phosphatase and/or protein kinase genes. Additional work is required to resolve these possibilities.     

Revue bibliographique: la maladie de la tache auréolée du blé

Tan spot caused by Pyrenophora tritici‐repentis is a wheat disease found worldwide which can cause significant losses. This disease is characterized by typical symptoms: a necrotic spot surrounded by chlorosis halo. On the basis of its ability to produce chlorosis and/or necrosis symptoms on a differential host set. Eight races of this pathogen are currently recognized. These symptoms are the result of a specific interaction between the host and at least three host specific toxins Ptr ToxA, Ptr ToxB and Ptr ToxC. This interaction seems to be a mirror image of the classical gene‐for‐gene described by Flore. This paper presents a first literature review in the French language, identifying the major aspects of this disease, its epidemiology and diversity of its causal agent.     

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.     

Identification of a Chlorosis-Inducing Toxin from Pyrenophora tritici-repentis and the Chromosomal Location of an Insensitivity Locus in Wheat

ABSTRACT Culture filtrate from Pyrenophora tritici-repentis race 1 isolate 78-62 contained a genotype-specific toxin which elicited extensive chlorosis on sensitive wheat genotypes. This toxin was partially purified using gel filtration, ion exchange, and reversed-phase chromatography. The chlorosis toxin was found to be a polar, nonionic, low-molecular-weight molecule. Wheat genotypes infiltrated with crude culture filtrate and partially purified chlorosis toxin exhibited the same chlorotic symptoms seen with conidial inoculations of isolate 78-62. All tested wheat genotypes that exhibited extensive chlorosis to the toxin also exhibited extensive chlorosis to conidial inoculations, and all wheat genotypes insensitive to the toxin did not exhibit extensive chlorosis to conidial inoculations. The recombinant inbred population derived from the cross W-7984 x Opata 85 segregated for chlorosis induction from infiltration with partially purified chlorosis toxin from isolate 78-62. The locus identified by the marker XGli1, associated with resistance to conidial inoculations from race 1 isolates Pti2 and 78-62 and race 3 isolate D308, also was associated with insensitivity to infiltration of crude culture filtrate and partially purified chlorosis toxin. The marker XGli1, located on the short arm of chromosome 1A, is linked to the insensitivity locus within 5.7 cM. We propose that this chlorosis toxin be designated Ptr ToxC.     

Genetic and Physical Mapping of a Gene Conditioning Sensitivity in Wheat to a Partially Purified Host-Selective Toxin Produced by Stagonospora nodorum

ABSTRACT A toxin, designated SnTox1, was partially purified from culture filtrates of isolate Sn2000 of Stagonospora nodorum, the causal agent of wheat leaf and glume blotch. The toxin showed selective action on several different wheat genotypes, indicating that it is a host-selective toxin (HST). The toxic activity was reduced when incubated at 50 degrees C and activity was eliminated when treated with proteinase K, suggesting that the HST is a protein. The synthetic hexaploid wheat W-7984 and hard red spring wheat Opata 85, the parents of the International Triticeae Mapping Initiative (ITMI) mapping population, were found to be sensitive and insensitive, respectively, to SnTox1. The ITMI mapping population was evaluated for toxin reaction and used to map the gene conditioning sensitivity. This gene, designated Snn1, mapped to the distal end of the short arm of chromosome 1B. The wheat cv. Chinese Spring (CS) and all CS nullisomic-tetrasomic lines were sensitive to the toxin, with the exception of N1BT1D. Insensitivity also was observed when the 1B chromosome of CS was substituted with the 1B chromosome of an insensitive accession of Triticum dicoccoides. In addition, a series of 1BS chromosome deletion lines were used to physically localize the sensitivity gene. Physical mapping indicated that Snn1 lies within a major gene-rich region on 1BS. This is the first report identifying a putative proteinaceous HST from S. nodorum and the chromosomal location of a host gene conferring sensitivity.     

Exploring de novo specificity: the Pyrenophora tritici‐repentis–barley interaction

Pyrenophora tritici‐repentis (Ptr) is a destructive fungal pathogen of wheat worldwide. In addition to wheat, Ptr has been isolated from various other hosts in the family Poaceae, yet the nature of its interaction with those hosts is unknown. The Ptr–barley relationship was explored and the existence of a specific interaction between Ptr and barley is described for the first time; symptom development on several barley genotypes was evaluated in bioassays and by toxin infiltration into barley leaves. Ptr ToxB‐producing isolates of the fungus were able to cause significant damage when inoculated onto certain barley genotypes, and Ptr ToxB was able to induce chlorosis in a highly selective manner when infiltrated into those same genotypes. Ptr–barley specificity is subtle and can break with slight changes in temperature after infection. To understand the infection process in barley, a cytological analysis and in planta fungal biomass estimation using quantitative PCR were performed. The fungus penetrates through the host epidermal cells and advances to colonize the mesophyll layer intercellularly, with the infection process on barley closely resembling that on wheat. Here, evidence is provided for a specific interaction between barley and Ptr, expanding understanding of Ptr host specificity and breaking the assumption that the highest level of specificity seen with Ptr is restricted to particular genotypes of the wheat host.     

