Two type III effector genes of Xanthomonas oryzae pv. oryzae control the induction of the host genes OsTFIIAγ1 and OsTFX1 during bacterial blight of rice

Two type III effector genes of Xanthomonas oryzae pv. oryzae control the induction of the host genes OsTFIIAγ1 and OsTFX1 during bacterial blight of rice
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DOI:
10.1073/pnas.0701742104
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发表时间:
2007-06-19
影响因子:
11.1
通讯作者:
White, Frank F.
White, Frank F.
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Sugio, Akiko;Yang, Bing;White, Frank F.

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水稻白叶枯病菌。水稻菌株pX099(A)诱导寄主基因Os8N3的表达,增加了寄主对白叶枯病的敏感性。在这里,我们发现pX099(A)以III型分泌系统依赖的方式影响另外两个基因的表达,一个编码bZIP转录因子(OsTFX1),另一个是位于1号染色体上的转录因子IIA的小亚基(OsTFIIA Gamma 1)。OsTFX1和OsTFIIA Gamma 1的诱导分别依赖于III型效应器基因pthXo6和pthXo7,这两个基因都编码转录激活器样(TAL)效应器家族中的两个先前未描述的成员。PthXo7是品系特异性的,可能反映了对水稻5号染色体上编码TFIIA小亚基第二形式的等位基因xa5介导的抗性的适应。PthXo6的缺失降低了病原菌的致病力,而OsTFX1的异位表达取消了pthXo6的完全致病力要求。稻瘟病菌X.oryzae pv.因此,Oryzae利用来自单个菌株的多个TAL效应器来调节多个宿主基因的表达,并且有证据支持相关宿主基因的表达有助于宿主对疾病的易感性的假设。
Xanthomonas oryzae pv. oryzae strain pX099(A) induces the expression of the host gene Os8N3, which results in increased host susceptibility to bacterial blight of rice. Here, we show that pX099(A) affects the expression of two additional genes in a type III secretion system-dependent manner, one encoding a bZIP transcription factor (OsTFX1) and the other the small subunit of the transcription factor IIA located on chromosome 1 (OsTFIIA gamma 1). Induction of OsTFX1 and OsTFIIA gamma 1 depended on the type III effector genes pthXo6 and pthXo7, respectively, both encoding two previously undescribed members of the transcription activator-like (TAL) effector family. pthXo7 is strain-specific and may reflect adaptation to the resistance mediated by xa5, an allele of OsTFIIA gamma 5 encoding a second form of the TFIIA small subunit on chromosome 5 of rice. The loss of pthXo6 resulted in reduced pathogen virulence, and ectopic expression of OsTFX1 abrogated the requirement for pthXo6 for full virulence. X. oryzae pv. oryzae therefore modulates the expression of multiple host genes using multiple TAL effectors from a single strain, and evidence supports the hypothesis that expression of the associated host genes contributes to host susceptibility to disease.