Infection of wheat seed by Pyrenophora tritici-repentis

1994 ◽  
Vol 72 (4) ◽  
pp. 510-519 ◽  
Author(s):  
A. M. C. Schilder ◽  
G. C. Bergstrom
Keyword(s):  
New York ◽  
Flag Leaf ◽  
Infection Process ◽  
Tan Spot ◽  
Seed Infection ◽  
Wheat Seed ◽  
Inoculum Concentration ◽  
Pyrenophora Tritici Repentis ◽  
Key Words Wheat ◽  
Late Stages

The seed infection process of Pyrenophora tritici-repentis, incitant of tan spot of wheat, was investigated, as were several influencing factors. Following inoculation of the wheat spike, P. tritici-repentis gained access to the seed by first colonizing the glume, lemma, or palea. Seed infection was first observed 3 d after inoculation, and infection incidence increased with time and with inoculum concentration. Wheat seeds were susceptible to infection by this fungus throughout most of their development, although inoculation at the milk stage resulted in the highest percentage of infected seeds. Susceptibility to foliar infection by P. tritici-repentis was not a good predictor of susceptibility to seed infection in four wheat cultivars tested in a glasshouse experiment, except perhaps in ‘BR 8’, which was significantly less susceptible than the other cultivars at early and late stages of seed development. In a field experiment, wheat seed infection by P. tritici-repentis occurred primarily after the early dough stage and was positively correlated with tan spot severity on the flag leaf shortly after anthesis. Key words: wheat, Pyrenophora tritici-repentis, Drechslera tritici-repentis, tan spot, seed infection, New York.

scholarly journals Evaluation of Pyrenophora tritici-repentis Infection of Wheat Heads

Agriculture ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 417
Author(s):  
Pao Theen See ◽  
Nikki Schultz ◽  
Caroline S. Moffat
Keyword(s):  
Recovery Rate ◽  
Pcr Detection ◽  
Tan Spot ◽  
Spore Suspension ◽  
Etiological Agent ◽  
Seed Infection ◽  
Grain Development ◽  
Spot Disease ◽  
Pyrenophora Tritici Repentis ◽  
Tan Spot Disease

The incidence of wheat head infection by Pyrenophora tritici-repentis (Ptr), the etiological agent of tan spot disease, was evaluated during grain development in a glasshouse experiment. Heads artificially inoculated with a Ptr spore suspension developed widespread brown spots across the spikelets, and mycelia and conidophores were observed on glumes and awns. Seeds of heavily infected heads were darkened and shrivelled, but no red smudge symptoms were apparent. The recovery rate of Ptr isolates from the inoculated wheat heads was low, and colonies that were re-isolated displayed an irregular morphology with reddish mycelia when grown on agar plates. The presence of Ptr on inoculated wheat heads was assessed directly via PCR detection, and a limitation of Ptr hyphae to proliferate beyond the point of contact of spore inoculum on floret tissues was observed. The systemic transmission of Ptr from infected seeds was minimal; however, saprophytic growth of the pathogen occurred on the senescing leaves of wheat plants grown from inoculated seeds. Thus, even though Ptr seed infection is not as common as foliar infection, infected seeds are still a source of disease inoculum and screening for pathogen contamination is advisable.

scholarly journals A Rainfall-Based Model for Predicting the Regional Incidence of Wheat Seed Infection by Stagonospora nodorum in New York

2002 ◽  
Vol 92 (5) ◽  
pp. 511-518 ◽  
Author(s):  
Denis A. Shah ◽  
Gary C. Bergstrom
Keyword(s):  
New York ◽  
Simple Model ◽  
Stagonospora Nodorum ◽  
Seed Infection ◽  
Independent Data ◽  
Wheat Seed ◽  
Binomial Probability ◽  
Actual Distribution ◽  
Central New York ◽  
Distribution Parameters

Our goal was to develop a simple model for predicting the incidence of wheat seed infection by Stagonospora nodorum across western and central New York in any given year. The distribution of the incidence of seed infection by S. nodorum across the region was well described by the beta-binomial probability distribution (parameters p and θ). Mean monthly rainfalls in May and in June across western and central New York were used to predict p. The binary power law was used to predict θ. The model was validated with independent data collected from New York. The predicted distribution of seed infection incidence was not statistically different from the actual distribution of the incidence of seed infection.

