Quorum Sensing Modulates the Epibiotic-Parasitic Relationship Between Actinomyces odontolyticus and Its Saccharibacteria epibiont, a Nanosynbacter lyticus Strain, TM7x.
Quorum Sensing Modulates the Epibiotic-Parasitic Relationship Between Actinomyces odontolyticus and Its Saccharibacteria epibiont, a Nanosynbacter lyticus Strain, TM7x.
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DOI：
10.3389/fmicb.2018.02049
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发表时间：
2018
影响因子：
5.2
通讯作者：
He X
中科院分区：
文献类型：
--
作者：
Bedree JK;Bor B;Cen L;Edlund A;Lux R;McLean JS;Shi W;He X
超小型专性寄生表生物 TM7x 是长期难以捉摸的糖杆菌门（以前的 TM7 门）中第一个也是唯一一个待培养的成员，在与其细菌宿主溶齿放线菌放线菌亚种 XH001 共培养中被分离出来。 TM7x 相关 XH001 共培养物的初始表型特征表明，与单一培养物的 XH001 相比，TM7x 存在下生物膜形成增强。 XH001 的基因组分析和先前发表的转录组分析还揭示了假定的 AI-2 群体感应 (QS) 操纵子的存在，该操纵子在 TM7x 与 XH001 关联时高度上调。该分析表明，XH001 中诱导程度最高的基因是 lsrB 直向同源基因，它编码自诱导物 (AI)-2 QS 信号分子的推定周质结合蛋白。进一步的基因组分析表明，XH001 中的 lsrB 操纵子是假定的杂合 AI-2/核糖转运操纵子，并且存在编码 AI-2 合酶的 luxS 直向同源物。在本研究中，研究了 AI-2 QS 在生物膜形成背景下 XH001 和 TM7x 之间的表生-寄生关系中的潜在作用。开发了 XH001 的遗传系统，以在 XH001 中产生 lsrB 和 luxS 基因缺失突变体。表型表征表明，lsrB 或 luxS 中的缺失突变不会影响 XH001 的生长动态、单物种生物膜形成能力，也不会影响其与 TM7x 关联的能力。 TM7x 与 XH001 的关联以 luxS 依赖性方式诱导 lsrB 基因表达。有趣的是，与野生型 XH001 不同，野生型 XH001 在与 TM7x 建立表生寄生关系后显示出显着增加的生物膜形成，XH001ΔlsrB 和 XH001ΔluxS 突变体在与 TM7x 相关时未能实现增强的生物膜形成。总之，当 XH001 和 TM7x 建立其表生-寄生关系时，我们证明了 AI-2 QS 在调节双物种生物膜形成中的重要作用。
The ultra-small, obligate parasitic epibiont, TM7x, the first and only current member of the long-elusive Saccharibacteria (formerly the TM7 phylum) phylum to be cultivated, was isolated in co-culture with its bacterial host, Actinomyces odontolyticus subspecies actinosynbacter, XH001. Initial phenotypic characterization of the TM7x-associated XH001 co-culture revealed enhanced biofilm formation in the presence of TM7x compared to XH001 as monoculture. Genomic analysis and previously published transcriptomic profiling of XH001 also revealed the presence of a putative AI-2 quorum sensing (QS) operon, which was highly upregulated upon association of TM7x with XH001. This analysis revealed that the most highly induced gene in XH001 was an lsrB ortholog, which encodes a putative periplasmic binding protein for the auto inducer (AI)-2 QS signaling molecule. Further genomic analyses suggested the lsrB operon in XH001 is a putative hybrid AI-2/ribose transport operon as well as the existence of a luxS ortholog, which encodes the AI-2 synthase. In this study, the potential role of AI-2 QS in the epibiotic-parasitic relationship between XH001 and TM7x in the context of biofilm formation was investigated. A genetic system for XH001 was developed to generate lsrB and luxS gene deletion mutants in XH001. Phenotypic characterization demonstrated that deletion mutations in either lsrB or luxS did not affect XH001’s growth dynamic, mono-species biofilm formation capability, nor its ability to associate with TM7x. TM7x association with XH001 induced lsrB gene expression in a luxS-dependent manner. Intriguingly, unlike wild type XH001, which displayed significantly increased biofilm formation upon establishing the epibiotic-parasitic relationship with TM7x, XH001ΔlsrB, and XH001ΔluxS mutants failed to achieve enhanced biofilm formation when associated with TM7x. In conclusion, we demonstrated a significant role for AI-2 QS in modulating dual-species biofilm formation when XH001 and TM7x establish their epibiotic-parasitic relationship.
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影响因子：
3.6
作者：
Bor B;Poweleit N;Bois JS;Cen L;Bedree JK;Zhou ZH;Gunsalus RP;Lux R;McLean JS;He X;Shi W
通讯作者：
Shi W
影响因子：
3.1
作者：
Fong, KP;Gao, L;Demuth, DR
通讯作者：
Demuth, DR
影响因子：
3.6
作者：
BASSLER, BL;WRIGHT, M;SILVERMAN, MR
通讯作者：
SILVERMAN, MR
影响因子：
64.8
作者：
Chen, X;Schauder, S;Hughson, FM
通讯作者：
Hughson, FM
影响因子：
4.4
作者：
Brinig, MM;Lepp, PW;Relman, DA
通讯作者：
Relman, DA