scholarly journals A Comparative Study of Pyrenophora Teres Drechs. F. Teres and Pyrenophora Teres Drechs. F. Maculata Smedeg. Cause of "Net" and "Spot" Type Net Blotch Respectively on New Zealand Barley

2021 ◽  
Author(s):  
◽  
Daphne Geraldine Carvalho

<p>Net blotch is caused by Pyrenophora teres Drechs. (stat. conid. Drechslera teres (Sacc.) Shoem., syn. Helminthosporium teres Sacc). P. teres produces symptoms which appear initially as small necrotic spots and streaks on the leaf. These increase to produce the characteristic net-like symptoms, which have given rise to the name net blotch. Sometimes, lesions develop from small necrotic spots, to form elliptical lesions. This is the "spot" type of P. teres and was first noticed in 1967 in isolates from North America, Mexico, Israel and Holland. It was thought that these isolates were mutants of P. teres. Since 1969 however, other workers have reported similar observations widely occurring in Norway, Denmark and Finland. Based on minor morphological differences, Ito and Kuribayashi proposed a new species, called P. japonica. Smedegård-Petersen disagreed, and showed that the spot-producing isolate represents a deviating type of P. teres, only differing from the usual "net" type in the symptoms induced on barley plants. He based his reasoning on morphological, cultural and genetical investigations. Consequently, Smedegård-Petersen described two new forms of the fungus, Pyrenophora teres Drechs. f. teres Smedeg., which produces the usual net lesions, and Pyrenophora teres Drechs. f. maculata Smedeg., which produces well defined dark brown circular or elliptical lesions without netting. The aim of the research undertaken in the present study was to conduct a comparative study on the morphology and fitness of a range of New Zealand "net" and "spot" type isolates. An attempt was also made at crossing a "net" type with a "spot" type. Although Smedegård-Petersen had stated that there was no morphological difference between the "net" and "spot" types, this project was undertaken because no research had been done on New Zealand isolates. Furthermore, different features were studied using different methods not used by other workers in studying P. teres. The only morphological difference that was distinctive was that the "spot" types of P. teres formed coremial strands, which were fan-like in morphology, which produced conidia in culture, and the "net" types did not. There was no way to tell the "net" isolates apart from the "spot" isolates, based on conidia colour, length, width, volume or the number of cells per conidium. One fact that did emerge, was that the longest conidia had the greatest number of cells per conidium and the reverse was also true. The germination of monoconidial isolates showed that there were no major differences in branching between the two types of P. teres. However, it was revealed that two germ tubes were capable of emerging from one cell in the "spot" isolates. All cells in a conidium in both the "net" and "spot" types were able to germinate, cells that germinated tended to be at opposite ends, and the first cell to germinate in a conidium was usually the cell at the hilum. Examination of the growth rates showed that there were no significant differences in the growth rates of the "net" and "spot" types when grown on MEA+B. The "spot" types were able to penetrate cellulose faster than the "net" types and hence may produce cellulose faster as well. ANT148, which had previously been an unknown type, was proved to be a "spot" type in the pathogenicity tests. It may have been the source of the New Zealand "spot" type inoculum because the seed it came from was imported into New Zealand in 1984, two years prior to the discovery of the "spot" type of P. teres in the South Island. Both forms of P. teres penetrated the leaf through the epidermal cell wall, and occasionally entered through the stomata. Even though the "spot" type may be present inside the leaf, the symptoms are not usually manifested until later, compared with the "net" type where the symptoms tend to be an indication of the amount of hyphae present in the leaf. In the screening of the progeny from the crossing, the "spot" type of P. teres had lost up to 78.9% of its resistance to triadimenol and flutriafol, when compared to the sensitivity tests carried out in 1986 and 1987. It is hypothesised that 13Y, the "net" type is dominant, and the "spot" type, KF2, recessive, as none of the progeny had any resistance to triadimenol or flutriafol, after undergoing somatic recombination. It was concluded that the "spot" and "net" types are two types of the same species, and there was not enough evidence to suggest otherwise. Further studies should be done, using more current isolates of the "net" and "spot" types of P. teres, and the old D. japonica isolates from New Zealand, to establish if the cultures identified as D. japonica, are different in any way.</p>

