The identification of a new gene for leaf pubescence introgressed into bread wheat from Triticum timopheevii Zhuk. and its manifestation in a different genotypic background

2021 ◽  
pp. 1-7
Author(s):  
A. V. Simonov ◽  
O. G. Smirnova ◽  
M. A. Genaev ◽  
T. A. Pshenichnikova

Abstract Leaf pubescence is widespread among higher plants. In bread wheat, a relationship was found between this trait and the efficiency of photosynthetic processes and productivity. In this work, we established the chromosomal localization of the gene for leaf pubescence introgressed from Triticum timopheevii into a bread wheat line 821 and studied its expression in the genetic background of two wheat cultivars differing in genetic control and phenotypic expression of pubescence. To obtain quantitative characteristics of pubescence in cultivars and hybrid populations, the LHDetect2 program was used, which makes it possible to estimate the length and number of trichomes on a leaf fold. A genetic analysis showed the dominant inheritance of the gene. Monosomic analysis F2 was used to establish chromosome localization and investigate the expression of the gene in cultivars Saratovskaya S29 (S29) and Diamant 2 (Dm2). As a result, the gene Hltt, introgressed from T. timopheevii, was identified and localized in the distal region of the long arm of 5A chromosome for the first time. In both F2 populations, the gene reduced the density of trichomes and formed long trichomes, uncharacteristic for the two recipient cultivars S29 and Dm2. A larger number of long trichomes was formed in the genetic background of S29, which carry the bread wheat gene Hl1 and Hl3 for leaf pubescence, than in Dm2. Development of substitution and isogenic lines with the fragment of introgression carrying the gene Hltt will allow determining function and assessing the adaptive significance of the gene more precisely.

1998 ◽  
Vol 78 (4) ◽  
pp. 683-687 ◽  
Author(s):  
Dapeng Bai ◽  
D. R. Knott ◽  
Janice Zale

Triticum timopheevii (Zhuk.) Zhuk. is noted for its resistance to diseases including leaf and stem rust of wheat. Only one gene (Lr18) for leaf rust resistance has been transferred from T. timopheevii to bread wheat. The objectives of this work were to study the inheritance of leaf rust resistance in five accessions of T. timopheevii and to transfer genes for resistance into durum and bread wheats. A diallel set of crosses was made among five T. timopheevii accessions that gave a fleck infection type with an isolate of leaf rust race CBB. None of the F2 populations of the 10 crosses segregated for resistance, indicating that the five accessions all had at least one gene for resistance in common. Several accessions were crossed and backcrossed twice to durum and to bread wheat. At least three genes for leaf rust resistance were transferred to durum wheat and one to bread wheat. The gene transferred to bread wheat and one of those transferred to durum wheat conditioned good resistance to a set of 10 diverse races of leaf rust. Resistance conditioned by all three genes was dominant in durum wheat but the one gene was recessive in bread wheat. Monosomic analysis of the bread wheat line showed that the gene is on chromosome 1A. It should be useful in breeding for leaf rust resistance in both durum and bread wheat. Key words: Triticum timopheevii, leaf rust resistance, durum wheat, bread wheat


Genome ◽  
1988 ◽  
Vol 30 (2) ◽  
pp. 99-102 ◽  
Author(s):  
Toshinobu Morikawa

Inheritance of the peroxidase isoenzymes of the flag leaf blade was examined by isoelectrofocusing in the hexaploid oats Avena byzantina cv. Kanota, Avena fatua ssp. compacta, and Avena sativa cv. Cherokee. Two independent peroxidase loci (Px0 and Px9) were detected in the F2 from the 'Kanota' × compacta cross. The Px0a derived from compacta expressed the highest peroxidase activity and was accompanied by a post-transcriptionally modified form or mozyme. A monosomic analysis of the Px0 and Px9 loci revealed that they were located on chromosomes 18 and 6, respectively. Phenotypic expression of the peroxidases varied in each genotye at the Px0 and Px9 loci. Phenotypes of the homozygote (Px0aPx0a) and the hemizygote (Px0a—) were similar to each other. The heterozygote (Px0aPx0b) had half the enzymatic activity of the others. Px9b of compacta was functional as a suppressor but that of 'Cherokee' was nonfunctional.Key words: monosomic analysis, peroxidase loci, isoenzyme, hexaploid oats.


2015 ◽  
Vol 8 (2) ◽  
Author(s):  
Kai Voss‐Fels ◽  
Matthias Frisch ◽  
Lunwen Qian ◽  
Stefan Kontowski ◽  
Wolfgang Friedt ◽  
...  

2020 ◽  
Vol 57 (6) ◽  
pp. 414-421 ◽  
Author(s):  
Christian Babbs ◽  
Jill Brown ◽  
Sharon W Horsley ◽  
Joanne Slater ◽  
Evie Maifoshie ◽  
...  

