A single system detects and protects the beneficial oral bacterium Streptococcus sp. A12 from a spectrum of antimicrobial peptides.
A single system detects and protects the beneficial oral bacterium Streptococcus sp. A12 from a spectrum of antimicrobial peptides.
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DOI：
10.1111/mmi.14703
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发表时间：
2021-07
影响因子：
3.6
通讯作者：
Burne RA
中科院分区：
文献类型：
--
作者：
Lee K;Kaspar JR;Rojas-Carreño G;Walker AR;Burne RA
共生细菌链球菌属。 A12 具有多种特性，可以促进与健康相关的口腔生物膜的稳定性，包括对龋齿病原体变形链球菌的明显拮抗作用。 LanFEG 型 ABC 转运蛋白 PcfFEG 赋予对羊毛硫抗生素乳链菌肽的耐受性，并增强 A12 与变形链球菌竞争的能力。在这里，我们研究了双组分系统 pcfRK 的 pcfFEG 和邻近基因的调节，以更好地了解 A12 的抗菌肽耐药性。 pcfFEG-pcfRK 的诱导是对乳链菌肽快速反应的主要机制。除了乳链菌肽之外，PcfFEG 还赋予 A12 对多种变形链球菌分离株产生的一系列羊毛硫抗生素和非羊毛硫抗生素抗菌肽的耐受性。 PcfFEG 的缺失导致双物种生物膜模型中 A12 和 S.mutans 的时空排列发生改变。 PcfFEG 或 PcfK 的缺失导致 pcfFEG 的组成型激活，并且 pcfFEG 的表达被 pcfK 突变体中的小肽抑制。 pcfR 或 pcfK 突变体的转录谱与功能基因组学相结合揭示了 PcfK 功能的特殊性以及一组对乳链菌肽敏感的新基因。总的来说，这些结果提供了基本见解，为设计基于微生物的疗法来控制口腔传染病奠定了基础。 LanFEG 型 ABC 转运蛋白 PcfFEG，在链球菌属中发现。 A12 赋予对羊毛硫抗生素乳链菌肽的耐受性，并且在 A12 中对于增强对龋齿病原体变形链球菌的防御至关重要。在这里，我们更深入地研究 pcfFEG 的调控，并探索其遗传连锁的双组分系统 pcfRK 的范围。我们获得了涉及 pcfFEGRK 表达的复杂调节回路的机制见解，并发现了在耐受乳链菌肽方面独立或与 PcfFEGRK 协同发挥作用的其他基因。
The commensal bacterium Streptococcus sp. A12 has multiple properties that may promote the stability of health-associated oral biofilms, including overt antagonism of the dental caries pathogen Streptococcus mutans. A LanFEG-type ABC transporter, PcfFEG, confers tolerance to the lantibiotic nisin and enhances the ability of A12 to compete against S. mutans. Here, we investigated the regulation of pcfFEG and adjacent genes for a two-component system, pcfRK, to better understand antimicrobial peptide resistance by A12. Induction of pcfFEG-pcfRK was the primary mechanism to respond rapidly to nisin. In addition to nisin, PcfFEG conferred tolerance by A12 to a spectrum of lantibiotic and non-lantibiotic antimicrobial peptides produced by a diverse collection of S. mutans isolates. Loss of PcfFEG resulted in altered spatio-temporal arrangement of A12 and S.mutans in a dual-species biofilm model. Deletion of PcfFEG or PcfK resulted in constitutive activation of pcfFEG and expression of pcfFEG was inhibited by small peptides in the pcfK mutant. Transcriptional profiling of pcfR or pcfK mutants combined with functional genomics revealed peculiarities in PcfK function and a novel panel of genes responsive to nisin. Collectively, the results provide fundamental insights that strengthen the foundation for design of microbial-based therapeutics to control oral infectious diseases. A LanFEG-type ABC transporter, PcfFEG, found in Streptococcus sp. A12 confers tolerance to lantibiotic nisin and is critical in A12 to mount defense against the dental caries pathogen, Streptococcus mutans. Here, we delve deeper into the regulation of pcfFEG and explore the scope of its genetically-linked two-component system, pcfRK. We gain mechanistic insights on the complex regulatory circuits involving pcfFEGRK expression and uncover additional genes that function independently or cooperatively with PcfFEGRK in tolerating nisin.
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DOI：
10.1093/bioinformatics/btu638
发表时间：
2015-01-15
期刊：
Bioinformatics (Oxford, England)
影响因子：
--
作者：
Anders S;Pyl PT;Huber W
通讯作者：
Huber W
影响因子：
3.2
作者：
Ahn, Sang-Joon;Burne, Robert A.
通讯作者：
Burne, Robert A.
影响因子：
4.4
作者：
Chakraborty, Brinta;Burne, Robert A.
通讯作者：
Burne, Robert A.
影响因子：
4.4
作者：
Bogaardt, Carlijn;van Tonder, Andries J.;Brueggemann, Angela B.
通讯作者：
Brueggemann, Angela B.
影响因子：
5.7
作者：
Conrads, Georg;Westenberger, Jacqueline;Abdelbary, Mohamed M. H.
通讯作者：
Abdelbary, Mohamed M. H.