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      RLP1.1, a novel wheat receptor-like protein gene, is involved in the defence response against Puccinia striiformis f. sp. tritici

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          Abstract

          Stripe rust, caused by Puccinia striiformis f. sp. tritici ( Pst), is one of the most serious diseases of wheat; therefore, exploring effective resistance-related genes is critical for breeding and studying resistance mechanisms. However, only a few stripe rust resistance genes and defence-related genes have been cloned. Moreover, transgenic wheat with enhanced stripe rust resistance has rarely been reported. Receptor-like proteins (RLPs) are known to be involved in defence and developmental pathways. In this research, a novel RLP gene TaRLP1.1 was characterized as an important stripe rust defence gene. TaRLP1.1 was screened by GeneChip and was found to be induced by Pst specifically in the resistant variety. Knock down of TaRLP1.1 in the stripe rust-resistant plants resulted in increased susceptibility to Pst, and phenolic autofluorogen accumulation at the pathogen–host interaction sites, usually correlated with the hypersensitive response, was decreased dramatically. However, when the TaRLP1.1 gene was transformed into the susceptible wheat variety Yangmai158, the transgenic plants showed highly increased resistance to Pst, and the hypersensitive response was enhanced at the infection sites. Meanwhile, the expression of pathogenesis-related genes decreased in the TaRLP1.1-silenced plants and increased in the TaRLP1.1-overexpressing plants. Thus, it was proposed that TaRLP1.1 greatly contributed to the hypersensitive response during the pathogen–host interaction. Along with the functional analysis, an evolutionary study of the TaRLP1 family was performed. Characterization of TaRLP1.1 may facilitate breeding for stripe rust resistance and better understanding of the evolution of the RLP genes in wheat.

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          A putative ABC transporter confers durable resistance to multiple fungal pathogens in wheat.

          Agricultural crops benefit from resistance to pathogens that endures over years and generations of both pest and crop. Durable disease resistance, which may be partial or complete, can be controlled by several genes. Some of the most devastating fungal pathogens in wheat are leaf rust, stripe rust, and powdery mildew. The wheat gene Lr34 has supported resistance to these pathogens for more than 50 years. Lr34 is now shared by wheat cultivars around the world. Here, we show that the LR34 protein resembles adenosine triphosphate-binding cassette transporters of the pleiotropic drug resistance subfamily. Alleles of Lr34 conferring resistance or susceptibility differ by three genetic polymorphisms. The Lr34 gene, which functions in the adult plant, stimulates senescence-like processes in the flag leaf tips and edges.
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            A kinase-START gene confers temperature-dependent resistance to wheat stripe rust.

            Stripe rust is a devastating fungal disease that afflicts wheat in many regions of the world. New races of Puccinia striiformis, the pathogen responsible for this disease, have overcome most of the known race-specific resistance genes. We report the map-based cloning of the gene Yr36 (WKS1), which confers resistance to a broad spectrum of stripe rust races at relatively high temperatures (25 degrees to 35 degrees C). This gene includes a kinase and a putative START lipid-binding domain. Five independent mutations and transgenic complementation confirmed that both domains are necessary to confer resistance. Yr36 is present in wild wheat but is absent in modern pasta and bread wheat varieties, and therefore it can now be used to improve resistance to stripe rust in a broad set of varieties.
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              Making sense of hormone crosstalk during plant immune responses.

              In response to biotic stress, crosstalk between plant hormonal signaling pathways prioritizes defense over other cellular functions. Some plant pathogens take advantage of this regulatory system by mimicking hormones that interfere with host immune responses to promote virulence. Here we discuss the various roles that crosstalk may play in response to pathogens with different infection strategies.
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                Author and article information

                Journal
                J Exp Bot
                J. Exp. Bot
                jexbot
                jexbot
                Journal of Experimental Botany
                Oxford University Press (UK )
                0022-0957
                1460-2431
                September 2013
                23 July 2013
                23 July 2013
                : 64
                : 12
                : 3735-3746
                Affiliations
                1National Key Laboratory of Crop Genetics and Germplasm Enhancement, Cytogenetics Institute, Nanjing Agricultural University , Nanjing, Jiangsu 210095, China
                2State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University , Yangling, Shaanxi 712100, China
                Author notes
                *To whom correspondence should be addressed. E-mail: pdchen@ 123456njau.edu.cn or caoaz@ 123456njau.edu.cn
                Article
                10.1093/jxb/ert206
                3745730
                23881396
                9a8c9323-9235-400d-9d3e-3dd421cefa29
                © The Author [2013]. Published by Oxford University Press on behalf of the Society for Experimental Biology.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                Page count
                Pages: 12
                Categories
                Research Paper

                Plant science & Botany
                disease resistance,hypersensitive response,receptor-like protein,stripe rust,transgenic,virus-induced gene silencing.

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