The rice (Oryza sativa) gene xa13 is a recessive resistance allele of Os-8N3, a member of the NODULIN3 (N3) gene family, located on rice chromosome 8. Os-8N3 is a susceptibility (S) gene for Xanthomonas oryzae pv oryzae, the causal agent of bacterial blight, and the recessive allele is defeated by strains of the pathogen producing any one of the type III effectors AvrXa7, PthXo2, or PthXo3, which are all members of the transcription activator-like (TAL) effector family. Both AvrXa7 and PthXo3 induce the expression of a second member of the N3 gene family, here named Os-11N3. Insertional mutagenesis or RNA-mediated silencing of Os-11N3 resulted in plants with loss of susceptibility specifically to strains of X. oryzae pv oryzae dependent on AvrXa7 or PthXo3 for virulence. We further show that AvrXa7 drives expression of Os-11N3 and that AvrXa7 interacts and binds specifically to an effector binding element within the Os-11N3 promoter, lending support to the predictive models for TAL effector binding specificity. The result indicates that variations in the TAL effector repetitive domains are driven by selection to overcome both dominant and recessive forms of resistance to bacterial blight in rice. The finding that Os-8N3 and Os-11N3 encode closely related proteins also provides evidence that N3 proteins have a specific function in facilitating bacterial blight disease.
水稻隱性抗病基因xa13是Os-8N3的等位基因，Os-8N3屬于結(jié)瘤素NODULIN3 (N3)基因家族的一員，位于8號(hào)染色體。Os-8N3是水稻感白葉枯病菌基因，而隱性等位基因的抗性能夠被那些產(chǎn)生III類效應(yīng)子AvrXa7、PthXo2或PthXo3的病原菌小種破壞，這些效應(yīng)子均屬于類轉(zhuǎn)錄激活因子（TAL）的效應(yīng)子家族成員。AvrXa7和PthXo3均能激活N3家族另一成員基因Os-11N3的表達(dá)。Os-11N3插入突變或者被RNA介導(dǎo)沉默后，對(duì)那些依賴AvrXa7和PthXo3的致病小種的特異感病性喪失。結(jié)果進(jìn)一步表明，AvrXa7驅(qū)動(dòng)Os-11N3的表達(dá)，并且AvrXa7可以與Os-11N3啟動(dòng)子特異的結(jié)合元件互作結(jié)合，這支持了之前預(yù)測(cè)的TAL效應(yīng)子特異結(jié)合模型。結(jié)果表明TAL效應(yīng)子重復(fù)結(jié)構(gòu)域受到了選擇，用來(lái)克服水稻顯性和隱性兩種形式的白葉枯抗性。Os-8N3和Os-11N3編碼親緣關(guān)系很近的蛋白，這為N3蛋白在促進(jìn)白葉枯發(fā)病過(guò)程中發(fā)揮特異作用提供了證據(jù)支持。