Lin Ying-Han, Romo Jesus A, Smith Trever C, Reyes Ann N, Karna S L Rajasekhar, Miller Christine L, Van Laar Tricia A, Yendapally Raghunandan, Chambers James P, Seshu J
South Texas Center for Emerging Infectious Diseases, Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA.
Department of Biology, California State University Fresno, Fresno, California, USA.
Infect Immun. 2017 Feb 23;85(3). doi: 10.1128/IAI.00684-16. Print 2017 Mar.
, the agent of Lyme disease, responds to numerous host-derived signals to alter adaptive capabilities during its enzootic cycle in an arthropod vector and mammalian host. Molecular mechanisms that enable to detect, channel, and respond to these signals have become an intense area of study for developing strategies to limit transmission/infection. Bioinformatic analysis of the borrelial genome revealed the presence of polyamine transport components (PotA, PotB, PotC, and PotD), while homologs for polyamine biosynthesis were conspicuously absent. Although is cotranscribed, the level of PotA was elevated under growth conditions mimicking unfed ticks compared to the level in fed ticks, while the levels of PotD were similar under the aforementioned conditions in Among several polyamines and polyamine precursors, supplementation of spermine or spermidine in the borrelial growth medium induced synthesis of major regulators of gene expression in , such as RpoS and BosR, with a concomitant increase in proteins that contribute to colonization and survival of in the mammalian host. Short transcripts of were elevated in response to spermidine, which was correlated with increased protein levels of RpoS. Transcriptional analysis of and ( ; ) in the presence of spermidine revealed the interplay of multiple regulatory factors in gene expression. The effect of spermidine on the levels of select borrelial proteins was also influenced by serum factors. These studies suggest that multiple host-derived signals/nutrients and their transport systems contribute to adaptation during the vector and vertebrate host phases of infection.
莱姆病病原体在节肢动物媒介和哺乳动物宿主的生态循环中，会对众多宿主来源的信号做出反应，以改变其适应能力。能够检测、传递并对这些信号做出反应的分子机制，已成为开发限制传播/感染策略的一个热门研究领域。对疏螺旋体基因组的生物信息学分析表明，存在多胺转运成分（PotA、PotB、PotC和PotD），而多胺生物合成的同源物则明显缺失。尽管PotA、PotB、PotC和PotD是共转录的，但与饱血蜱相比，在模拟未进食蜱的生长条件下，PotA的水平升高，而PotD的水平在上述条件下相似。在几种多胺和多胺前体中，在疏螺旋体生长培养基中添加精胺或亚精胺可诱导疏螺旋体中基因表达主要调节因子（如RpoS和BosR）的合成，同时有助于疏螺旋体在哺乳动物宿主中定殖和存活的蛋白质也随之增加。亚精胺可使疏螺旋体的短转录本升高，这与RpoS蛋白水平的增加相关。在亚精胺存在的情况下对rpoS和bosR（rpoS；bosR）的转录分析揭示了疏螺旋体基因表达中多种调节因子的相互作用。血清因子也会影响亚精胺对特定疏螺旋体蛋白水平的影响。这些研究表明，多种宿主来源的信号/营养物质及其转运系统在感染的媒介和脊椎动物宿主阶段有助于疏螺旋体的适应。
