Identification of a new resistance gene to septoria tritici blotch in wheat

Door het screenen van lijnen en wilde verwanten van tarwe, is een nieuw resistentiegen tegen STB (Septoria tritici blotch) gevonden

A first genome assembly of the barley fungal pathogen Pyrenophora teres f. teres

Background: Pyrenophora teres f. teres is a necrotrophic fungal pathogen and the cause of one of barley's most important diseases, net form of net blotch. Here we report the first genome assembly for this species based solely on short Solexa sequencing reads of isolate 0-1. The assembly was validated by comparison to BAC sequences, ESTs, orthologous genes and by PCR, and complemented by cytogenetic karyotyping and the first genome-wide genetic map for P. teres f. teres. Results: The total assembly was 41.95 Mbp and contains 11,799 gene models of 50 amino acids or more. Comparison against two sequenced BACs showed that complex regions with a high GC content assembled effectively. Electrophoretic karyotyping showed distinct chromosomal polymorphisms between isolates 0-1 and 15A, and cytological karyotyping confirmed the presence of at least nine chromosomes. The genetic map spans 2477.7 cM and is composed of 243 markers in 25 linkage groups, and incorporates simple sequence repeat markers developed from the assembly. Among predicted genes, non-ribosomal peptide synthetases and efflux pumps in particular appear to have undergone a P. teres f. teres-specific expansion of non-orthologous gene families. Conclusions: This study demonstrates that paired-end Solexa sequencing can successfully capture coding regions of a filamentous fungal genome. The assembly contains a plethora of predicted genes that have been implicated in a necrotrophic lifestyle and pathogenicity and presents a significant resource for examining the bases for P. teres f. teres pathogenicity

Identification and chromosomal location of major genes for resistance to Pyrenophora teres in a doubled-haploid barley population

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

Pyrenophora teres: profile of an increasingly damaging barley pathogen

Pyrenophora teres, causal agent of net blotch of barley, exists in two forms, designated P. teres f. teres and P. teres f. maculata, which induce net form net blotch (NFNB) and spot form net blotch (SFNB), respectively. Significantly more work has been performed on the net form than on the spot form although recent activity in spot form research has increased because of epidemics of SFNB in barley-producing regions. Genetic studies have demonstrated that NFNB resistance in barley is present in both dominant and recessive forms, and that resistance/susceptibility to both forms can be conferred by major genes, although minor quantitative trait loci have also been identified. Early work on the virulence of the pathogen showed toxin effector production to be important in disease induction by both forms of pathogen. Since then, several laboratories have investigated effectors of virulence and avirulence, and both forms are complex in their interaction with the host. Here, we assemble recent information from the literature that describes both forms of this important pathogen and includes reports describing the host-pathogen interaction with barley. We also include preliminary findings from a genome sequence survey.Taxonomy: Pyrenophora teres Drechs. Kingdom Fungi; Phylum Ascomycota; Subphylum Pezizomycotina; Class Dothideomycete; Order Pleosporales; Family Pleosporaceae; Genus Pyrenophora, form teres and form maculata.Identification: To date, no clear morphological or life cycle differences between the two forms of P. teres have been identified, and therefore they are described collectively. Towards the end of the growing season, the fungus produces dark, globosely shaped pseudothecia, about 1-2 mm in diameter, on barley. Ascospores measuring 18-28 μm × 43-61 μm are light brown and ellipsoidal and often have three to four transverse septa and one or two longitudinal septa in the median cells. Conidiophores usually arise singly or in groups of two or three and are lightly swollen at the base. Conidia measuring 30-174 μm × 15-23 μm are smoothly cylindrical and straight, round at both ends, subhyaline to yellowish brown, often with four to six pseudosepta. Morphologically, P. teres f. teres and P. teres f. maculata are indistinguishable.Host range: Comprehensive work on the host range of P. teres f. teres has been performed; however, little information on the host range of P. teres f. maculata is available. Hordeum vulgare and H. vulgare ssp. spontaneum are considered to be the primary hosts for P. teres. However, natural infection by P. teres has been observed in other wild Hordeum species and related species from the genera Bromus, Avena and Triticum, including H. marinum, H. murinum, H. brachyantherum, H. distichon, H. hystrix, B. diandrus, A. fatua, A. sativa and T. aestivum (Shipton ., 1973, Rev. Plant Pathol. 52:269-290). In artificial inoculation experiments under field conditions, P. teres f. teres has been shown to infect a wide range of gramineous species in the genera Agropyron, Brachypodium, Elymus, Cynodon, Deschampsia, Hordelymus and Stipa (Brown et al., 1993, Plant Dis. 77:942-947). Additionally, 43 gramineous species were used in a growth chamber study and at least one of the P. teres f. teres isolates used was able to infect 28 of the 43 species tested. However, of these 28 species, 14 exhibited weak type 1 or 2 reactions on the NFNB 1-10 scale (Tekauz, 1985). These reaction types are small pin-point lesions and could possibly be interpreted as nonhost reactions. In addition, the P. teres f. teres host range was investigated under field conditions by artificially inoculating 95 gramineous species with naturally infected barley straw. Pyrenophora teres f. teres was re-isolated from 65 of the species when infected leaves of adult plants were incubated on nutrient agar plates; however, other than Hordeum species, only two of the 65 host species exhibited moderately susceptible or susceptible field reaction types, with most species showing small dark necrotic lesions indicative of a highly resistant response to P. teres f. teres. Although these wild species have the potential to be alternative hosts, the high level of resistance identified for most of the species makes their role as a source of primary inoculum questionable.Disease symptoms: Two types of symptom are caused by P. teres. These are net-type lesions caused by P. teres f. teres and spot-type lesions caused by P. teres f. maculata. The net-like symptom, for which the disease was originally named, has characteristic narrow, dark-brown, longitudinal and transverse striations on infected leaves. The spot form symptom consists of dark-brown, circular to elliptical lesions surrounded by a chlorotic or necrotic halo of varying width

