Chromosome engineering-mediated introgression and molecular mapping of novel Aegilops speltoides-derived resistance genes for tan spot and Septoria nodorum blotch diseases in wheat

2019 ◽  
Vol 132 (9) ◽  
pp. 2605-2614 ◽  
Author(s):  
Wei Zhang ◽  
Xianwen Zhu ◽  
Mingyi Zhang ◽  
Gongjun Shi ◽  
Zhaohui Liu ◽  
...  

2019 ◽  
Vol 7 (6) ◽  
pp. 809-818 ◽  
Author(s):  
Wenjing Hu ◽  
Xinyao He ◽  
Susanne Dreisigacker ◽  
Carolina P. Sansaloni ◽  
Philomin Juliana ◽  
...  


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 ◽  
...  


2016 ◽  
Vol 6 (12) ◽  
pp. 4139-4150 ◽  
Author(s):  
Simerjot K Virdi ◽  
Zhaohui Liu ◽  
Megan E Overlander ◽  
Zengcui Zhang ◽  
Steven S Xu ◽  
...  

Abstract Tan spot and Septoria nodorum blotch (SNB) are important diseases of wheat caused by the necrotrophic fungi Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively. The P. tritici-repentis necrotrophic effector (NE) Ptr ToxB causes tan spot when recognized by the Tsc2 gene. The NE ToxA is produced by both pathogens and has been associated with the development of both tan spot and SNB when recognized by the wheat Tsn1 gene. Most work to study these interactions has been conducted in common wheat, but little has been done in durum wheat. Here, quantitative trait loci (QTL) analysis of a segregating biparental population indicated that the Tsc2-Ptr ToxB interaction plays a prominent role in the development of tan spot in durum. However, analysis of two biparental populations indicated that the Tsn1-ToxA interaction was not associated with the development of tan spot, but was strongly associated with the development of SNB. Pa. nodorum expressed ToxA at high levels in infected Tsn1 plants, whereas ToxA expression in P. tritici-repentis was barely detectable, suggesting that the differences in disease levels associated with the Tsn1-ToxA interaction were due to differences in pathogen expression of ToxA. These and previous results together indicate that: (1) the effects of Tsn1-ToxA on tan spot in common wheat can range from nonsignificant to highly significant depending on the host genetic background; (2) Tsn1-ToxA is not a significant factor for tan spot development in durum wheat; and (3) Tsn1-ToxA plays a major role in SNB development in both common and durum wheat. Durum and common wheat breeders alike should strive to remove both Tsc2 and Tsn1 from their materials to achieve disease resistance.



2019 ◽  
Vol 20 (21) ◽  
pp. 5432 ◽  
Author(s):  
Pawan Kumar Singh ◽  
Sukhwinder Singh ◽  
Zhiying Deng ◽  
Xinyao He ◽  
Zakaria Kehel ◽  
...  

Tan spot (TS) and Septoria nodorum blotch (SNB) induced by Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively, cause significant yield losses and adversely affect grain quality. The objectives of this study were to decipher the genetics and map the resistance to TS and SNB in the PBW343/Kenya Nyangumi (KN) population comprising 204 F6 recombinant inbred lines (RILs). Disease screening was performed at the seedling stage under greenhouse conditions. TS was induced by P. tritici-repentis isolate MexPtr1 while SNB by P. nodorum isolate MexSN1. Segregation pattern of the RILs indicated that resistance to TS and SNB in this population was quantitative. Diversity Array Technology (DArTs) and simple sequence repeats (SSRs) markers were used to identify the quantitative trait loci (QTL) for the diseases using inclusive composite interval mapping (ICIM). Seven significant additive QTLs for TS resistance explaining 2.98 to 23.32% of the phenotypic variation were identified on chromosomes 1A, 1B, 5B, 7B and 7D. For SNB, five QTLs were found on chromosomes 1A, 5A, and 5B, explaining 5.24 to 20.87% of the phenotypic variation. The TS QTL on 1B chromosome coincided with the pleiotropic adult plant resistance (APR) gene Lr46/Yr29/Pm39. This is the first report of the APR gene Lr46/Yr29/Pm39 contributing to TS resistance.



Euphytica ◽  
2004 ◽  
Vol 137 (2) ◽  
pp. 203-223 ◽  
Author(s):  
Xiu-Qiang Huang ◽  
Marion S. Röder


2011 ◽  
Vol 124 (3) ◽  
pp. 577-583 ◽  
Author(s):  
Hiroomi Kai ◽  
Kinuko Takata ◽  
Morihiro Tsukazaki ◽  
Masahiko Furusho ◽  
Takahide Baba


2021 ◽  
Vol 12 ◽  
Author(s):  
Michael G. Francki ◽  
Esther Walker ◽  
Christopher J. McMullan ◽  
W. George Morris

Septoria nodorum blotch (SNB) is a necrotrophic disease of wheat prominent in some parts of the world, including Western Australia (WA) causing significant losses in grain yield. The genetic mechanisms for resistance are complex involving multiple quantitative trait loci. In order to decipher comparable or independent regulation, this study identified the genetic control for glume compared to foliar resistance across four environments in WA against 37 different isolates. High proportion of the phenotypic variation across environments was contributed by genotype (84.0% for glume response and 82.7% for foliar response) with genotype-by-environment interactions accounting for a proportion of the variation for both glume and foliar response (14.7 and 16.2%, respectively). Despite high phenotypic correlation across environments, most of the eight and 14 QTL detected for glume and foliar resistance using genome wide association analysis (GWAS), respectively, were identified as environment-specific. QTL for glume and foliar resistance neither co-located nor were in LD in any particular environment indicating autonomous genetic mechanisms control SNB response in adult plants, regulated by independent biological mechanisms and influenced by significant genotype-by- environment interactions. Known Snn and Tsn loci and QTL were compared with 22 environment-specific QTL. None of the eight QTL for glume or the 14 for foliar response were co-located or in linkage disequilibrium with Snn and only one foliar QTL was in LD with Tsn loci on the physical map. Therefore, glume and foliar response to SNB in wheat is regulated by multiple environment-specific loci which function independently, with limited influence of known NE-Snn interactions for disease progression in Western Australian environments. Breeding for stable resistance would consequently rely on recurrent phenotypic selection to capture and retain favorable alleles for both glume and foliar resistance relevant to a particular environment.



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