Virulence of Icelandic Pyrenophora teres f. teres populations and resistance of Icelandic spring barley lines

The causal agent of the barley net blotch disease, Pyrenophora teres, is known for its high level of diversity due to sexual reproduction. Different pathotypes, defined by a virulence combination, even within the same fields are frequently found and virulence between locations can vary considerably. Evaluation of virulence patterns of a pathogen population is essential for breeding resistant cultivars suitable for specific locations. To identify virulence patterns in Icelandic Pyrenophora teres f. teres (Ptt) isolates, twenty single spore isolates of Ptt were collected from seven locations in Iceland and analysed with AFLP markers. Principle Coordinate Analysis (PCoA) revealed Icelandic Ptt isolates clustering away from reference isolates from Austria, Finland, Sweden, Switzerland, UK, and USA. Hierarchical clustering grouped the Icelandic isolates into three distinct groups. Furthermore, the virulence of these twenty isolates was tested on 16 barley differential lines and revealed high variation in their virulence. Twenty-one barley cultivars commonly used in Iceland showed high susceptibility towards inoculation with Icelandic Ptt isolates.

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

<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>

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

<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>

Breeding barley for durable resistance to net and spot forms of net blotch

This chapter focuses on breeding barley for durable resistance to net and spot forms of net blotch. It starts by reviewing how Pyrenophora teres f. teres can cause net form net blotch. The chapter then goes on to examine the molecular markers that can be identified to provide resistances to net form net blotch. A section on the population dynamics of barley–P. teres f. teres interactions is also provided. The chapter also reviews how breeding crops with specific genes can help to create durable resistance to net form blotch. It moves on to discuss how Pyrenophora teres Drechs. f. maculata can cause spot form net blotch and how identifying specific molecular markers can help provide resistance to this form of net blotch. The chapter concludes by highlighting the importance of combining durable resistance to both forms of net blotch.

Genetic mapping of host resistance to the Pyrenophora teres f. maculata isolate 13IM8.3

Spot form net blotch (SFNB), caused by the necrotrophic fungal pathogen Pyrenophora teres f. maculata (Ptm), is a foliar disease of barley that results in significant yield losses in major growing regions worldwide. Understanding the host-parasite interactions between pathogen virulence/avirulence genes and the corresponding host susceptibility/resistance genes is important for the deployment of genetic resistance against SFNB. Two recombinant inbred mapping populations were developed to characterize genetic resistance/susceptibility to the Ptm isolate 13IM8.3, which was collected from Idaho (ID). An Illumina Infinium array was used to produce a genome-wide marker set. Quantitative trait loci (QTL) analysis identified ten significant resistance/susceptibility loci, with two of the QTL being common to both populations. One of the QTL on 5H appears to be novel, while the remaining loci have been reported previously. Single nucleotide polymorphisms (SNPs) closely linked to or delimiting the significant QTL have been converted to user-friendly markers. Loci and associated molecular markers identified in this study will be useful in genetic mapping and deployment of the genetic resistance to SFNB in barley.