Mating Type Locus-Specific Polymerase Chain Reaction Markers for Differentiation of Pyrenophora teres f. teres and P. teres f. maculata, the Causal Agents of Barley Net Blotch

Lu S Platz G J Edwards M C and Friesen T L 2010 Mating type locus specific polymerase chain reaction markers for differentiation of Pyrenophora teres f teres and P teres f maculata the causal agents of barley net blotch Phytopathology 100 1298-1306 Fourteen single nucleotide polymorphisms (SNPs) were identified at the mating type (MAT) loci of Pyrenophora teres f teres (Ptt) which causes net form (NF) net blotch and P tens f maculata (Ptm) which causes spot form (SF) net blotch of barley MAT specific SNP primers were developed for polymerase chain reaction (PCR) and the two forms were differentiated by distinct PCR products PttMATI 1 (1 143 bp) and PttMATI 2 (1 421 bp) for NF MAT1 1 and MATI 2 isolates PanMATI (194 bp) and PtmMAT1 2 (939 bp) for SF MAT1 1 and MAT1 2 isolates respectively Specificity was validated using 37 NF and 17 SF isolates collected from different geographic regions Both MAT1 and MAT1 2 SNP primers retained respective specificity when used in duplex PCR No cross reactions were observed with DNA from P graminea P trawl repent is or other ascomycetes or barley Single or mixed infections of the two different forms were also differentiated This study provides the first evidence that the limited SNPs at the MAT locus are sufficient for distinguishing closely related heterothallic ascomycetes at subspecies levels thus allowing pathogenicity and mating type characteristics of the fungus to be determined simultaneously Methods presented will facilitate pathogen detection disease management and epidemiological studie

Mating Type Locus-Specific Polymerase Chain Reaction Markers for Differentiation of Pyrenophora teres f. teres and P. teres f. maculata, the Causal Agents of Barley Net Blotch

Lu S Platz G J Edwards M C and Friesen T L 2010 Mating type locus specific polymerase chain reaction markers for differentiation of Pyrenophora teres f teres and P teres f maculata the causal agents of barley net blotch Phytopathology 100 1298-1306 Fourteen single nucleotide polymorphisms (SNPs) were identified at the mating type (MAT) loci of Pyrenophora teres f teres (Ptt) which causes net form (NF) net blotch and P tens f maculata (Ptm) which causes spot form (SF) net blotch of barley MAT specific SNP primers were developed for polymerase chain reaction (PCR) and the two forms were differentiated by distinct PCR products PttMATI 1 (1 143 bp) and PttMATI 2 (1 421 bp) for NF MAT1 1 and MATI 2 isolates PanMATI (194 bp) and PtmMAT1 2 (939 bp) for SF MAT1 1 and MAT1 2 isolates respectively Specificity was validated using 37 NF and 17 SF isolates collected from different geographic regions Both MAT1 and MAT1 2 SNP primers retained respective specificity when used in duplex PCR No cross reactions were observed with DNA from P graminea P trawl repent is or other ascomycetes or barley Single or mixed infections of the two different forms were also differentiated This study provides the first evidence that the limited SNPs at the MAT locus are sufficient for distinguishing closely related heterothallic ascomycetes at subspecies levels thus allowing pathogenicity and mating type characteristics of the fungus to be determined simultaneously Methods presented will facilitate pathogen detection disease management and epidemiological studie