2021 ◽  
Author(s):  
◽  
Daphne Geraldine Carvalho

<p>Net blotch is caused by Pyrenophora teres Drechs. (stat. conid. Drechslera teres (Sacc.) Shoem., syn. Helminthosporium teres Sacc). P. teres produces symptoms which appear initially as small necrotic spots and streaks on the leaf. These increase to produce the characteristic net-like symptoms, which have given rise to the name net blotch. Sometimes, lesions develop from small necrotic spots, to form elliptical lesions. This is the "spot" type of P. teres and was first noticed in 1967 in isolates from North America, Mexico, Israel and Holland. It was thought that these isolates were mutants of P. teres. Since 1969 however, other workers have reported similar observations widely occurring in Norway, Denmark and Finland. Based on minor morphological differences, Ito and Kuribayashi proposed a new species, called P. japonica. Smedegård-Petersen disagreed, and showed that the spot-producing isolate represents a deviating type of P. teres, only differing from the usual "net" type in the symptoms induced on barley plants. He based his reasoning on morphological, cultural and genetical investigations. Consequently, Smedegård-Petersen described two new forms of the fungus, Pyrenophora teres Drechs. f. teres Smedeg., which produces the usual net lesions, and Pyrenophora teres Drechs. f. maculata Smedeg., which produces well defined dark brown circular or elliptical lesions without netting. The aim of the research undertaken in the present study was to conduct a comparative study on the morphology and fitness of a range of New Zealand "net" and "spot" type isolates. An attempt was also made at crossing a "net" type with a "spot" type. Although Smedegård-Petersen had stated that there was no morphological difference between the "net" and "spot" types, this project was undertaken because no research had been done on New Zealand isolates. Furthermore, different features were studied using different methods not used by other workers in studying P. teres. The only morphological difference that was distinctive was that the "spot" types of P. teres formed coremial strands, which were fan-like in morphology, which produced conidia in culture, and the "net" types did not. There was no way to tell the "net" isolates apart from the "spot" isolates, based on conidia colour, length, width, volume or the number of cells per conidium. One fact that did emerge, was that the longest conidia had the greatest number of cells per conidium and the reverse was also true. The germination of monoconidial isolates showed that there were no major differences in branching between the two types of P. teres. However, it was revealed that two germ tubes were capable of emerging from one cell in the "spot" isolates. All cells in a conidium in both the "net" and "spot" types were able to germinate, cells that germinated tended to be at opposite ends, and the first cell to germinate in a conidium was usually the cell at the hilum. Examination of the growth rates showed that there were no significant differences in the growth rates of the "net" and "spot" types when grown on MEA+B. The "spot" types were able to penetrate cellulose faster than the "net" types and hence may produce cellulose faster as well. ANT148, which had previously been an unknown type, was proved to be a "spot" type in the pathogenicity tests. It may have been the source of the New Zealand "spot" type inoculum because the seed it came from was imported into New Zealand in 1984, two years prior to the discovery of the "spot" type of P. teres in the South Island. Both forms of P. teres penetrated the leaf through the epidermal cell wall, and occasionally entered through the stomata. Even though the "spot" type may be present inside the leaf, the symptoms are not usually manifested until later, compared with the "net" type where the symptoms tend to be an indication of the amount of hyphae present in the leaf. In the screening of the progeny from the crossing, the "spot" type of P. teres had lost up to 78.9% of its resistance to triadimenol and flutriafol, when compared to the sensitivity tests carried out in 1986 and 1987. It is hypothesised that 13Y, the "net" type is dominant, and the "spot" type, KF2, recessive, as none of the progeny had any resistance to triadimenol or flutriafol, after undergoing somatic recombination. It was concluded that the "spot" and "net" types are two types of the same species, and there was not enough evidence to suggest otherwise. Further studies should be done, using more current isolates of the "net" and "spot" types of P. teres, and the old D. japonica isolates from New Zealand, to establish if the cultures identified as D. japonica, are different in any way.</p>


Genome ◽  
2006 ◽  
Vol 49 (7) ◽  
pp. 855-859 ◽  
Author(s):  
T L Friesen ◽  
J D Faris ◽  
Z Lai ◽  
B J Steffenson

Net blotch, caused by Pyrenophora teres, is one of the most economically important diseases of barley worldwide. Here, we used a barley doubled-haploid population derived from the lines SM89010 and Q21861 to identify major quantitative trait loci (QTLs) associated with seedling resistance to P. teres f. teres (net-type net blotch (NTNB)) and P. teres f. maculata (spot-type net blotch (STNB)). A map consisting of simple sequence repeat (SSR) and amplified fragment length polymorphism (AFLP) markers was used to identify chromosome locations of resistance loci. Major QTLs for NTNB and STNB resistance were located on chromosomes 6H and 4H, respectively. The 6H locus (NTNB) accounted for as much as 89% of the disease variation, whereas the 4H locus (STNB resistance) accounted for 64%. The markers closely linked to the resistance gene loci will be useful for marker-assisted selection.Key words: disease resistance, Drechslera teres, molecular markers.


