scholarly journals Resistance to Tan Spot and Stagonospora nodorum Blotch in Wheat-Alien Species Derivatives

Plant Disease ◽  
2008 ◽  
Vol 92 (1) ◽  
pp. 150-157 ◽  
Author(s):  
R. E. Oliver ◽  
X. Cai ◽  
R.-C. Wang ◽  
S. S. Xu ◽  
T. L. Friesen

Tan spot (caused by Pyrenophora tritici-repentis) and Stagonospora nodorum blotch (SNB) (caused by Stagonospora nodorum) are destructive fungal diseases of wheat (Triticum aestivum) throughout the world. Host plant resistance is thought to be an efficient and economical method of control. The objective of the present study was to identify novel sources of tan spot and SNB resistance in wheat genotypes derived from the crosses between wheat and alien species. Evaluations were conducted at the seedling stage in a growth chamber with 100% relative humidity. For each genotype, three replications were used for each disease. Among the 199 wheat-alien species derivatives evaluated, 65 exhibited resistance to tan spot and 30 showed resistance to SNB similar to BR34, a Brazilian wheat line used as the resistant control. Eleven derivatives were resistant to both diseases. Reactions of the derivatives and their respective wheat parents to tan spot and SNB suggest that resistance genes in the derivatives are derived from alien species. These derivatives can serve as desirable bridges for introgression of resistance genes from alien species to cultivated wheat, and could contribute novel and effective tan spot and SNB resistance to wheat breeding.

Plant Disease ◽  
2015 ◽  
Vol 99 (10) ◽  
pp. 1333-1341 ◽  
Author(s):  
Zhaohui Liu ◽  
Ibrahim El-Basyoni ◽  
Gayan Kariyawasam ◽  
Guorong Zhang ◽  
Allan Fritz ◽  
...  

Tan spot and Stagonospora nodorum blotch (SNB), often occurring together, are two economically significant diseases of wheat in the Northern Great Plains of the United States. They are caused by the fungi Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively, both of which produce multiple necrotrophic effectors (NE) to cause disease. In this work, 120 hard red winter wheat (HRWW) cultivars or elite lines, mostly from the United States, were evaluated in the greenhouse for their reactions to the two diseases as well as NE produced by the two pathogens. One P. nodorum isolate (Sn4) and four Pyrenophora tritici-repentis isolates (Pti2, 331-9, DW5, and AR CrossB10) were used separately in the disease evaluations. NE sensitivity evaluation included ToxA, Ptr ToxB, SnTox1, and SnTox3. The numbers of lines that were rated highly resistant to individual isolates ranged from 11 (9%) to 30 (25%) but only six lines (5%) were highly resistant to all isolates, indicating limited sources of resistance to both diseases in the U.S. adapted HRWW germplasm. Sensitivity to ToxA was identified in 83 (69%) of the lines and significantly correlated with disease caused by Sn4 and Pti2, whereas sensitivity to other NE was present at much lower frequency and had no significant association with disease. As expected, association mapping located ToxA and SnTox3 sensitivity to chromosome arm 5BL and 5BS, respectively. A total of 24 potential quantitative trait loci was identified with −log (P value) > 3.0 on 12 chromosomes, some of which are novel. This work provides valuable information and tools for HRWW production and breeding in the Northern Great Plains.


2006 ◽  
Vol 96 (8) ◽  
pp. 885-889 ◽  
Author(s):  
P. K. Singh ◽  
J. L. Gonzalez-Hernandez ◽  
M. Mergoum ◽  
S. Ali ◽  
T. B. Adhikari ◽  
...  

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.


2007 ◽  
Vol 114 (5) ◽  
pp. 855-862 ◽  
Author(s):  
W. Tadesse ◽  
M. Schmolke ◽  
S. L. K. Hsam ◽  
V. Mohler ◽  
G. Wenzel ◽  
...  

2009 ◽  
Vol 99 (8) ◽  
pp. 906-912 ◽  
Author(s):  
Justin D. Faris ◽  
Timothy L. Friesen

The wheat Tsn1 gene on chromosome 5B confers sensitivity to a host-selective toxin produced by the pathogens that cause tan spot and Stagonospora nodorum blotch (SNB) known as Ptr ToxA and SnToxA, respectively (hereafter referred to as ToxA). A compatible Tsn1–ToxA interaction is known to play a major role in conferring susceptibility of hexaploid (common) wheat to SNB. However, a recent study by another group suggested that the Tsn1–ToxA interaction was not relevant in conferring susceptibility of the tetraploid (durum) wheat cv. Langdon (LDN). Here, we reevaluated the role of the Tsn1–ToxA interaction in governing SNB susceptibility using the same mapping population and Stagonospora nodorum isolate (Sn2000) as were used in the previous study. Results of our quantitative trait locus analysis showed that the Tsn1 locus accounted for 95% of the variation in SNB. In addition, inoculation of the mapping population with two ToxA-knockout strains of Sn2000 revealed that the entire population was resistant. Furthermore, several LDN Tsn1-disrupted mutants were evaluated and found to be resistant to SNB. Together, these results prove unequivocally that Tsn1 is the only factor present along chromosome 5B that governs response to SNB in this population and that a compatible Tsn1–ToxA interaction is necessary for the manifestation of disease. Therefore, the results from the previous study are refuted.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jyotirmoy Halder ◽  
Jinfeng Zhang ◽  
Shaukat Ali ◽  
Jagdeep S. Sidhu ◽  
Harsimardeep S. Gill ◽  
...  

