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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Integrated regulatory responses of fimB to N-acetylneuraminic (sialic) acid and GlcNAc in Escherichia coli K-12.
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Integrated regulatory responses of fimB to N-acetylneuraminic (sialic) acid and GlcNAc in Escherichia coli K-12.

机译：fimB对大肠杆菌K-12中N-乙酰神经氨酸（唾液酸）和GlcNAc的整合调控反应。

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摘要

Bacterial-host attachment by means of bacterial adhesins is a key step in host colonization. Phase variation (reversible on-off switching) of the type 1 fimbrial adhesin of Escherichia coli involves a DNA inversion catalyzed by FimB (switching in either direction) or FimE (mainly on-to-off switching). fimB is separated from the divergent yjhATS operon by a large (1.4 kbp) intergenic region. Short ( approximately 28 bp) cis-active elements (regions 1 and 2) close to yjhA stimulate fimB expression and are required for sialic acid (Neu(5)Ac) sensitivity of its expression [El-Labany, S., Sohanpal, B. K., Lahooti, M., Akerman, R. & Blomfield, I. C. (2003) Mol. Microbiol. 49, 1109-1118]. Here, we show that whereas NanR, a sialic acid-response regulator, binds to region 1, NagC, a GlcNAc-6P-responsive protein, binds to region 2 instead. The NanR- and NagC-binding sites lie adjacent to deoxyadenosine methylase (Dam) methylation sites (5'-GATC) that are protected from modification, and the two regulators are shown to be required for methylation protection at regions 1 and 2, respectively. Mutations in nanR and nagC diminish fimB expression, and both fimB expression and FimB recombination are inhibited by GlcNAc (3- and >35-fold, respectively). Sialic acid catabolism generates GlcNAc-6-P, and whereas GlcNAc disrupts methylation protection by NagC alone, Neu(5)Ac inhibits the protection mediated by both NanR and NagC as expected. Type 1 fimbriae are proinflammatory, and host defenses enhance the release of both Neu(5)Ac and GlcNAc by a variety of mechanisms. Inhibition of type 1 fimbriation by these amino sugars may thus help balance the interaction between E. coli and its hosts.
机译：通过细菌粘附素的细菌-宿主附着是宿主定殖的关键步骤。大肠杆菌1型纤维粘附素的相变（可逆开关控制）涉及通过FimB（向任一方向转换）或FimE（主要是开关转换）催化的DNA转化。 fimB与发散的yjhATS操纵子之间有一个较大的（1.4 kbp）基因间区域。靠近yjhA的短（约28 bp）顺式活性元件（区域1和2）刺激fimB表达，是唾液酸（Neu（5）Ac）敏感的表达所必需的[El-Labany，S.，Sohanpal，BK ，Lahooti，M.，Akerman，R.和Blomfield，IC（2003）Mol。微生物。 49，1109-1118]。在这里，我们显示，NanR（一种唾液酸响应调节剂）与区域1结合，而NagC（一种GlcNAc-6P响应蛋白）与区域2结合。 NanR和NagC结合位点与被保护免于修饰的脱氧腺苷甲基化（Dam）甲基化位点（5'-GATC）相邻，并且显示两个调节剂分别是区域1和2甲基化保护所必需的。 nanR和nagC中的突变会减少fimB表达，而fimB表达和FimB重组均受到GlcNAc的抑制（分别为3倍和> 35倍）。唾液酸分解代谢产生GlcNAc-6-P，而GlcNAc破坏仅NagC的甲基化保护作用，而Neu（5）Ac抑制NanR和NagC介导的保护作用。 1型菌毛是促炎性的，宿主防御通过多种机制增强Neu（5）Ac和GlcNAc的释放。这些氨基糖抑制1型纤维化可能因此有助于平衡大肠杆菌与其宿主之间的相互作用。

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