1990 ◽  
Vol 70 (2) ◽  
pp. 473-480 ◽  
Author(s):  
C. G. J. VAN DEN BERG ◽  
B. G. ROSSNAGEL

Spot-type net blotch, incited by Pyrenophora teres f. maculata has become widespread in Saskatchewan. This study was conducted to evaluate the effect of the fungicide Tilt (propiconazole) on the severity of spot-type net blotch, grain yield and yield components in spring barley. The susceptible cultivar Elrose was subjected to five schedules of foliar application of Tilt at Medstead, Shellbrook and Saskatoon, Saskatchewan in 1985 and 1986. The moderately susceptible cultivar Argyle was included in the experiments conducted in 1986. Results show that Tilt controlled spot-type net blotch in Elrose. However, the effective period was limited. A single application did not control spot-type net blotch in cases with rapid disease development. Application of Tilt at Zadoks growth stages 31 and 49 would be required to provide reliable control in a susceptible cultivar. Control of spot-type net blotch increased grain yield. A single application of Tilt increased grain yield up to 23% over the untreated control. In most cases, a double application of Tilt did not increase grain yield over a timely single application. Increased grain yield was associated with increased kernel weight. The correlation coefficient between grain yield and kernel weight ranged from 0.82 to 0.88. Tilt had no effect on a healthy crop of Elrose and the moderately susceptible cultivar Argyle.Key words: Pyrenophora teres f. maculata, Hordeum vulgare L., propiconazole, barley


Plant Disease ◽  
2010 ◽  
Vol 94 (4) ◽  
pp. 480-480 ◽  
Author(s):  
Z. H. Liu ◽  
T. L. Friesen

Net blotch of barley (Hordeum vulgare L.) caused by the fungus Pyrenophora teres (anamorph Drechslera teres) is found in two forms, net form net blotch (NFNB) and spot form net blotch (SFNB). When inoculated on susceptible varieties, P. teres f. teres produces lesions with a characteristic net-like pattern surrounded by necrosis or chlorosis (NFNB), whereas P. teres f. maculata produces lesions consisting of spots surrounded by necrosis or chlorosis (SFNB). Recently, epidemics of SFNB have occurred throughout the world (4). Currently, net blotch is a significant foliar disease of barley in the North Dakota-Northwestern Minnesota agricultural region, a leading barley-production area. Diseased barley leaf tissue was collected annually from 2004 to 2008 in Fargo and Langdon, ND. Diseased leaves were incubated to promote sporulation. Ten single-spore isolates of P. teres collected from each location each year were tested for virulence by inoculation on 20 commonly used barley net blotch differential lines. Among the 100 isolates collected, one isolate collected in Fargo in 2006 (FGOH06Pt-8) and one isolate collected in Langdon in 2008 (LDNH08Pt-4) were identified as P. teres f. maculata due to their induction of spot-type lesions across the differential set. Conidial morphology of the two isolates was similar to P. teres f. teres isolates. A pathogenicity test of all isolates was performed on regional barley cvs. Tradition, Robust, and Lacey as well as barley lines Rika and Kombar (1) as previously described (3). The net form isolate 0-1 and spot form isolate DEN2.6 (obtained from B. Steffenson, University of Minnesota) were used as controls. The P. teres f. teres isolate 0-1 produced typical net type symptoms on all barley lines except the resistant line Rika, in which only small, dark spots were observed. DEN2.6 produced pin-point spot-like lesions with an extensive yellow halo on Robust, Lacey, Rika, and Kombar, but without chlorosis on Tradition. The two newly identified isolates induced elliptical spot-type lesions measuring 3 × 6 mm, larger than those produced by P. teres f. maculata isolate DEN 2.6, suggesting a higher level of virulence. We constructed a neighbor-joining phylogenetic tree using ClustalW2 ( http://www.ebi.ac.uk/ ) based on sequence identity of the internal transcribed spacer (ITS) region from 0-1 (GenBank No. GU014819), DEN2.6 (GenBank No. GU014820), FGOH06Pt-8 (GenBank No. GU014821), and LDNH08Pt-4 (GenBank No. GU014822) as well as P. teres f. maculata, P. teres f. teres, and P. tritici-repentis (causal agent of tan spot of wheat) accessions obtained from GenBank (2). All P. teres isolates clustered together and were clearly separated from the P. tritici-repentis cluster. Isolates FGOH06Pt-8 and LDNH08Pt-4 had identical ITS sequences and differed from DEN2.6 by only a single nucleotide. To our knowledge, this is the first report of P. teres f. maculata in North Dakota. Resistance to SFNB should now be considered in local barley breeding programs and cultivar releases. Reference: (1) M. Abu Qamar. Theor. Appl. Genet. 117:1261, 2008. (2) R. M. Andrie et al. Fungal Genet. Biol. 45:363, 2008. (3) Z. Lai et al. Fungal Genet. Biol. 44:323, 2007. (4) M. S. McLean et al. Crop Pasture Sci. 60:303, 2009.


