Development Of Tan Spot Research Articles

Association Mapping of Resistance to Tan Spot in the Global Durum Panel.

Tan spot, caused by the necrotrophic fungal pathogen Pyrenophora tritici-repentis (Ptr), is an important disease of durum and common wheat worldwide. Compared with common wheat, less is known about the genetics and molecular basis of tan spot resistance in durum wheat. We evaluated 510 durum lines from the Global Durum Wheat Panel (GDP) for sensitivity to the necrotrophic effectors (NEs) Ptr ToxA and Ptr ToxB and for reaction to Ptr isolates representing races 1 to 5. Overall, susceptible durum lines were most prevalent in South Asia, the Middle East, and North Africa. Genome-wide association analysis showed that the resistance locus Tsr7 was significantly associated with tan spot caused by races 2 and 3, but not races 1, 4, or 5. The NE sensitivity genes Tsc1 and Tsc2 were associated with susceptibility to Ptr ToxC- and Ptr ToxB-producing isolates, respectively, but Tsn1 was not associated with tan spot caused by Ptr ToxA-producing isolates, which further validates that the Tsn1-Ptr ToxA interaction does not play a significant role in tan spot development in durum. A unique locus on chromosome arm 2AS was associated with tan spot caused by race 4, a race once considered avirulent. A novel trait characterized by expanding chlorosis leading to increased disease severity caused by the Ptr ToxB-producing race 5 isolate DW5 was identified, and this trait was governed by a locus on chromosome 5B. We recommend that durum breeders select resistance alleles at the Tsr7, Tsc1, Tsc2, and the chromosome 2AS loci to obtain broad resistance to tan spot.

Development of wheat leaf blotches depending on soil tillage system

Conservative soil tillage is considered as the main tool to preserve soil fertility, to reduce gas emissions, and to save financial and labour resources. However, majority of researchers have found that different systems of reduced soil tillage increase the occurrence of slugs, weeds and diseases, including wheat diseases. The aim of the present study was to determine the impact of reduced soil tillage on the severity of winter wheat leaf blotches. The influence of different soil tillage systems and crop rotation on the severity of winter wheat disease was evaluated in a two-factorial experiment: A – soil tillage system (A1 – traditional soil tillage with ploughing at the depth of 22–24 cm); A2 – reduced soil tillage with disc harrowing up to the depth of 10 cm); and B – different crop rotations (B1 – continuous winter wheat; B2 – winter wheat and oilseed rape were grown; B3 – crop rotation). The severity of diseases was determined approximately every 10 days during the whole vegetation season, the total disease impact was estimated by calculating the area under the disease progress curve. Tan spot, caused by Pyrenophora tritici-repentis and Septoria tritici blotch, caused by Zymoseptoria tritici dominated in trials during the entire research period. Soil tillage is the most important factor promoting the development of tan spot, continuous wheat sowings also increased the severity of tan spot. The development of Septoria tritici blotch did not depend on the agronomic practice applied.

DISEASE MONITORING TO DETERMINE THE LEVEL OF SPREAD AND DEVELOPMENT OF THE PATHOGEN PYRENOPHORA TRITICI-REPENTIS IN KAZAKHSTAN

Tan spot, caused by the fungus Pyrenophora tritici-repentis, is economically important foliar disease in Kazakhstan. Monitoring of crops in the farms of the Almaty region was carried out to determine the spread and degree of development of tan spot, as well as the collection of infectious wheat material for further study of virulence. The aim of the study is disease monitoring and to identify the genotypic potential of resistance to tan spot of cultivated wheat cultivars. As a result of the research, 18 (52.9%) cultivars and lines (Karasai, Matai, Bogarnaya-56, Taza, Kozha, Daulet, Asiada, BARU, Kazakhtanskii yantar, Satti, Kazkhastanskaya 10, Almaly, Zhetisu, Naz, Bezostaya 1, Brazilskaya elita, Brazilskaya ozimaya and Bezostaya 100) resistant to tan spot were identified. As a result of the selection and genetic study of promising wheat lines and cultivars, it is shown that it is recommended to use selected promising wheat lines and cultivars in Almaty region, which showed resistance to diseases, as a promising material in breeding for disease resistance. In the future, these 18 cultivars will be studied at subsequent stages of the breeding process in order to create new high-yielding varieties of winter wheat.