BackgroundDeletions removing 100s–1000s kb of DNA, and variable numbers of poorly characterised genes, are often found in patients with a wide range of developmental abnormalities. In such cases, understanding the contribution of the deletion to an individual’s clinical phenotype is challenging.MethodsHere, as an example of this common phenomenon, we analysed 41 patients with simple deletions of ~177 to ~2000 kb affecting one allele of the well-characterised, gene dense, distal region of chromosome 16 (16p13.3), referred to as ATR-16 syndrome. We characterised deletion extents and screened for genetic background effects, telomere position effect and compensatory upregulation of hemizygous genes.ResultsWe find the risk of developmental and neurological abnormalities arises from much smaller distal chromosome 16 deletions (~400 kb) than previously reported. Beyond this, the severity of ATR-16 syndrome increases with deletion size, but there is no evidence that critical regions determine the developmental abnormalities associated with this disorder. Surprisingly, we find no evidence of telomere position effect or compensatory upregulation of hemizygous genes; however, genetic background effects substantially modify phenotypic abnormalities.ConclusionsUsing ATR-16 as a general model of disorders caused by CNVs, we show the degree to which individuals with contiguous gene syndromes are affected is not simply related to the number of genes deleted but depends on their genetic background. We also show there is no critical region defining the degree of phenotypic abnormalities in ATR-16 syndrome and this has important implications for genetic counselling.


PLoS Genetics ◽  
2009 ◽  
Vol 5 (3) ◽  
pp. e1000399 ◽  
Author(s):  
Tali Gidalevitz ◽  
Thomas Krupinski ◽  
Susana Garcia ◽  
Richard I. Morimoto

1988 ◽  
Vol 76 (6) ◽  
pp. 933-940 ◽  
Author(s):  
J. C. Sanz ◽  
G. Hueros ◽  
J. M. Gonzalez ◽  
N. Jouve

2020 ◽  
Vol 24 (6) ◽  
pp. 557-567
Author(s):  
I. V. Porotnikov ◽  
O. Yu. Antonova ◽  
O. P. Mitrofanova

Bread wheat (Triticum aestivum L.), the varieties of which are widely used for the grain production, is difficultly crossable with related species of Triticeae Dum. This factor limits the chance of introduction of alien genetic material into the wheat gene pool and the possibility of new varieties breeding with good adaptation to adverse environmental factors. The crossability between wheat and related species is controlled by Kr1-Kr4 genes (Crossability with Rye, Hordeum and Aegilops spp.) and the SKr gene (Suppressor of crossability). SKr and Kr1 have the largest influence on the trait. In the case of the recessive alleles, these genes do not function and the quantity of hybrid seeds after pollination with alien species can achieve more than 50 %. SKr is located on 5BS between the GBR0233 and Xgwm234 markers, closely linked with the markers Xcfb341, TGlc2 and gene12. Kr1 was mapped on 5BL, proximally to the Ph1 gene, between the EST-SSR markers Xw5145 and Xw9340. The markers of SKr were used to control the transfer of its recessive allele into other wheat genotypes, which made it possible to obtain highly crossable forms. However, the advantages of using the SKr and Kr1 markers in marker-assisted selection and in the screening of ex situ collections are not sufficiently studied. The published Kr1 sequence for varieties with different crossability offers great prospects, because it will be possible to create allele-specific markers. In this review, the following issues are considered: genetic resources created by wheat and rye hybridization, the geographical distribution of easy-to-cross forms of wheat, genetic control of the wheat and rye compatibility, advances of the use of molecular markers in the mapping of Kr-genes and their transmission control.


2019 ◽  
Author(s):  
Christian Babbs ◽  
Jill Brown ◽  
Sharon W. Horsley ◽  
Joanne Slater ◽  
Evie Maifoshie ◽  
...  

AbstractBackgroundSporadic deletions removing 100s-1000s kb of DNA, and variable numbers of poorly characterised genes, are often found in patients with a wide range of developmental abnormalities. In such cases, understanding the contribution of the deletion to an individual’s clinical phenotype is challenging.MethodsHere, as an example of this common phenomenon, we analysed 34 patients with simple deletions of ∼177 to ∼2000 kb affecting one allele of the well characterised, gene dense, distal region of chromosome 16 (16p13.3), referred to as ATR-16 syndrome. We characterised precise deletion extent and screened for genetic background effects, telomere position effect and compensatory up regulation of hemizygous genes.ResultsWe find the risk of developmental and neurological abnormalities arises from much smaller terminal chromosome 16 deletions (∼400 kb) than previously reported. Beyond this, the severity of ATR-16 syndrome increases with deletion size, but there is no evidence that critical regions determine the developmental abnormalities associated with this disorder. Surprisingly, we find no evidence of telomere position effect or compensatory upregulation of hemizygous genes, however, genetic background effects substantially modify phenotypic abnormalities.ConclusionsUsing ATR-16 as a general model of disorders caused by sporadic copy number variations, we show the degree to which individuals with contiguous gene syndromes are affected is not simply related to the number of genes deleted but also depends on their genetic background. We also show there is no critical region defining the degree of phenotypic abnormalities in ATR-16 syndrome and this has important implications for genetic counselling.


Sign in / Sign up

Export Citation Format

Share Document