1999 ◽  
Vol 35 (No. 4) ◽  
pp. 115-120 ◽  
Author(s):  
V. Minařiková ◽  
I. Polišenská

One of t he diseases that have become i mportant in the Czech Republ ic recently is net blotch of ba rley caused by Pyrenophora teres (Died.) Drechs., with the imperfect stale Drechslera teres. In 1 995-1997 infected leaves of both spring and winter barley were collected in various stands and climatic regions. Al most 400 isolates of the pathogen were obtained and tested for virulence using a differential set (Cl 5791. CI 2750, CI 9819, C 8755, Stcudclli, Harbin, C 29192, CI 739, Tifang. and the suscepti ble control Beate). To assess their reaction, the laboratory method for testing leaf segments on benzimidazole was used. The most stable resistant responses, compared also with previous tests from 1991-1994, were found in Cl 739 and Tifang where the frequency of viru lent isolates did not exceed I 0% of all tested ones. These genotypes should be involved in practical breeding of barley for resistance to the pathogen.


1983 ◽  
Vol 63 (3) ◽  
pp. 631-639 ◽  
Author(s):  
J. C. SUTTON ◽  
P. STEELE

Effects of systemic fungicides on progress of net blotch, caused by Pyrenophora teres, were examined in field plots. Disease intensities and apparent infection rates (r values) in barley grown from carbathiin-treated seeds were similar to those of the checks 29–30 days and later. Etaconazole used as a seed treatment reduced disease intensities for about 29–42 days, but r values later accelerated and exceeded those of the checks. Propiconazole applied to the foliage at early tillering reduced r for about 12 days, but disease subsequently progressed more rapidly than in the checks. Applications of propiconazole at spike emergence reduced r for 13–15 days. According to the observed r values and disease intensities, the following temporal relationships of fungicide applications and disease progress were recognized: (1) period of reduced epidemic rates; (2) period of accelerated epidemic rates; (3) period of epidemiologic impact of the fungicide (the summation of 1 and 2). Seed treatments and tillering sprays failed to increase barley yields significantly. However, when propiconazole was applied at spike emergence, or at both tillering and spike emergence, 1000-kernel weights increased by 17.3% and 17.8%, respectively, at one location, and grain yields by 14.2% and 19.1% at a second location.Key words: Etaconazole, propiconazole, carbathiin, epidemiology, Pyrenophora teres, Drechslera teres


2007 ◽  
Vol 97 (8) ◽  
pp. 907-915 ◽  
Author(s):  
Abolfazl Sarpeleh ◽  
Hugh Wallwork ◽  
David E. A. Catcheside ◽  
Max E. Tate ◽  
Amanda J. Able

Pyrenophora teres, the causal agent of net blotch of barley (Hordeum vulgare L.), induces a combination of necrosis and extensive chlorosis in susceptible barley cultivars. Cell-free filtrates from both net and spot forms of P. teres; P. teres f. sp. teres, and P. teres f. sp. maculata were found to contain phytotoxic low molecular weight compounds (LMWCs) and proteinaceous metabolites which appear to be responsible for different components of the symptoms induced by the two forms of the pathogen in a susceptible cultivar of barley (cv. Sloop). Proteins induced only brown necrotic spots or lesions similar to those induced by the pathogens 72 h after inoculation. In contrast, LMWCs induced general chlorosis seen 240 h after inoculation but not the localized necrosis. Neither hydrolyzed or heat- or protease-treated proteinaceous metabolites induced the symptoms. This is the first report of the involvement of proteins produced by P. teres in symptom development during net blotch disease of barley.


