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酮戊二酸转运蛋白 KgtP 通过 III 型分泌系统分泌,并有助于稻黄单胞菌 pv.oryzae 的毒力。

Ketoglutarate transport protein KgtP is secreted through the type III secretion system and contributes to virulence in Xanthomonas oryzae pv. oryzae.

机构信息

Laboratory for Monitoring and Management for Plant Pests and Diseases (Ministry of Education of China), College of Plant Protection, Nanjing Agricultural University, Nanjing, China.

出版信息

Appl Environ Microbiol. 2012 Aug;78(16):5672-81. doi: 10.1128/AEM.07997-11. Epub 2012 Jun 8.

Abstract

The phytopathogenic prokaryote Xanthomonas oryzae pv. oryzae is the causal agent of bacterial leaf blight (BB) of rice and utilizes a type III secretion system (T3SS) to deliver T3SS effectors into rice cells. In this report, we show that the ketoglutarate transport protein (KgtP) is secreted in an HpaB-independent manner through the T3SS of X. oryzae pv. oryzae PXO99(A) and localizes to the host cell membrane for α-ketoglutaric acid export. kgtP contained an imperfect PIP box (plant-inducible promoter) in the promoter region and was positively regulated by HrpX and HrpG. A kgtP deletion mutant was impaired in bacterial virulence and growth in planta; furthermore, the mutant showed reduced growth in minimal media containing α-ketoglutaric acid or sodium succinate as the sole carbon source. The reduced virulence and the deficiency in α-ketoglutaric acid utilization by the kgtP mutant were restored to wild-type levels by the presence of kgtP in trans. The expression of OsIDH, which is responsible for the synthesis of α-ketoglutaric acid in rice, was enhanced when KgtP was present in the pathogen. To our knowledge, this is the first report demonstrating that KgtP, which is regulated by HrpG and HrpX and secreted by the T3SS in Xanthomonas oryzae pv. oryzae, transports α-ketoglutaric acid when the pathogen infects rice.

摘要

植物病原原核生物稻黄单胞菌 pv. 稻致病变种是水稻细菌性条斑病(BB)的病原体,它利用 III 型分泌系统(T3SS)将 T3SS 效应器输送到水稻细胞中。在本报告中,我们表明酮戊二酸转运蛋白(KgtP)通过稻黄单胞菌 pv. 稻致病变种 PXO99(A)的 T3SS 以 HpaB 非依赖性的方式分泌,并定位于宿主细胞膜以输出α-酮戊二酸。kgtP 在启动子区域包含一个不完美的 PIP 盒(植物诱导启动子),并受 HrpX 和 HrpG 的正调控。kgtP 缺失突变体在细菌毒力和在植物体内的生长方面受到损害;此外,该突变体在含有α-酮戊二酸或琥珀酸钠作为唯一碳源的最小培养基中的生长受到抑制。kgtP 缺失突变体的毒力降低和α-酮戊二酸利用不足通过在转基因中存在 kgtP 恢复到野生型水平。负责在水稻中合成α-酮戊二酸的 OsIDH 的表达在病原体中存在 KgtP 时增强。据我们所知,这是第一个报道表明 KgtP 受 HrpG 和 HrpX 调控并通过稻黄单胞菌 pv. 稻致病变种的 T3SS 分泌,当病原体感染水稻时,它可以运输α-酮戊二酸。

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