Yellow leaf spot of winter bread wheat in the Saratov region

The purpose of the current work was to study the development of tan spot, the causative agent of yellow leaf spot Pyrenophora tritici-repentis (Died) Drechsler on winter bread wheat in the conditions of the Saratov region of Russia. In 2018–2019 there was carried out an estimation of the resistance of 33 winter bread wheat samples to the causative agent of yellow leaf spot. It was established that the varieties “Gostianum 237” and “Levoberezhnaya 1” were characterized by a high level of resistance in the fields. There were identified such weak susceptible varieties as “Victoria 95”, “Gubernia”, “Mironovskaya 808”, “Donskaya bezostaya”, “Smuglyanka”, “Kalach 60”, “111-96 / Zhemchuzhina Povolzhiya”, “L 329 / Urozhaynaya”, “Gubernia / Zhemchuzhina Povolzhiya”, “Saratovskaya 90/ Ukraina”, “L 503 / M Freeman”, “81-93 / (Saratovskaya 11 / Kharkov 82)”. There was identified a moderate damage in the varieties “Lutenscens 230”, “Saratovskaya 80”, “Saratovskaya 90 / 14431 M”, “Sozvesdie”, “Anastasia”, “Saratovskaya 8 / Yubilyar”. The varieties “Zhemchuzhina Povolzhiya”, “Saratovskaya 17”, “Elvira”, “Saratovskaya 8 / B.Z.D.”, “(26-72 / N 49)/(L 15 / Pia)/Sar. 8)”, “Saratovskaya 8 / Yubilyar”, “L 503 / M Freeman”, “30-99/(Saratovskaya 11 / Kharkovskaya 82)”, “Sharada / L 31-98”, “346-06 / L 1334-5”, “Saratovskaya 90”, “L 329 / Saratovskaya ubileynaya”, “Istok/(Saratovskaya 90 / L 503)”, “Brigantina / Don 74” were found susceptible to the pathogen. It was identified that the proportion of winter soft wheat samples resistant to Pyrenophora tritici-repentis was 42% of the total number of varieties studied. There was studied dynamics of Pyrenophora tritici-repentis development in the winter soft wheat variety “Saratovskaya90”. It was found out that the damage degree of the winter bread wheat variety “Saratovskaya90” greatly depended upon the remoteness of the sowings from the source of infection.

IDENTIFICATION WHEAT GENOTYPES RESISTANT TO TAN SPOT PYRENOPHORA TRITICI-REPENTIS

Intensified wheat production, changes in cultural practices including shifts from conventional tillage to reduced tillage practices, and wheat monoculture involving cultivation of susceptible cultivars has resulted in development of tan spot to epidemic proportions in Kazakhstan. Pyrenophora tritici-repentis, causal agent of tan spot on wheat. In recent years, there has been increasing distribution and harmfulness of P. tritici-repentis on wheat. The aim of the study was to identify and select wheat germplasm resistant to tan spot P. tritici-repentis using molecular markers. The results of field evaluation showed resistant reaction to tan spot in 76 wheat varieties (68%). Molecular screening of wheat germplasm was carried out based on the reaction to the fungal inoculum and to host-specific toxins (HST) produced by the P. tritici-repentis. The wheat germplasm insensitive to the toxins HST Ptr ToxA and Ptr ToxB was selected. As a result of molecular screening of 111 wheat genotypes using SSR marker Xfcp623 linked to insensitivity gene to the selective toxin Ptr ToxA of tan spot, 31 carriers of effective tsn1 gene were identified, which accounted for 27,9% of the genotypes studied. Ten samples of wheat (Jubileynaya 60, TOO11/TOOOO7, F3.71/TRM/VORONA/3/OC14, NANJTNG 82149 KAUZ, ECHA/LI115, Akmola 2, Kazakh-stanskaya rannespelaya, Kazakhstanskaya 25, 428g/MK-122A and 190-Naz/GF55) are characterized with complex resistance to the races Ptr 1 and 5, as well as to 2 toxins (ToxA and ToxB) and to the Septoria nodorum blotch isolate SNB7k. 20 promising wheat lines resistant to tan spot were selected. These genotypes also showed a moderate and high level of field resistance and recommended to use in the breeding programs for resistance to tan spot.

