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More insight into the importance of BRI1 in the disease resistance of uzu requires more in-depth studies of the receptor protein activity in barley derivatives and T-DNA mutants of Brachypodium.
Here we investigate the resistance of uzu barley derivatives to more diseases and use a combination of transcriptomic and biochemical studies to determine how these uzu derivatives differ in defences and BR signaling as compared to their parental barley genotypes.
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Patients diagnosed with Celiac disease must follow a gluten-free diet — a diet essentially free of wheat and its derivatives, barley, rye and malts — to avoid further abdominal pain or complications, according to the Celiac Disease Foundation.
Celiac Disease (CD) is an autoimmune disease characterized by damage to the small intestine, triggered by gluten ingestion from wheat, rye and barley and their derivatives in genetically susceptible individuals [ 1, 2].
Gluten is the protein found in grains such as wheat, barley, and rye and derivatives of these grains such as malt and triticale.
The semi-dwarf uzu derivatives of barley cvs.
In Table 2, all (putatively) identified T2 derivatives in barley are listed.
Goddard et al. [ 12] also reported that a T-DNA insertion in the 5′ untranslated region of BRI1 homolog in Brachypodium distachyon resulted in a similar disease resistance response as observed in the uzu derivatives of barley.
The literature suggests that the uzu derivative of barley is less responsive to BR [ 11].
Pathogenicity tests were used to compare the response of these two semi-dwarf uzu derivatives and their parental barley lines to the obligate pathogen Barley Stripe Mosaic Virus (BSMV), the necrotrophic net blotch pathogen Pyrenophora teres and the toxigenic hemibiotrophic fungus Fusarium culmorum that causes Fusarium head blight (FHB, also known as scab disease of cereals).
It is a primary induced gamma-ray mutant derivative of the barley cultivar Maythorpe, and is known to contain a mutation in Breviaristatum-e (Ari-e).
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