Effect of substituting spray-dried plasma protein for milk products in starter pig diets

Two growth trials utilizing 444 weaned pigs were conducted to determine the efficacy of substituting spray-dried porcine plasma protein (PP) for dried skim milk (DSM) and/or dried whey (DW) in starter pig diets. Trial 1 was a field study in which 240 pigs were fed either a control diet containing 20% DSM and 20% DW during phase I (0 to 14 d postweaning) and 15% DW and 5% select menhaden fishmeal in phase II (14 to 28 d postweaning) of the 28 d trial. Plasma protein was substituted on a lysine basis for DSM in the phase I diet and for DW in the phase IT diet. Diets were isolactose in both phases. Pigs fed the diets containing PP grew faster and consumed more feed from d 0 to 7 than pigs fed the control. However, pigs fed the control diet compensated during wk 2 to achieve equal performance during phase 1. No treatment differences were detected during phase II or in overall performance. In Trial 2, 204 pigs were allotted to one of the following treatments: 1) control diet containing 20% DSM and 20& DW, 2) as 1 with casein replacing soybean meal (lysine basis; all milk protein), 3) as 1 with PP and lactose replacing 20% DSM (lysine and lactose basis), 4) as 3 with starch replacing lactose (wt/wt), 5) as 1 with PP and lactose replacing DSM and DW (lysine and lactose basis), 6) as 5 with starch replacing lactose, 7) corn-soybean meal plus 20% DW Pigs fed diets containing PP grew faster and consumed more feed than pigs fed the control, casein, or 20% DW diets from 0 to 14 d postweaning. Similarly, overall gains were significantly greater for pigs fed PP than pigs fed the control, casein, and DW diets. Also, pigs fed PP consumed greater quantities of feed over the entire trial than those pigs fed the control or casein diets. Serum was collected on d 13 and analyzed for blood urea nitrogen. Blood urea N was higher for pigs fed PP, indicating that the amino acids in PP are more available to the pig, but not all are utilized for protein synthesis. Skinfold thickness was measured on d 7 following intradermal injections of protein extracts of PP soybean meal and DSM; these data indicate that PP and DSM cause extremely small changes in skinfold thickness compared to soybean proteins. Based on the results of these experiments, PP has an equal, if not better, feeding value than milk protein

Pivoting from Arabidopsis to wheat to understand how agricultural plants integrate responses to biotic stress

International audienceIn this review, we argue for a research initiative on wheat's responses to biotic stress. One goal is to begin a conversation between the disparate communities of plant pathology and entomology. Another is to understand how responses to a variety of agents of biotic stress are integrated in an important crop. We propose gene-for-gene interactions as the focus of the research initiative. On the parasite's side is an Avirulence (Avr) gene that encodes one of the many effector proteins the parasite applies to the plant to assist with colonization. On the plant's side is a Resistance (R) gene that mediates a surveillance system that detects the Avr protein directly or indirectly and triggers effector-triggered plant immunity. Even though arthropods are responsible for a significant proportion of plant biotic stress, they have not been integrated into important models of plant immunity that come from plant pathology. A roadblock has been the absence of molecular evidence for arthropod Avr effectors. Thirty years after this evidence was discovered in a plant pathogen, there is now evidence for arthropods with the cloning of the Hessian fly's vH13 Avr gene. After reviewing the two models of plant immunity, we discuss how arthropods could be incorporated. We end by showing features that make wheat an interesting system for plant immunity, including 479 resistance genes known from agriculture that target viruses, bacteria, fungi, nematodes, insects, and mites. It is not likely that humans will be subsisting on Arabidopsis in the year 2050. It is time to start understanding how agricultural plants integrate responses to biotic stress