Genetic control and chromosomal location of Triticum timopheevii-derived resistance to septoria nodorum blotch in durum wheat

Genome ◽  
1995 ◽  
Vol 38 (2) ◽  
pp. 332-338 ◽  
Author(s):  
H. Ma ◽  
G. R. Hughes

The genetic control of resistance, expressed as restricted lesion development in seedling plants, to septoria nodorum blotch of wheat was studied under controlled environmental conditions, using the parental, F1, F2, F3, BC1F1, and BC1F2 generations of crosses of Triticum timopheevii-derived resistant durum lines S3-6, S9-10, and S12-1 with the susceptible durum cv. Sceptre. The seedling resistance of these three resistant sources, derived from T. timopheevii (PI 290518), was monogenically controlled. The chromosomal location of the resistance gene identified was determined by crossing the complete set of 'Langdon' – 'Chinese Spring' D-genome disomic substitution lines with S12-1. Tests of the F1 and F2 generations of each cross indicated that only chromosome 3A was associated with resistance. Therefore, the resistance gene is considered to be located on chromosome 3A and has been designated temporarily as SnbTM.Key words: Leptosphaeria nodorum, Stagonospora nodorum, Phaeosphaeria nodorum, glume blotch, disease resistance, substitution lines, Triticum durum.

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

Genome ◽  
1988 ◽  
Vol 30 (2) ◽  
pp. 229-233 ◽  
Author(s):  
C. F. Konzak ◽  
L. R. Joppa

The durum wheat (Triticum turgidum L. var. durum) cultivar 'Vic' was treated with the chemical mutagen N-methyl-N′-nitrosourea and among the M2 progeny a mutant with "chocolate chaff" (designated cc) was identified. Genetic analyses indicated that chocolate chaff is due to a single recessive gene mutation. The penetrance of the gene for chocolate chaff was environmentally influenced and varied from dark blotches on the glumes to complete coloration of culms as well as spikes. To determine the chromosomal location of the gene, the mutant was crossed with a set of 'Langdon' durum disomic substitution lines in which each of the 14 A- and B-genome chromosomes of durum wheat were replaced by their respective D-genome homoeologues. The segregation of cc was normal in all of the crosses except for those with the 7D(7A) and 7D(7B) lines. Cytogenetic analysis indicated that the gene was located on chromosome 7B, and that chromosome 7D has a gene that prevents the expression of cc when present in one or more copies. It was shown that the 'Langdon' D-genome disomic substitution lines can be used to determine the chromosomal location of genes in tetraploid wheat.Key words: Triticum turgidum, aneuploid, chromosome substitution, monosomic, cytogenetics.


Genome ◽  
1988 ◽  
Vol 30 (2) ◽  
pp. 222-228 ◽  
Author(s):  
L. R. Joppa ◽  
N. D. Williams

A complete set of disomic substitution lines have been developed in the tetraploid wheat cultivar Langdon (Triticum turgidum L. var. durum). These aneuploid lines each have a pair of durum wheat homoeologues replaced by a pair of D-genome chromosomes transferred from 'Chinese Spring' hexaploid wheat. They can be used to determine the chromosomal location of genes, to transfer chromosomes from one cultivar or line of tetraploid wheat to another, to study the cytogenetics of tetraploid wheat, to determine gene linkages, and to identify chromosomes involved in translocations. Their phenotypic characteristics, their cytogenetic behavior, and suggested methods for their use are described.Key words: cytogenetics, monosomic, chromosome transmission, telosomic, chromosome substitution.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Huyen T. T. Phan ◽  
Eiko Furuki ◽  
Lukas Hunziker ◽  
Kasia Rybak ◽  
Kar-Chun Tan

