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细菌中碳代谢与毒力之间的相关性。

Correlations between carbon metabolism and virulence in bacteria.

作者信息

Poncet Sandrine, Milohanic Eliane, Mazé Alain, Abdallah Jamila Nait, Aké Francine, Larribe Mireille, Deghmane Ala-Eddine, Taha Muhamed-Kheir, Dozot Marie, De Bolle Xavier, Letesson Jean Jacques, Deutscher Josef

出版信息

Contrib Microbiol. 2009;16:88-102. doi: 10.1159/000219374. Epub 2009 Jun 2.

Abstract

Bacteria have developed several mechanisms which allow the preferred utilization of the most efficiently metabolizable carbohydrates when these organisms are exposed to a mixture of carbon sources. Interestingly, the same or similar mechanisms are used by some pathogens to control various steps of their infection process. The efficient metabolism of a carbon source might serve as signal for proper fitness. Alternatively, the presence of a specific carbon source might indicate to bacterial cells that they thrive in infection-related organs, tissues or cells and that specific virulence genes should be turned on or switched off. Frequently, virulence gene regulators are affected by changes in carbon source availability. For example, expression of the gene encoding the Streptococcus pyogenes virulence regulator Mga is controlled by the classical carbon catabolite repression (CCR) mechanism operative in Firmicutes. The activity of PrfA, the major virulence regulator in Listeria monocytogenes, seems to be controlled by the phosphorylation state of phosphotransferase system(PTS) components. In Vibrio cholerae synthesis of HapR, which regulates the expression of genes required for motility, is controlled via the Crp/cAMP CCR mechanism, whereas synthesis of Salmonella enterica HilE, which represses genes in a pathogenicity island, is regulated by the carbohydrate-responsive, PTS-controlled Mlc.

摘要

当细菌暴露于碳源混合物时,它们已发展出多种机制,以便优先利用最易代谢的碳水化合物。有趣的是,一些病原体利用相同或相似的机制来控制其感染过程的各个步骤。碳源的有效代谢可能作为适当适应性的信号。或者,特定碳源的存在可能向细菌细胞表明它们在与感染相关的器官、组织或细胞中茁壮成长,并且特定的毒力基因应该开启或关闭。毒力基因调节因子经常受到碳源可用性变化的影响。例如,编码化脓性链球菌毒力调节因子Mga的基因表达受厚壁菌门中起作用的经典碳分解代谢物阻遏(CCR)机制控制。单核细胞增生李斯特菌的主要毒力调节因子PrfA的活性似乎受磷酸转移酶系统(PTS)组分的磷酸化状态控制。在霍乱弧菌中,调节运动所需基因表达的HapR的合成通过Crp/cAMP CCR机制控制,而抑制致病岛中基因的肠炎沙门氏菌HilE的合成则由碳水化合物响应的、PTS控制的Mlc调节。

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