Identification of quantitative trait loci conferring resistance to tan spot in a biparental population derived from two Nebraska hard red winter wheat cultivars

Tan spot, caused by Pyrenophora tritici-repentis (Ptr), is a destructive foliar disease in all types of cultivated wheat worldwide. Genetics of tan spot resistance in wheat is complex, involving insensitivity to fungal-produced necrotrophic effectors (NEs), major resistance genes, and quantitative trait loci (QTL) conferring race-nonspecific and race-specific resistance. The Nebraska hard red winter wheat (HRWW) cultivar ‘Wesley’ is insensitive to Ptr ToxA and highly resistant to multiple Ptr races, but the genetics of resistance in this cultivar is unknown. In this study, we used a recombinant inbred line (RIL) population derived from a cross between Wesley and another Nebraska cultivar ‘Harry’ (Ptr ToxA sensitive and highly susceptible) to identify QTL associated with reaction to tan spot caused by multiple races/isolates. Sensitivity to Ptr ToxA conferred by the Tsn1 gene was mapped to chromosome 5B as expected. The Tsn1 locus was a major susceptibility QTL for the race 1 and race 2 isolates, but not for the race 2 isolate with the ToxA gene deleted. A second major susceptibility QTL was identified for all the Ptr ToxC-producing isolates and located to the distal end of the chromosome 1A, which likely corresponds to the Tsc1 locus. Three additional QTL with minor effects were identified on chromosomes 7A, 7B, and 7D. This work indicates that both Ptr ToxA-Tsn1 and Ptr ToxC-Tsc1 interactions are important for tan spot development in winter wheat, and Wesley is highly resistant largely due to the absence of the two tan spot sensitivity genes.

Importance of Agronomic Practice on the Control of Wheat Leaf Diseases

Soil tillage and crop rotation are considered important tools in wheat leaf disease control; however, the results of investigations are inconsistent. The aim of the present study was to determine the effect of the soil tillage system and cropping sequence on the development of winter wheat leaf diseases in 2012–2017. The disease development was assessed in a two-factor experiment: (a) soil tillage system; and (b) crop rotation. Foliar fungicides were used uniformly in all variants. The results showed that tan spot (caused by Pyrenophora tritici-repentis) dominated in 2012, 2013, and 2016, but the level of Septoria tritici blotch (Zymoseptoria tritici) was essentially lower and exceeded the severity of tan spot only in 2015. The agronomic practice used significantly influenced only the development of tan spot. Reduced soil tillage and continuous wheat sowing substantially increased tan spot severity, especially when both practices were used simultaneously. Short crop rotation (only wheat and oilseed rape) provided sufficient control of tan spot in ploughed fields, whereas in non-ploughed fields, the level of this disease did not decrease. The results could be explained by differences in the pathogens’ life cycle: P. tritici-repentis ascospores in wheat debris is the main source of infection; in contrast, Z. tritici spreads by conidia from living plants.

Silicon suppresses tan spot development on wheat infected by Pyrenophora tritici-repentis

Tan spot caused by Pyrenophora tritici-repentis is the main foliar diseases of wheat in Brazil. The effect of silicon (Si) on the components of resistance of a susceptible (Fundacep Horizonte) and a moderately resistant (Quartzo) wheat cultivar was studied in a controlled environment. Silicon was supplied as calcium silicate in the soil 30 days before sowing. At the booting stage, a conidial suspension of the fungus was sprayed onto the flag leaves of potted plants, which were incubated under moist conditions for 48 h. Afterwards, inoculated leaves were assessed for: incubation period (IP), infection efficiency (IE), area under lesion size curve (AULSC), lesion size (LS), severity (SEV) and area under severity curve (AUSC). Foliar Si concentrations were quantified at the end of the evaluations. Si supply to plants increased leaf Si concentration in 233% for Fundacep Horizonte (from 4.8 to 16.0 g kg−1 of dry matter) and 211% for Quartzo (from 5.3 to 16.5 g kg−1 of dry matter). In the Si + treatments, IP was longer by 24 and 17 h, IE declined by 53.5 and 65.5%, LS (at 264 h after inoculation) by 4.6 mm (from 9.5 to 4.9 mm) and 5.9 mm (from 8.2 to 2.3 mm), and SEV by 53% (from 54.4 to 18.8%) and 88% (from 47.7 to 5.5%) respectively, for the Fundacep Horizonte and Quartzo cultivars. The Si x cultivar interaction was not significant for AULSC and AUSC, and these variables were reduced by 55.8 and 80.8%, respectively, in plants supplied with Si. In conclusion, Si enhanced the resistance of wheat plants to tan spot development by affecting several resistance components, regardless of the resistance level of the cultivar. However, the greatest reduction in tan spot development by Si supply was observed when using a moderately resistant cultivar.

