Ectopic activation of the rice NLR heteropair RGA4/RGA5 confers resistance to bacterial blight and bacterial leaf streak diseases

                5.901
                Mathilde Hutin, Stella Cé, sari, Vé, ronique Chalvon, Corinne Michel, Tuan Tu Tran, Jens Boch, Ralf Koebnik, Boris Szurek, Thomas Kroj
                The Plant Journal, 2016, 88(1): 43-55  DOI: 10.1111/tpj.13231;      追溯原文......本站官方QQ群:62473826

                Bacterial blight (BB) and bacterial leaf streak (BLS) are important diseases in Oryza sativa caused by Xanthomonas oryzae pv. oryzae (Xoo) and Xanthomonas oryzae pv. oryzicola (Xoc), respectively. In both bacteria, transcription activator‐like (TAL) effectors are major virulence determinants that act by transactivating host genes downstream of effector‐binding elements (EBEs) bound in a sequence‐specific manner. Resistance to Xoo is mostly related to the action of TAL effectors, either by polymorphisms that prevent the induction of susceptibility (S) genes or by executor (R) genes with EBEs embedded in their promoter, and that induce cell death and resistance. For Xoc, no resistance sources are known in rice. Here, we investigated whether the recognition of effectors by nucleotide binding and leucine‐rich repeat domain immune receptors (NLRs), the most widespread resistance mechanism in plants, is also able to stop BB and BLS. In one instance, transgenic rice lines harboring the AVR1‐CO39 effector gene from the rice blast fungus Magnaporthe oryzae, under the control of an inducible promoter, were challenged with transgenic Xoo and Xoc strains carrying a TAL effector designed to transactivate the inducible promoter. This induced AVR1‐CO39 expression and triggered BB and BLS resistance when the corresponding Pi‐CO39 resistance locus was present. In a second example, the transactivation of an auto‐active NLR by Xoo‐delivered designer TAL effectors resulted in BB resistance, demonstrating that NLR‐triggered immune responses efficiently control Xoo. This forms the foundation for future BB and BLS disease control strategies, whereupon endogenous TAL effectors will target synthetic promoter regions of Avr or NLR executor genes.

                異位激活水稻NLR異源對(duì)RGA4/RGA5會(huì)賦予對(duì)白葉枯病和細(xì)菌性條斑病的抗性

                白葉枯病(BB)和細(xì)菌性條斑病(BLS)是兩種重要的水稻病害,分別是由白葉枯病菌(Xoo)和細(xì)菌性條斑病菌(Xoc)引起的。在這兩種病原菌中,類轉(zhuǎn)錄激活因子(TAL)效應(yīng)子通過以序列特異的方式,反式激活效應(yīng)子結(jié)合元件束(EBEs)的下游宿主基因,是主要的毒性決定因素。對(duì)Xoo的抗性主要與TAL效應(yīng)子的作用相關(guān),通過多態(tài)性抑制對(duì)感病基因的誘導(dǎo)或者將EBEs嵌入到抗病基因的啟動(dòng)子內(nèi),這會(huì)誘導(dǎo)細(xì)胞死亡和抗病性。而對(duì)于Xoc,在水稻中還沒有已知的抗性資源。本文中,我們分析了核苷酸結(jié)合和富含亮氨酸重復(fù)結(jié)構(gòu)域免疫受體(NLRs)對(duì)效應(yīng)子的識(shí)別是否也會(huì)阻止BB和BLS,NLRs是植物中最普遍的抗性機(jī)制。在一個(gè)實(shí)例中,包含來源于稻瘟病菌的AVR1-CO39效應(yīng)子基因的轉(zhuǎn)基因植株,在可誘導(dǎo)啟動(dòng)子的控制下,通過轉(zhuǎn)基因的攜帶設(shè)計(jì)好能夠反式激活誘導(dǎo)性啟動(dòng)子的TAL效應(yīng)子的Xoo和Xoc菌株進(jìn)行鑒定。當(dāng)對(duì)應(yīng)Pi-CO39抗性位點(diǎn)存在時(shí),這會(huì)誘導(dǎo)AVR1-CO39的表達(dá)和引發(fā)對(duì)BB和BLS的抗性。在第二個(gè)例子中,Xoo傳遞設(shè)計(jì)好的TAL效應(yīng)子對(duì)自激活NLR的反式激活會(huì)導(dǎo)致對(duì)BB的抗性,表明NLR引發(fā)的免疫應(yīng)答能夠有效控制Xoo。內(nèi)源TAL效應(yīng)子能夠作用于Avr或NLR抗性基因的合成啟動(dòng)子區(qū)域,這能夠用于未來建立控制BB和BLS的策略。


                基因列表
                  稻瘟病抗性基因 Pia; RGA4; Os11gRGA4
                  NB-LRR蛋白編碼基因 Pi5; PiCO39; RGA5; Os11gRGA5
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