Mutagenesis of 18 Type III Effectors Reveals Virulence Function of XopZPXO99 in Xanthomonas oryzae pv. oryzae
Mutagenesis of 18 Type III Effectors Reveals Virulence Function of XopZPXO99 in Xanthomonas oryzae pv. oryzae
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DOI：
10.1094/mpmi-23-7-0893
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发表时间：
2010-07-01
影响因子：
3.5
通讯作者：
Yang, Bing
中科院分区：
文献类型：
--
作者：
Song, Congfeng;Yang, Bing
米黄斑病菌 (Xanthonzonas oryzae pv.)米曲霉依靠 III 型分泌系统 (T3SS) 将效应子转移到宿主细胞中，从而引起水稻白叶枯病。所有在 X. oryzae pv. 中具有已知功能的 III 型 (T3) 效应子。 oryzae 属于转录激活因子样 (TAL) 效应子家族。然而，基因组中还存在其他非 TAL 相关效应基因，尽管它们在毒力中的作用及其作用方式尚未阐明。在这里，我们报告了 18 个非 TAL T3 效应基因突变体的产生，并鉴定了一个有助于菌株 PX099(A) 毒力的突变体。 XopZ(PXO99) 编码一个预测的 1,414 个氨基酸的蛋白质，其功能未知。由于基因组中 212 kb 的重复，PX099A 包含该基因的两个相同副本。具有一个 XopZ (PXO99) 拷贝敲除突变的菌株没有表现出任何明显的毒力缺陷。然而，与 PX099(A) 相比，XopZ(PXO99) 两个拷贝均发生突变的菌株在病灶长度和细菌增殖方面表现出较低的毒力。 XopZ（PXO99）的一个基因组拷贝的引入使突变体恢复到完全毒力。 XopZ(PXO99) 在本塞姆氏烟草叶片中的瞬时表达抑制了宿主的基础防御，而宿主的基础防御是由 PX099A 的 T3SS 突变体诱导的，这表明 XopZ(PXO99) 在米 X. oryzae pv 期间干扰宿主先天免疫的作用。米酵母感染。 XopZ(PXO99) 相关基因存在于所有黄单胞菌属中。其基因组序列已确定，表明此类效应基因在黄单胞菌属的发病机制中具有保守作用。我们的结果表明，XopZ(PXO99) 编码一种新的 T3 效应子，并对米 X. oryzae pv 具有毒力。用于水稻白叶枯病的水稻菌株。
Xanthonzonas oryzae pv. oryzae depends on a type III secretion system (T3SS) to translocate effectors into host cells for its ability to cause bacterial blight of rice. All type III (T3) effectors with known function in X. oryzae pv. oryzae belong to a family of transcription activator-like (TAL) effectors. However, other, non TAL-related effector genes are present in the genome, although their role in virulence and their mode of action have yet to be elucidated. Here, we report the generation of mutants for 18 non-TAL T3 effector genes and the identification of one that contributes to the virulence of strain PX099(A). XopZ(PXO99) encodes a predicted 1,414-amino-acid protein of unknown function. PX099A contains two identical copies of the gene due to a duplication of 212 kb in the genome. Strains with knockout mutations of one copy of XopZ(PXO99) did not exhibit any visible virulence defect. However, strains with mutations in both copies of XopZ(PXO99) displayed reduced virulence in terms of lesion length and bacterial multiplication compared with PX099(A). The introduction of one genomic copy of XopZ(PXO99) restores the mutant to full virulence. Transient expression of XopZ(PXO99) in Nicotiana benthamiana leaves suppresses host basal defense, which is otherwise induced by a T3SS mutant of PX099A, suggesting a role for XopZ(PXO99) in interfering with host innate immunity during X. oryzae pv. oryzae infection. XopZ(PXO99)-related genes are found in all Xanthomonas spp. whose genomic sequences have been determined, suggesting a conserved role for this type of effector gene in pathogenesis of Xanthomonas spp. Our results indicate that XopZ(PXO99) encodes a novel T3 effector and contributes virulence to X. oryzae pv. oryzae strains for bacterial blight of rice.