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Os8N3是水稻白叶枯病的一个宿主感病基因。

Os8N3 is a host disease-susceptibility gene for bacterial blight of rice.

作者信息

Yang Bing, Sugio Akiko, White Frank F

机构信息

Department of Plant Pathology, Kansas State University, Manhattan, KS 66506.

Department of Plant Pathology, Kansas State University, Manhattan, KS 66506

出版信息

Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10503-10508. doi: 10.1073/pnas.0604088103. Epub 2006 Jun 23.

Abstract

Many bacterial diseases of plants depend on the interaction of type III effector genes of the pathogen and disease-susceptibility genes of the host. The host susceptibility genes are largely unknown. Here, we show that expression of the rice gene Os8N3, a member of the MtN3 gene family from plants and animals, is elevated upon infection by Xanthomonas oryzae pv. oryzae strain PXO99(A) and depends on the type III effector gene pthXo1. Os8N3 resides near xa13, and PXO99(A) failed to induce Os8N3 in rice lines with xa13. Silencing of Os8N3 by inhibitory RNA produced plants that were resistant to infection by strain PXO99(A) yet remained susceptible to other strains of the pathogen. The effector gene avrXa7 from strain PXO86 enabled PXO99(A) compatibility on either xa13- or Os8N3-silenced plants. The findings indicate that Os8N3 is a host susceptibility gene for bacterial blight targeted by the type III effector PthXo1. The results support the hypothesis that X. oryzae pv. oryzae commandeers the regulation of otherwise developmentally regulated host genes to induce a state of disease susceptibility. Furthermore, the results support a model in which the pathogen induces disease susceptibility in a gene-for-gene manner.

摘要

许多植物细菌性疾病取决于病原体的III型效应子基因与宿主感病基因之间的相互作用。宿主感病基因大多未知。在此,我们表明水稻基因Os8N3(动植物中MtN3基因家族的一个成员)在受到水稻白叶枯病菌菌株PXO99(A)感染后表达上调,且依赖于III型效应子基因pthXo1。Os8N3位于xa13附近,在带有xa13的水稻品系中,PXO99(A)无法诱导Os8N3表达。通过抑制性RNA使Os8N3沉默后产生的植株对PXO99(A)菌株的感染具有抗性,但对该病原体的其他菌株仍敏感。来自菌株PXO86的效应子基因avrXa7使PXO99(A)能在xa13沉默或Os8N3沉默的植株上致病。这些发现表明Os8N3是水稻白叶枯病的一个宿主感病基因,受III型效应子PthXo1靶向作用。这些结果支持了水稻白叶枯病菌操纵原本受发育调控的宿主基因的调控以诱导感病状态这一假说。此外,这些结果支持了病原体以基因对基因的方式诱导感病性的模型。

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