Red smudge in durum wheat reduces seedling vigour

1996 ◽  
Vol 76 (2) ◽  
pp. 321-324 ◽  
Author(s):  
M. R. Fernandez ◽  
R. M. DePauw ◽  
J. M. Clarke ◽  
L. P. Lefkovitch
Keyword(s):  
Durum Wheat ◽  
Triticum Turgidum ◽  
Tan Spot ◽  
Wheat Seed ◽  
Seedling Vigour ◽  
Pyrenophora Tritici Repentis ◽  
Percent Germination ◽  
Seminal Roots ◽  
Early Seedling ◽  
Early Seedling Development

The effect of red smudge, caused by Pyrenophora tritici-repentis (Died.) Drechs, on germination and early seedling development of four durum wheat (Triticum turgidum L. var. durum Desf.) cultivars was examined using artificially and naturally infected seeds. Rate of germination was similar for red smudged and healthy seeds. Percent germination of naturally infected, but not of artificially infected seeds, was lower for the red smudge than for the control treatments. The number of seminal roots was also lower for the naturally infected than for the control seeds. Lengths of the longest seminal root and of the coleoptile at 12 d were greater in the control than in the disease treatments, regardless of whether the seeds were naturally or artificially infected. It was concluded that red smudge of durum wheat seed reduced seedling vigour. There was transmission of P. tritici-repentis to the coleoptile but not to the true leaves. Key words: Red smudge, tan spot transmission, seedling vigour, durum wheat

scholarly journals First Report of Tan Spot of Wheat Caused by Pyrenophora tritici-repentis in the Pacific Northwest

Plant Disease ◽  
2003 ◽  
Vol 87 (2) ◽  
pp. 203-203
Author(s):  
T. L. Peever ◽  
T. D. Murray
Keyword(s):  
New York ◽  
Pacific Northwest ◽  
Sequence Similarity ◽  
Triticum Aestivum L ◽  
Tan Spot ◽  
Morphological Description ◽  
Morphological Identification ◽  
First Report ◽  
Pyrenophora Tritici Repentis ◽  
The Pacific

In late May 2001, lesions resembling tan spot were observed on lower leaves of winter wheat (Triticum aestivum L.) in early boot stage in Nez Perce County, ID. Abundant sporulation was observed from tan lesions with chlorotic haloes after 2 days incubation in a moist chamber at room temperature. Conidia were multicelled, straw colored, approximately 100 × 15 µm, rounded at the apex, and borne singly on dark brown conidiophores. The fungus fit the morphological description of Drechslera tritici-repentis (Died.) Shoemaker, the anamorphic state of Pyrenophora tritici-repentis (Died.) Drechs. (2). Three single-conidial isolates were sampled from infected plants in a 5 × 1 m area of the affected field and induced to sporulate. Two of the isolates were used to spray-inoculate 3-week-old susceptible wheat (cv. Madsen) in the greenhouse (one plant per isolate, 1 × 105 conidia/ml), and tan spot lesions were apparent 3 to 5 days after inoculation with both isolates. DNA was extracted from all three isolates, and the entire nuclear ribosomal internal transcribed spacer (ITS) was amplified with ITS1 and ITS4 primers (4). Similarly, 610 bp of the 5′ end of the glyceraldehyde-3-phosphate-dehydrogenase gene (gpd) was amplified with gpd-1 and gpd-2 primers (1). ITS and gpd amplicons were direct-sequenced on both strands, and alignment revealed that all three isolates were identical for both regions. A BLAST search of the NCBI database with the ITS sequence revealed P. tritici-repentis accessions AY004808 and AF071348 and D. tritici-repentis accession AF163060 as the closest matches with 100, 99.8, and 98.8% sequence similarity, respectively. A similar search with the gpd sequence revealed P. tritici-repentis accessions AY004838 and AF081370 and P. bromi accession AY004839 as the closest matches with 100, 100, and 99.0% sequence similarity, respectively. These results, coupled with the morphological identification and inoculation results, confirm the identity of the fungus as P. tritici-repentis. Although reported on other grass hosts in the region (3), to our knowledge, this is the first report of tan spot of wheat in the Pacific Northwest. This disease has been of little concern to wheat producers in the Pacific Northwest due to low rainfall and relative humidity during the growing season. References: (1) M. L. Berbee et al. Mycologia 91:964, 1999. (2) M. B. Ellis, Dematiaceous Hyphomycetes. CMI, Kew, Surrey, UK. 1971. (3) R. Sprague. Diseases of Cereals and Grasses in North America (Fungi, Except Smuts and Rusts). Ronald Press Co. New York, 1950. (4) T. J. White et al. Pages 315–322 in: PCR Protocols: A Guide to Methods and Applications. Academic Press Inc., New York, 1990.