Virulence assessment of Australian Pyrenophora tritici-repentis isolates

The virulence of 57 Australian isolates of Pyrenophora tritici-repentis (Ptr), a necrotrophic fungal pathogen responsible for the major wheat disease tan spot, was assessed through plant infection assays. Isolates collected from the northern, southern, and western wheat-cropping regions of Australia were evaluated against 16 Australian bread wheat cultivars under controlled growth conditions. Following infection, the wheat panel displayed varying disease symptoms ranging from tiny necrotic specks to spreading chlorotic and necrotic lesions. Analysis of variance indicated that the wheat cultivar exhibited a greater effect on the disease response, explaining 62.7% of the variation, in comparison to the isolate (10.4%). The interaction between the cultivar and the isolate was statistically significant and was attributed to 9.8% of the total variation. All Ptr isolates examined were able to cause disease, but did not display a clear distinction in virulence on the wheat panel investigated, instead showing subtle differences in aggressiveness. Based on the disease responses, there was no obvious pattern between isolate aggressiveness and cropping region. Some cultivars, such as Hydra, exhibited an effective level of resistance in relation to the panel of isolates tested. All 57 Ptr isolates were found to possess the ToxA effector gene and lack the ToxB effector gene. The gene expression level of ToxA was up-regulated at 3 days postinfection in both ToxA-sensitive and -insensitive cultivars, independent of ToxA–Tsn1 recognition.     

Identification and Molecular Mapping of a Gene Conferring Resistance to Pyrenophora tritici-repentis Race 3 in Tetraploid Wheat

ABSTRACT 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 F(2) generation and of the F(4:5) and F(6:7) families indicated that a single recessive gene controlled resistance to necrosis induced by race 3 in the cross studied.     

Genetic Control of Resistance to Tan Necrosis Induced by Pyrenophora tritici-repentis, Races 1 and 2, in Spring and Winter Wheat Genotypes

ABSTRACT 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 F(1) and F(2) generations, and of F(2:3) and F(2:8) 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.     

Detection and characterization of QoI resistance in Pyrenophora tritici-repentis populations causing tan spot of wheat in Argentina

Tan spot, caused by the fungus Pyrenophora tritici-repentis (Ptr), is a disease that has become more prevalent and intense in wheat crops in Argentina in recent years. Failure to control the disease with strobilurin fungicides, which were once effective, has been observed in different zones where wheat is grown. However, whether or not true resistance is present in the pathogen population in the region is not scientifically confirmed. This study evaluated the sensitivity of numerous Ptr isolates to representative QoI fungicides used in Argentina through in vitro and in planta assays, as well as through molecular analysis. Eighty-two monosporic isolates obtained in different locations in the north and south of Buenos Aires province in 2014, 2016, and 2018 were tested to determine sensitivity to selected QoI fungicides in conidial germination and mycelial inhibition assays, as well as in molecular analysis. Conidial germination was not inhibited at 1 µg/ml of azoxystrobin, trifloxystrobin, and pyraclostrobin. On the other hand, mycelial growth was inhibited by 59%, 56%, and 86% at 100 µg/ml of azoxystrobin, trifloxystrobin, and pyraclostrobin, respectively. The molecular analysis detected the G143A mutation in the cytb gene of all the 82 Ptr isolates, but the F129L and G137R substitutions were not present. This study documents the G143A mutation conferring QoI resistance in Ptr in South America. The findings of this study are key for future decisions regarding use of fungicide and rotation in the region.     

Genetic and molecular analyses in crosses of race 2 and race 7 of albugo Candida

ABSTRACT The inheritance of avirulence and polymorphic molecular markers in Albugo candida, the cause of white rust of crucifers, was studied in crosses of race 2 (Ac2), using isolates MiAc2-B1 or MiAc2-B5 (metalaxyl-insensitive and virulent to Brassica juncea cv. Burgonde) with race 7 (Ac7), using isolate MsAc7-A1 (metalaxyl-sensitive and virulent to B. rapa cv. Torch). Hybrids were obtained via co-inoculation onto a common susceptible host. Putative F(1) progeny were selfed to produce F(2) progeny. The parents and F(1) progeny were examined for virulence on the differential cultivars B. juncea cv. Burgonde and B. rapa cv. Torch. Segregation of avirulence or virulence of F(2) populations was analyzed on cv. Torch. Putative F(1) hybrids were confirmed by random amplified polymorphic DNA markers specific for each parent. Avirulence or virulence of F (2) progeny to B. rapa cv. Torch suggested 3:1 in each of three populations, supporting the hypothesis of a single dominant avirulence gene. Amplified fragment length polymorphism markers also segregated in regular Mendelian fashion among F(2) progeny derived from two F(1) hybrids (Cr2-5 and Cr2-7) of Cross-2. This first putative avirulence gene in A. candida was designated AvrAc1. These results suggest that a single dominant gene controls avirulence in race Ac2 to B. rapa cv. Torch and provides further evidence for the gene-for-gene relationship in the Albugo-Brassica pathosystem.     

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.