1989 ◽  
Vol 40 (4) ◽  
pp. 745 ◽  
Author(s):  
TN Khan

The effect of spot-type net blotch (Drechslera teres (Sacc.) Shoem.) on yield was studied in fourteen field experiments located at two sites over seven years in the area where the disease occurs; the northern cereal belt of south-west Western Australia. An overall reduction of 26% in grain yield occurred associated with spot-type net blotch infection. The yield losses varied depending upon season, date of sowing and cultivar. Disease was found to reduce 100 grain weight and number of ears/m2, but number of grains/ear were not affected. Regression analysis supported the above negative effect of disease on yield in general, but in a few cases disease and yield were positively correlated. The Area Under Curve (AUC) model was considered most appropriate and percentage yield loss (L) was estimated as L = 0.0233 AUC. Using this relationship, potential losses in yields of cvv. Beeeher and O'Connor were estimated to be 34% and 29%, respectively. The application of this relationship is suggested to be limited to short season environments similar to the northern cereal belt of Western Australia. A need to understand factors which modify the yield response to this disease is highlighted.


Plant Disease ◽  
2004 ◽  
Vol 88 (10) ◽  
pp. 1162-1162
Author(s):  
S. A. Pereyra ◽  
S. E. Germán

In September 2003, leaves exhibiting spot-type lesions similar to those produced by Cochliobolus sativus Drechs. ex Dastur were widely observed in six commercial barley crops of cvs. Norteña Daymán, Norteña Carumbé, and MUSA 936 in Soriano and Río Negro provinces, the main barley production region in western Uruguay. Spot lesions were tan to dark brown, circular to elliptical, and 3 to 10 mm in diameter. Larger lesions were surrounded by a chlorotic margin of varying width. Affected leaf pieces (10 to 15) from each field were placed in a moist chamber for 2 days to promote sporulation. A fungus identified morphologically as Pyrenophora teres (Died.) Drechs. (1) was consistently isolated from infected leaves. However, symptoms did not correspond to the net-type lesions of net blotch commonly produced by P. teres f. sp. teres in Uruguay. Three monoconidial cultures were obtained by transferring single conidia to potato dextrose agar and then to 10% V8 juice agar and incubated at 20 to 22°C with a 12-h photoperiod for 10 days. Adding sterile water to each plate and gently rubbing the surface with a microscope slide prepared inoculum for pathogenicity tests. Conidia concentration was adjusted to 1 × 104 conidia per ml. Sixty-eight barley genotypes from Uruguay, ICARDA/CIMMYT, and North Dakota were grown in the greenhouse for 2 weeks at 20 to 22°C with a 14-h photoperiod. For each monoconidial isolate, three seedlings of each genotype were inoculated at the three-leaf stage 15 to 16 days after seeding with 0.4 ml of the inoculum suspension with an airbrush inoculator. A drop of Tween 20 was added per 40 ml of inoculum suspension. One set of each genotype was inoculated with sterile water as a control. Seedlings were placed in a dew chamber at 20°C and 100% relative humidity in the dark for 24 h and then returned to prior conditions. The first lesions developed after 7 to 9 days. Leaves two and three of the plants were visually rated for disease (3) 13 days after inoculation. Control plants were disease free. The most susceptible reactions were observed on cvs. Norteña Daymán, MUSA 936, and line CLE 230 (Uruguay). Symptoms were similar in shape and size to those observed in the fields. The most resistant infection types were observed on several Uruguayan and North Dakota advanced lines. The fungus was consistently reisolated from inoculated plants. On the basis of morphology and symptoms produced, the pathogen was identified (2) as P. teres. f. sp. maculata Smedeg. To our knowledge, this is the first report of this fungus causing spot-like symptoms of net blotch in Uruguay. References: (1) M. B. Ellis. Dematiaceous hyphomycetes, CABI, Oxon, UK, 1971. (2) V. Smedergaard-Petersen. Pages 124–144 in: R. Vet. Agr. Univ. Yearbook, Copenhagen, 1971. (3) A. Tekauz. Can. J. Plant Pathol.7:181, 1985.


2003 ◽  
Vol 56 ◽  
pp. 251-256 ◽  
Author(s):  
M.G. Cromey ◽  
R.A. Parkes

Drechslera teres f sp teres causes net blotch of barley While it is usually controlled adequately by fungicides episodes of fungicide insensitivity have led to periodic outbreaks of severe net blotch in New Zealand Disease resistance is an alternative control method but resistance may not be durable due to the development and spread of new pathotypes of D teres In New Zealand the use of disease resistance has been hampered by a lack of information on pathogenic variation in D teres Samples of net blotch were collected from barley crops and field trials and single conidium isolates of D teres f sp teres were produced These were inoculated onto internationally recognised differential barley cultivars Disease reactions were assessed and pathogenic variation in the New Zealand D teres population determined Some differential cultivars were resistant to all isolates tested but others were susceptible to one or more of the isolates While pathogenic variation was identified in the New Zealand D teres f sp teres population the extent of variation was less than indicated in some overseas studies


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