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

2006 ◽  
Vol 96 (8) ◽  
pp. 885-889 ◽  
Author(s):  
P. K. Singh ◽  
J. L. Gonzalez-Hernandez ◽  
M. Mergoum ◽  
S. Ali ◽  
T. B. Adhikari ◽  
...  
Keyword(s):  
Resistance Genes ◽  
Molecular Mapping ◽  
Recombinant Inbred Lines ◽  
Tetraploid Wheat ◽  
Recessive Gene ◽  
Tan Spot ◽  
Substitution Lines ◽  
Disease Reaction ◽  
Pyrenophora Tritici Repentis ◽  
The Cross

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 F2 generation and of the F4:5 and F6:7 families indicated that a single recessive gene controlled resistance to necrosis induced by race 3 in the cross studied.

scholarly journals Expression of the ToxA and PtrPf2 genes of the phytopathogenic fungus Pyrenophora tritici-repentis at the beginning of the infection process

2019 ◽  
Author(s):  
Nina V. Mironenko ◽  
Alexandra S. Orina ◽  
Nadezhda M. Kovalenko
Keyword(s):  
Transcription Factor ◽  
Wheat Variety ◽  
Infection Process ◽  
Phytopathogenic Fungus ◽  
In Planta ◽  
Effector Gene ◽  
Pyrenophora Tritici Repentis ◽  
Wheat Leaves ◽  
Necrotrophic Effector

This study shows that the necrotrophic effector gene ToxA is differentially expressed in isolates of P. tritici-repentis fungus at different time periods after inoculation of the wheat variety Glenlea which has the gene Tsn1 controlling sensitivity to the necrosis inducing toxin Ptr ToxA. Two P. tritici-repentis isolates with different ability to cause necrosis on the leaves of Glenlea variety (nec + and nec-) and with different expression level of ToxA and gene of factor transcription PtrPf2 in vitro were used for analysis. Isolates of P. tritici-repentis are characterized by the differential expression of ToxA in planta. The expression of the ToxA gene in P. tritici-repentis ToxA+ isolates significantly increased when infected the wheat leaves compared to ToxA expression results obtained in vitro. The levels of ToxA expression in both isolates differed significantly after 24, 48 and 96 hours after inoculation, however, the dynamics of the trait change over time were similar. However, the highest ToxA expression in the virulent (nec+) isolate in contrast with the avirulent (nec-) isolate was observed at a point of 48 hours. Whereas the expression of regulating transcription factor PtrPf2 in planta differed imperceptibly from expression in vitro throughout the observation period. Obviously, the role of the fungal transcription factor in regulating the effector gene expression weakens in planta, and other mechanisms regulating the expression of pathogen genes at the biotrophic stage of the disease develop.

Characterization of Pyrenophora tritici-repentis in Tunisia and Comparison with a Global Pathogen Population

Plant Disease ◽  
2021 ◽  
Author(s):  
Marwa Laribi ◽  
Alireza Akhavan ◽  
Sarrah M'Barek ◽  
Amor Yahyaoui ◽  
Stephen Ernest Strelkov ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Geographic Origin ◽  
Tan Spot ◽  
Pcr Analysis ◽  
Group Method ◽  
Region Of Origin ◽  
Pyrenophora Tritici Repentis ◽  
Pair Group ◽  
Necrotrophic Effector

Pyrenophora tritici-repentis (Ptr) causes tan spot, an important foliar disease of wheat. A collection of Ptr isolates from Tunisia, located in one of the main secondary centers of diversification of durum wheat, was tested for phenotypic race classification based on virulence on a host differential set, and for the presence of the necrotrophic effector (NE) genes ToxA, ToxB , and toxb by PCR analysis. While races 2, 4, 5, 6, 7, and 8 were identified according to their virulence phenotypes, PCR testing indicated the presence of ‘atypical’ isolates that induced necrosis on the wheat differential ‘Glenlea’, but lacked the expected ToxA gene, suggesting the involvement of other NEs in the Ptr/wheat interaction. Genetic diversity and the Ptr population structure were explored further by examining 59 Tunisian isolates and 35 isolates from Algeria, Azerbaijan, Canada, Iran, and Syria using 24 simple sequence repeat markers. Average genetic diversity, overall gene flow and percentage polymorphic loci were estimated as 0.58, 2.09 and 87%, respectively. Analysis of molecular variance showed that 81% of the genetic variance occurred within populations and 19% between populations. Cluster analysis by the unweighted pair group method indicated that ToxB- isolates grouped together and were distantly related to ToxB+ isolates. Based on Nei’s analysis, the global collection clustered into two distinct groups according to their region of origin. The results suggest that both geographic origin and the host-specificity imposed by different NEs can lead to differentiation among Ptr populations.

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