The sensitivity of Canadian wheat genotypes to the necrotrophic effectors produced by Pyrenophora tritici-repentis

Pyrenophora tritici-repentis (Ptr), the cause of tan spot of wheat, is a foliar pathogen of economic importance worldwide. Tan spot development is associated with the production of necrotrophic effectors (Ptr ToxA, Ptr ToxB and Ptr ToxC) that serve as fungal pathogenicity and/or virulence factors. The objective of this study was to investigate the sensitivity to each of these effectors in a collection of 100 Canadian wheat cultivars representing all wheat classes and developed over a century by various Canadian breeding programmes. Heterologously expressed, His-tagged Ptr ToxA and Ptr ToxB, and spore germination fluids possessing putative Ptr ToxC activity, were produced and used to screen the cultivars for sensitivity. Of the 100 wheat cultivars tested, 92 were sensitive to at least one effector, 68 were sensitive to Ptr ToxA, 63 were sensitive to Ptr ToxC and 24 were sensitive to Ptr ToxB. Only eight cultivars were insensitive to all three effectors. These results reflect the widespread sensitivity in Canadian wheat cultivars to these necrotrophic effectors, with sensitivity to Ptr ToxA and the putative Ptr ToxC found consistently to be more common than Ptr ToxB sensitivity. The predominance of Ptr ToxA and Ptr ToxC sensitivity in Canadian wheat is consistent with the prevalence of races 1 (Ptr ToxA + Ptr ToxC producer) and 2 (Ptr ToxA producer) of Ptr in North America, and could reflect a competitive advantage for Ptr ToxA-producing isolates in the pathogen population.

Diseases of leaves in triticale and spelt in Ukrainian Polissia

There were studied the peculiarities of fungal diseases of triticale and spelt in the conditions of Ukrainian Polissia. It was found that Septoria leaf blotch and powdery mildew have a dominant role in the pathogenic complex of both cultures as their relative shares are 34.0 and 23.0% respectively in the complex of triticale leaf mycoses, and 52.0 and 36.0% respectively in the complex of spelt leaf mycoses. It was noted that such diseases as tan spot, brown leaf rust and snow mold rarely occurred on winter triticale plants, and such diseases as ascochyta leaf blight, spot blotch and Fusarium disease were episodic in nature. Development of tan spot and spot blotch on spelt plants had non-systematic character. It was established that on spelt wheat level of disease severity is lower and number of pathogens is less

Inverse gene-for-gene interactions contribute additively to tan spot susceptibility in wheat.

Tan spot susceptibility is conferred by multiple interactions of necrotrophic effector and host sensitivity genes. Tan spot of wheat, caused by Pyrenophora tritici-repentis, is an important disease in almost all wheat-growing areas of the world. The disease system is known to involve at least three fungal-produced necrotrophic effectors (NEs) that interact with the corresponding host sensitivity (S) genes in an inverse gene-for-gene manner to induce disease. However, it is unknown if the effects of these NE-S gene interactions contribute additively to the development of tan spot. In this work, we conducted disease evaluations using different races and quantitative trait loci (QTL) analysis in a wheat recombinant inbred line (RIL) population derived from a cross between two susceptible genotypes, LMPG-6 and PI 626573. The two parental lines each harbored a single known NE sensitivity gene with LMPG-6 having the Ptr ToxC sensitivity gene Tsc1 and PI 626573 having the Ptr ToxA sensitivity gene Tsn1. Transgressive segregation was observed in the population for all races. QTL mapping revealed that both loci (Tsn1 and Tsc1) were significantly associated with susceptibility to race 1 isolates, which produce both Ptr ToxA and Ptr ToxC, and the two genes contributed additively to tan spot susceptibility. For isolates of races 2 and 3, which produce only Ptr ToxA and Ptr ToxC, only Tsn1 and Tsc1 were associated with tan spot susceptibility, respectively. This work clearly demonstrates that tan spot susceptibility in this population is due primarily to two NE-S interactions. Breeders should remove both sensitivity genes from wheat lines to obtain high levels of tan spot resistance.

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

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.