Abstract Background In the late 1920s, A. E. Watkins collected about 7000 landrace cultivars (LCs) of bread wheat (Triticum aestivum L.) from 32 different countries around the world. Among which 826 LCs remain viable and could be a valuable source of superior/favorable alleles to enhance disease resistance in wheat. In the present study, a core set of 121 LCs, which captures the majority of the genetic diversity of Watkins collection, was evaluated for identifying novel sources of resistance against tan spot, Stagonospora nodorum blotch (SNB), and Fusarium Head Blight (FHB). Results A diverse response was observed in 121 LCs for all three diseases. The majority of LCs were moderately susceptible to susceptible to tan spot Ptr race 1 (84%) and FHB (96%) whereas a large number of LCs were resistant or moderately resistant against tan spot Ptr race 5 (95%) and SNB (54%). Thirteen LCs were identified in this study could be a valuable source for multiple resistance to tan spot Ptr races 1 and 5, and SNB, and another five LCs could be a potential source for FHB resistance. GWAS analysis was carried out using disease phenotyping score and 8807 SNPs data of 118 LCs, which identified 30 significant marker-trait associations (MTAs) with -log10 (p-value) > 3.0. Ten, five, and five genomic regions were found to be associated with resistance to tan spot Ptr race 1, race 5, and SNB, respectively in this study. In addition to Tsn1, several novel genomic regions Q.Ts1.sdsu-4BS and Q.Ts1.sdsu-5BS (tan spot Ptr race 1) and Q.Ts5.sdsu-1BL, Q.Ts5.sdsu-2DL, Q.Ts5.sdsu-3AL, and Q.Ts5.sdsu-6BL (tan spot Ptr race 5) were also identified. Our results indicate that these putative genomic regions contain several genes that play an important role in plant defense mechanisms. Conclusion Our results suggest the existence of valuable resistant alleles against leaf spot diseases in Watkins LCs. The single-nucleotide polymorphism (SNP) markers linked to the quantitative trait loci (QTLs) for tan spot and SNB resistance along with LCs harboring multiple disease resistance could be useful for future wheat breeding.


2019 ◽  
Vol 22 (8) ◽  
pp. 978-986 ◽  
Author(s):  
A. М. Kokhmetova ◽  
Sh. Ali ◽  
Z. Sapakhova ◽  
M. N. Atishova

Pyrenophora tritici-repentis(Ptr) is the causative agent of tan spot, one of the yield limiting diseases of wheat, rapidly increasing in wheat growing countries including Kazakhstan. The aim of this study was the identifcation of wheat genotypes with resistance to Ptr race 1 and race 5 and their host­selective effectors (toxins) Ptr ToxA and Ptr ToxB. A common wheat collection of 41 accessions (38 experimental and 3 controls) was characterized using the molecular markersXfcp623andXBE444541, diagnostic for theTsn1andTsc2genes conferring sensitivity to fungal toxins. The coincidence of the markerXBE444541with resistance to race 5 was 92.11 %, and with Ptr ToxB, 97.37 %. Genotyping results using the markerXfcp623confrmed the expected response to Ptr ToxA; the presence/absence of the markerXfcp623completely (100 %) coincided with sensitivity/resistance to race 1 and Ptr ToxA. This demonstrates the reliability of the diagnostic markerXfcp623for identifying wheat genotypes with resistance to the fungus and insensitivity to Ptr ToxA. The study of the reaction of wheat germplasm to the fungal inoculation and toxin infltration showed that out of 38 genotypes analyzed 30 (78 %) exhibited resistance to both race 1 and race 5, and insensitivity to toxins Ptr ToxA and ToxB. Of most signifcant interest are eight wheat genotypes that showed resistance/insensitivity both to the two races and two toxins. The results of phenotyping were reconfrmed by the molecular markers used in this study. Sensitivity to Ptr ToxB is not always correlated with susceptibility to race 5 and is dependent on the host’s genetic background of the wheat genotype, i. e. on a specifc wheat genotype. The results of the study are of interest for increasing the efciency of breeding based on the elimination of the genotypes with the dominant allelesTsn1andTsc2sensitive to the toxins Ptr ToxA and ToxB. The genotypes identifed will be used in wheat breeding for resistance to tan spot.


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