...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Science Signaling >Gene expression kinetics governs stimulus-specific decoration of the Salmonella outer membrane
【24h】

Gene expression kinetics governs stimulus-specific decoration of the Salmonella outer membrane

机译：基因表达动力学治理刺激特异性的沙门氏菌外膜的装饰

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Lipid A is the innermost component of the lipopolysaccharide (LPS) molecules that occupy the outer leaflet of the outer membrane in Gram-negative bacteria. Lipid A is recognized by the host immune system and targeted by cationic antimicrobial compounds. In Salmonella enterica serovar Typhimurium, the phosphates of lipid A are chemically modified by enzymes encoded by targets of the transcriptional regulator PmrA. These modifications increase resistance to the cationic peptide antibiotic polymyxin B by reducing the negative charge of the LPS. We report the mechanism by which Salmonella produces different lipid A profiles when PmrA is activated by low Mg2+ versus a mildly acidic pH. Low Mg2+ favored modification of the lipid A phosphates with 4-amino-4-deoxy-l-aminoarabinose (l-Ara4N) by activating the regulatory protein PhoP, which initially increased the LPS negative charge by promoting transcription of lpxT, encoding an enzyme that adds an additional phosphate group to lipid A. Later, PhoP activated PmrA posttranslationally, resulting in expression of PmrA-activated genes, including those encoding the LpxT inhibitor PmrR and enzymes responsible for the incorporation of l-Ara4N. By contrast, a mildly acidic pH favored modification of the lipid A phosphates with a mixture of l-Ara4N and phosphoethanolamine (pEtN) by simultaneously inducing the PhoP-activated lpxT and PmrA-activated pmrR genes. Although l-Ara4N reduces the LPS negative charge more than does pEtN, modification of lipid A phosphates solely with l-Ara4N required a prior transient increase in lipid A negative charge. Our findings demonstrate how bacteria tailor their cell surface to different stresses, such as those faced inside phagocytes.
机译：脂A是脂多糖（LPS）分子的最内部成分，其占据外膜的外膜在革兰氏阴性细菌中。脂质A被宿主免疫系统认识到并由阳离子抗微生物化合物靶向。在沙门氏菌肠道血吸虫血硫核核核尿精中，脂质A的磷酸盐通过通过转录调节剂PMRA的靶向编码的酶化学改性。通过降低LPS的负电荷，这些修饰通过降低负电荷而增加对阳离子肽抗生素多粘蛋白B的抵抗力。我们报告了当PMRA由低Mg2 +与温和酸性pH激活时，沙门氏菌产生不同的脂质的机制。低Mg2 +通过激活调节蛋白蛋白酶通过促进LPXT的转录，通过激活4-氨基-4-脱氧-1-氨基喹啉（L-ARA4N）的脂质用4-氨基-4-脱氧-L-氨基氨基糖（L-ARA4N）的脂质的改性。将另外的磷酸盐组添加到脂A中。后来，PHOP后期后期的PMRA，导致PMRA活化基因的表达，包括编码LPXT抑制剂PMRR和负责掺入L-ARA4N的酶的酶。相比之下，通过同时诱导PHOP活化的LPXT和PMRA活化的PMRR基因，轻微酸性pH利益改性用L-ARA4N和磷酸乙醇胺（PETN）的混合物。尽管L-ARA4N降低了LPS负电荷，但彼得不仅仅是脂质的改性，仅使用L-ARA4N的磷酸盐，所需的脂质的脂质增加负电荷。我们的研究结果表明，细菌如何定制其细胞表面与不同的应力，例如面对吞噬细胞的那些。

著录项

  • 来源
    《Science Signaling》 |2018年第529期|共11页
  • 作者

    Hong Xinyu; Chen H. Deborah; Groisman Eduardo A.;

  • 作者单位

    Yale Sch Med Dept Cell Biol 295 Congress Ave New Haven CT 06536 USA;

    Yale Sch Med Dept Microbial Pathogenesis 295 Congress Ave New Haven CT 06536 USA;

    Yale Sch Med Dept Microbial Pathogenesis 295 Congress Ave New Haven CT 06536 USA;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号