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一种重氮二醇盐信号上调毒力因子并促进在植物中的存活。

A Diazeniumdiolate Signal in Upregulates Virulence Factors and Promotes Survival in Plants.

作者信息

Guo Qiang, Vitro Caitlin N, Crawford Drake M, Li Bo

机构信息

MOA Key Laboratory of Pest Monitoring and Green Management, College of Plant Protection, China Agricultural University, Beijing 100193, China.

Department of Chemistry, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, U.S.A.

出版信息

Mol Plant Microbe Interact. 2024 Nov;37(11):776-783. doi: 10.1094/MPMI-06-24-0069-R. Epub 2024 Nov 27.

Abstract

infects a wide variety of crops. The () is conserved across many strains and is responsible for producing an extracellular chemical signal, leudiazen. Disruption of the gene in pv. () UMAF0158 alleviated tomato chlorosis caused by this bacterium. We showed that deletion of the entire reduced UMAF0158 population in tomato leaflets. Leudiazen restored the signaling activity of the deletion mutant at a concentration as low as 10 nM. Both the diazeniumdiolate and isobutyl groups of leudiazen are critical for this potent signaling activity. Transcriptional analysis showed that and leudiazen induce the expression of as well as an uncharacterized gene cluster, RS17235-RS17245. We found that this cluster enhances the survival of UMAF0158 in planta and is widely distributed in strains. Our results demonstrate that plays prominent roles in the virulence and growth of . The and -like signaling systems in different bacteria likely regulate diverse microbe-host interactions. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.

摘要

感染多种作物。()在许多菌株中是保守的,负责产生一种细胞外化学信号,即leudiazen。在pv.()UMAF0158中该基因的破坏减轻了由这种细菌引起的番茄黄化。我们表明,整个()的缺失减少了番茄小叶中UMAF0158的数量。Leudiazen在低至10 nM的浓度下恢复了缺失突变体的信号活性。Leudiazen的重氮二醇盐和异丁基基团对这种强大的信号活性都至关重要。转录分析表明,()和leudiazen诱导()以及一个未表征的基因簇RS17235 - RS17245的表达。我们发现这个簇增强了UMAF0158在植物中的存活能力,并且在()菌株中广泛分布。我们的结果表明,()在()的毒力和生长中起着重要作用。不同细菌中的()和()样信号系统可能调节多种微生物 - 宿主相互作用。[公式:见正文] 版权所有© 2024作者。这是一篇根据知识共享署名4.0国际许可协议分发的开放获取文章。

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