Resistance to Tan Spot and Insensitivity to Ptr ToxA in Wheat

ABSTRACTTan spot, caused by the fungus Pyrenophora tritici‐repentis, is an important foliar disease of wheat (Triticum aestivum L.) worldwide. Growing resistant cultivars is an effective approach to reduce the losses caused by the disease. To identify resistance genes in common wheat, 380 wheat accessions from different geographical origins were evaluated for resistance to P. tritici‐repentis race 1, the predominant race in the Great Plains of the United States and western Canada, and insensitivity to Ptr ToxA, a host‐selective toxin produced by race 1. Most accessions tested (60%) were resistant and only 93 accessions (24%) were as susceptible as TAM 105, the susceptible control. Among 379 accessions, 230 were insensitive to Ptr ToxA, but only 158 of them showed resistance to race 1. A weak correlation between tan spot score and sensitivity to Ptr ToxA suggests that pathogenicity factors other than Ptr ToxA (like Ptr ToxC) also contributed to tan spot development in these accessions. The accessions with resistance to tan spot identified in this study should be useful sources for developing new tan spot resistant cultivars.

Identification of novel tan spot resistance QTLs using an SSR-based linkage map of tetraploid wheat

Durum wheat (Triticum turgidum L. subsp. durum ,2 n= 4x = 28, AABB) is an important cereal used for making pasta products. Compared with bread wheat, durum wheat receives less attention in genetic and genomic studies. In this research, a tetraploid wheat doubled haploid (DH) population derived from the cross between the durum wheat cultivar 'Lebsock' and the T. turgidum subsp. carthlicum (2n = 4x = 28, AABB) accession PI 94749 was developed. The population consisted of 146 lines and was used to construct linkage maps of all 14 chromosomes. The maps consisted of 280 SSR markers and spanned 2,034.1 cM with an average density of one marker per 7.2 cM. The DH population and the whole genome linkage maps were then used to identify QTLs associ- ated with tan spot resistance. The DH population was inoculated separately with two Ptr ToxA-producing isolates (Pti2 and 86-124) representing races 1 and 2, respectively, of Pyrenophora tritici-repentis, and five resistance QTLs were detected on chromosome arms 3AS, 3BL, 5AL and 7BL. Together, the QTLs explained a total of 46 and 41% of the phenotypic variation for reaction to Pti2 and 86-124, respectively. The Tsn1-Ptr ToxA interaction was not a significant factor in tan spot development in this population, and none of the QTLs corresponded to previously identified loci known to confer insensitivity to host-selective toxins (HSTs) produced by P. tritici-repentis. This result, together with those of other similar studies, indicates that the wheat-P. tritici-repentis pathosystem involves more factors than currently published host-toxin interactions. The DH population and genetic maps reported here will be useful for genetic dissection of important agronomic traits as well as the identification and development of markers for marker-assisted selection (MAS).

EndophyticChaetomium globosumreduces development of tan spot in wheat caused byPyrenophora tritici-repentis

Endophytic Chaetomium reduced the development of disease caused by Pyrenophora tritici-repentis in wheat leaves. Chaetomium globosum isolate NC-1 and its culture filtrate, applied to leaves 3, 7 and 14 days before inoculation with the pathogen, reduced the development of tan spot in treated leaves of the susceptible cv. Morocco. The disease reduction differed between host cultivars. Disease reduction was more pronounced in cv. Leichhardt than cv. Morocco. Inoculation of the endophyte or its culture filtrate led to accumulation of extracellular proteins in host tissues indicating activation of host defences. The intercellular washing fluid of endophyte-inoculated leaves lacked an inhibitory effect on the pathogen in vitro, and the inhibitory proteinaceous compound produced by the endophyte in vitro was not detected in the intercellular washing fluid of endophyte-infected leaves. The antagonistic effect of the endophyte against the pathogen in planta was probably due to activation of host defences rather than direct antagonism.

Role of Host Sensitivity to Ptr ToxA in Development of Tan Spot of Wheat

ABSTRACT 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 F(2)-derived F(6) 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.