AbstractThe fungus Parastagonospora nodorum is the causal agent of septoria nodorum leaf blotch (SNB) and glume blotch which are common in many wheat growing regions in the world. The disease is complex and could be explained by multiple interactions between necrotrophic effectors secreted by the pathogen and matching susceptibility genes in wheat. An Australian P. nodorum population was clustered into five groups with contrasting properties. This study was set to identify their pathogenicity profiles using a diverse wheat panel of 134 accessions which are insensitive to SnToxA and SnTox1 in both in vitro and in vivo conditions. SNB seedling resistance/susceptibility to five representative isolates from the five clusters, responses to crude culture-filtrates (CFs) of three isolates and sensitivity to SnTox3 semi-purified effector together with 11,455 SNP markers have been used for linkage disequilibrium (LD) and association analyses. While quantitative trait loci (QTL) on 1D, 2A, 2B, 4B, 5B, 6A, 6B, 7A, 7D chromosomes were consistently detected across isolates and conditions, distinct patterns and isolate specific QTL were also observed among these isolates. In this study, SnTox3–Snn3-B1 interaction for the first time in Australia and SnTox3–Snn3-D1 interaction for the first time in bread wheat were found active using wild-type isolates. These findings could be due to new SnTox3 haplotype/isoform and exotic CIMMYT/ICARDA and Vavilov germplasm used, respectively. This study could provide useful information for dissecting novel and different SNB disease components, helping to prioritise research targets and contributing valuable information on genetic loci/markers for marker-assisted selection in SNB resistance wheat breeding programme.


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.


Genome ◽  
1990 ◽  
Vol 33 (4) ◽  
pp. 515-520 ◽  
Author(s):  
D. L. Klindworth ◽  
N. D. Williams ◽  
L. R. Joppa

The supernumerary spikelet (SS) trait of durum wheat (Triticum turgidum L.), including the ramified and four-rowed spike traits, is characterized by an increased number of spikelets per spike. Chromosomal location of the SS gene(s) was determined by crossing the ramified spike line PI349056 to the set of 'Langdon' D-genome disomic substitution lines. Double monosomic F1 plants were backcrossed to PI349056 and the testcross F1 plants were classified for chromosome pairing and spike type. Segregation for spike type was observed in the testcross F2. Data indicated that the major SS gene was located on chromosome 2A. Subsequent crosses with the 'Langdon' 2A telosomics indicated that the major SS gene was located on the short arm of chromosome 2A. Segregation of the testcross F2 indicated that a minor SS gene was located on chromosome 2B. Results also indicated that inhibitors of SS may be located on the D-genome chromosomes and an additional experiment was designed to test this hypothesis. Eight D-genome monosomic addition lines were developed by backcrossing PI349056 from one to three times to plants containing D-genome univalents. The test populations contained two cytological types of plants, disomics having 14 pairs of durum chromosomes and D-genome monosomic additions having 14 pairs of durum chromosomes plus a D-genome monosome. Comparison of these two types of plants indicated that chromosome 2D (from 'Chinese Spring' wheat) had a strong inhibitor of SS expression.Key words: Triticum, branched spike, ramified spike, four-rowed spike, cytogenetics.


Weed Science ◽  
2004 ◽  
Vol 52 (1) ◽  
pp. 83-90 ◽  
Author(s):  
James A. Anderson ◽  
Leanne Matthiesen ◽  
Justin Hegstad

An induced mutation of the common wheat (2n = 6x = 42, AABBDD genomes) cultivar ‘Fidel’ has been shown to provide resistance to the imidazolinone class of herbicides. This class of herbicide gives broad-spectrum weed control including the weedy relative of wheat, jointed goatgrass (2n = 4x = 28, CCDD genomes). Because wheat and jointed goatgrass share a common genome, genes present on the D genome may transfer between the two species as a result of natural hybridization and selective pressures. Our objectives were to determine which genome of common wheat contained the herbicide resistance gene in the mutated Fidel and to genetically map its position. We investigated the chromosomal location of this gene using both durum (2n = 4x = 28, AABB genomes) and common wheat (6x) backgrounds. From crosses of durum wheat genotypes as the recurrent parent with mutated Fidel (cv. 9804, resistant), only BC1plants containing chromosome 6D (inherited from cv. 9804) were resistant to applications of labeled rates of imazamox, an imidazolinone herbicide. No other D-genome chromosome was absolutely associated with herbicide resistance. To confirm this chromosomal location and genetically map the position of this gene, two populations of F3families from the cross of cv. 9804 to the common wheat cultivars ‘Cashup’ and ‘Madsen’ were screened for reaction to imazamox, followed by genetic mapping with microsatellite markers. Two linked microsatellite markers were associated with the resistance trait, and one of them,Xgdm127, was located to chromosome 6D using aneuploid stocks, confirming the location of this gene on 6D. These results indicate that this resistance gene is in the genome that common wheat shares with jointed goatgrass. Therefore, imidazolinone-resistant wheat will need to be carefully managed to minimize the occurrence and spread of resistant jointed goatgrass, whether such plants arise because of hybridization with resistant common wheat or by independent mutation, a frequent occurrence with this herbicide class.


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