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Página 1 a partir de 63 resultados
[Comparative genetic analysis of the hexaploid wheat Triticum petropavlovskyi Udasz. et Migusch. and Triticum aestivum L].
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A poorly studied species of hexaploid wheat Triticum petropavlovskyi Udacz. et Migusch. was compared with common wheat Triticum aestivum L. by means of monosomic and genetic analyses of F2 hybrids. Triticum petropavlovskyi was found to carry 13 dominant genes determining its morphological and
Proteomic analysis of 'hybrid necrosis' in wheat (Triticum aestivum) leaves
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Wheat hybrid necrosis has been genetically characterised for many years, but the specific gene(s) and the protein products involved in the processes remains unknown. In this study, protein expression in the base (B), mid (M) and tip (T) segments of the FL-2 leaves of a necrotic hybrid, PZF1 and its
[Dynamics of hybrid necrosis genes in Russian cultivars of common wheat (Triticum aestivum L.)].
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Study of necrosis genotypes of 72 Russian cultivars of winter common wheat has confirmed a tendency towards "washing off" of genotypes with the Ne1 gene. Fifty-six percent of cultivars have the genotype ne1ne1Ne2Ne2, and 44% have the genotype ne1ne1ne2ne2; i.e., they are free of hybrid necrosis
Protective action of epidermal growth factor and a fraction from Triticum vulgare extract in mouse tail necrosis.
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Several peptide growth factors, including EGF, are known to protect endothelium from oxygen-related damage or ischemia-reperfusion, in vitro experiments show that such protective effect involves endogenous endothelium-related factors like nitric oxide and prostanoids. However, in vivo demonstrations
A novel intergeneric hybrid in the Triticeae: Triticum aestivum x Psathyrost achys juncea.
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Two hybrid embryos of intergeneric origin between Triticum aestivum cv Fukuho (2n=6x=42, AABBDD) and Psathyrostachys juncea (2n=2x=14, NN) were successfully rescued. One hybrid plant had the expected chromosome number of 28 (ABDN), whereas the second plant had 35 chromosomes. The average meiotic
[New data on the distribution of hybrid necrosis genes in winter bread wheat (Triticum aestivum L.) cultivars].
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Hybrid necrosis genotypes have been identified in 125 Russian cultivars of winter bread wheat. More than half of them (56%) carry the Ne2 gene (genotype ne1ne1Ne2Ne2); others are free of necrosis genes (genotype ne1ne1ne2ne2). The possible causes of the increase in the Ne2 allele frequency and the
Triticum aestivum Sprouts Extract Inhibits Azoymethane (AOM)/Dextran Sodium Sulfate (DSS)-Induced Colon Carcinogenesis in Mice.
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Chronic intestinal inflammation is critical risk factor of colorectal cancer. Triticum aestivum sprouts have been reported to provide a number of health benefits and used as a dietary supplement. In this study, the authors investigated the regulatory effects of T. aestivum sprouts ethanol extract
Ne2 encodes protein(s) and the altered RuBisCO could be the proteomics leader of hybrid necrosis in wheat (Triticum aestivum L.).
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Wheat hybrid necrosis is caused by the interaction of two dominant complementary genes, Ne1 and Ne2, located on chromosome arms 5BL and 2BS, respectively. The sequences of Ne1 or Ne2 have not yet been identified. It is also not known whether Ne1 and Ne2 are structural or regulatory genes.
A gene for resistance to a necrosis-inducing isolate of Pyrenophora tritici-repentis located on 5BL of Triticum aestivum cv. Chinese Spring.
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Several sources of high-level resistance to tan spot caused by Pyrenophora tritici-repentis have been identified in hexaploid wheat (Triticum aestivum L.). This study was conducted to determine the number and chromosome location of a gene(s) in the cultivar Chinese Spring (CS) that confers
Triticum aestivum sprout extract attenuates 2,4‑dinitrochlorobenzene‑induced atopic dermatitis‑like skin lesions in mice and the expression of chemokines in human keratinocytes.
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Atopic dermatitis (AD) is a common chronic, recurring, inflammatory skin disease. A number of researchers have been seeking safe AD therapies for a long time. Triticum aestivum sprouts (TAEE), known as wheatgrass, are one of the most widely used health foods worldwide. They show numerous beneficial
Triticum vulgare Extract Modulates Protein-Kinase B and Matrix Metalloproteinases 9 Protein Expression in BV-2 Cells: Bioactivity on Inflammatory Pathway Associated with Molecular Mechanism Wound Healing.
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Matrix metalloproteinases (MMPs) are a large family of ubiquitously expressed zinc-dependent enzymes with proteolitic activities. They are expressed in physiological situations and pathological conditions involving inflammatory processes including epithelial to mesenchymal transition (EMT), neuronal
Low temperature-induced necrosis shows phenotypic plasticity in wheat triploid hybrids.
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Hybrid necrosis sometimes appears in triploid hybrids between tetraploid wheat and Aegilops tauschii Coss. Two types of hybrid necrosis (type II and type III) were observed when cultivar Langdon was used as female parent for hybrid production. Type II necrosis symptoms occurred only under low
The relationship of leaf rust resistance gene Lr13 and hybrid necrosis gene Ne2m on wheat chromosome 2BS.
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CONCLUSIONS
Genetic and mutational analyses of wheat leaf rust resistance gene Lr13 and hybrid necrosis gene Ne2 m indicated that they are the same gene. Hybrid necrosis in wheat characterized by chlorosis and eventual necrosis of plant tissues in certain wheat hybrids is controlled by the
Tagging and validation of a major quantitative trait locus for leaf rust resistance and leaf tip necrosis in winter wheat cultivar forno.
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ABSTRACT A major leaf rust (Puccinia triticina) resistance quantitative trait locus (QTL) (QLrP.sfr-7DS) previously has been described on chromosome 7DS in the winter wheat (Triticum aestivum) cv. Forno. It was detected in a population of single-seed descent (SSD) lines derived from the cross Arina
Molecular mapping of hybrid necrosis genes Ne1 and Ne2 in hexaploid wheat using microsatellite markers.
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Hybrid necrosis is the gradual premature death of leaves or plants in certain F1 hybrids of wheat (Triticum aestivum L.), and it is caused by the interaction of two dominant complementary genes Ne1 and Ne2 located on chromosome arms 5BL and 2BS, respectively. To date, molecular markers linked to
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