Tan spot development peculiarities in Latvia

Tan spot, caused by Pyrenophora tritici-repentis (Died.) Drechs., anamorph Drechslera tritici-repentis is one of the most important wheat diseases in the world, especially in the regions of intensive wheat growing. Tan spot had established for the first time in Latvia in 1994. Epidemic of this disease was observed in Latvia in 1998. Development of tan spot were investigated in field experiments at the Research and Training Farm “Peterlauki” of Latvia University of Agriculture in 1998–2001. Level of incidence and severity of tan spot differed depending on varieties and years. Severity of the disease was 16–71% in 1999; 0.1–5% in 2000 and 4–18% in 2001 depending on varieties at the time of ripening. 1999 summer was extremely dry, and development of disease was not observed. Explosion of disease was observed at the second half of June in 2000 and 2001, without reference to varieties. Date of increasing start differed, but in all cases important development was observed after flowering. Rate of increasing of disease was very high, during two weeks severity of disease increased from 0.1 till maximum of severity. Amount and frequency of rainy differed in 2000 and 2001, but increase on disease was very similar, it means, we need more information about favourable conditions for Drechslera tritici-repentis. Sexual stage Pyrenophora tritici-repentis was observed in Latvia for the first time. Further investigations are necessary, because relationships between meteorological conditions and stages of development are unclear.

The Effect of Plant Height on Tan Spot on Durum Wheat in Southern Saskatchewan.

Tan spot [caused by Pyrenophora tritici-repentis (Died.) Drechs.] is the most important leaf disease of durum wheat (Triticum turgidum L. var. durum). Most of the durum cultivars in western Canada are of conventional height but development of shorter cultivars is desirable. Changes in microenvironment resulting from a height reduction might cause greater leaf spot development. The effect of plant height on tan spot of durum wheat was determined in five pairs of genotypes near-isogenic for plant height and five randomly selected populations, each with a semidwarf and a conventional height parent. These were grown in five environments in Saskatchewan (1996-1998 at Swift Current, 1997-1998 at Indian Head), and evaluated for tan spot reaction in a growth chamber. There was no difference in tan spot reaction under controlled conditions between short and tall genotype(s) in each pair or population, although there were differences within each height category. Under field conditions, short genotypes had either equal or greater disease than tall genotypes. Contrasts between all short and tall genotypes also showed that the tall had less disease in 1998 at Indian Head (9.8 for tall, 10.2 for short) and in all years at Swift Current (9.5 and 9.9 in 1996, 8.1 and 8.7 in 1997, 8.5 and 8.9 in 1998, for tall and short, respectively). However, there was genetic variability within populations, with some short having equal or less disease than tall genotypes. Some of these short genotypes also had a low tan spot lesion type under controlled conditions. We conclude that plant height could affect tan spot development in durum wheat under conditions prevalent in southern Saskatchewan, and that this is probably mediated by canopy density.

The Effect of Plant Height on Tan Spot on Durum Wheat in Southern Saskatchewan

Tan spot [caused by Pyrenophora tritici-repentis (Died.) Drechs.] is the most important leaf disease of durum wheat (Triticum turgidum L. var. durum). Most of the durum cultivars in western Canada are of conventional height but development of shorter cultivars is desirable. Changes in microenvironment resulting from a height reduction might cause greater leaf spot development. The effect of plant height on tan spot of durum wheat was determined in five pairs of genotypes near-isogenic for plant height and five randomly selected populations, each with a semidwarf and a conventional height parent. These were grown in five environments in Saskatchewan (1996–1998 at Swift Current, 1997–1998 at Indian Head), and evaluated for tan spot reaction in a growth chamber. There was no difference in tan spot reaction under controlled conditions between short and tall genotype(s) in each pair or population, although there were differences within each height category. Under field conditions, short genotypes had either equal or greater disease than tall genotypes. Contrasts between all short and tall genotypes also showed that the tall had less disease in 1998 at Indian Head (9.8 for tall, 10.2 for short) and in all years at Swift Current (9.5 and 9.9 in 1996, 8.1 and 8.7 in 1997, 8.5 and 8.9 in 1998, for tall and short, respectively). However, there was genetic variability within populations, with some short having equal or less disease than tall genotypes. Some of these short genotypes also had a low tan spot lesion type under controlled conditions. We conclude that plant height could affect tan spot development in durum wheat under conditions prevalent in southern Saskatchewan, and that this is probably mediated by canopy density.

A single gene encodes a selective toxin causal to the development of tan spot of wheat.

The identification and characterization of pathogenicity factors are essential to an understanding of the molecular events that regulate the interaction of plant-pathogenic microbes with their hosts. We have isolated the gene that encodes a host-selective toxic protein produced by the fungus Pyrenophora tritici-repentis and confirmed that this gene functions in the plant as the primary determinant of pathogenicity in the Pyrenophora-wheat interaction. These results demonstrate that a single gene encodes the production of a host-selective toxin and that transformation of this gene into a non-toxin-producing isolate of P. tritici-repentis leads to both toxin production and pathogenicity.