Quorum Sensing N-acyl Homoserine Lactones-SdiA Suppresses Escherichia coli-Pseudomonas aeruginosa Conjugation through Inhibiting traI Expression.

Quorum Sensing N-acyl Homoserine Lactones-SdiA Suppresses Escherichia coli-Pseudomonas aeruginosa Conjugation through Inhibiting traI Expression.
复制标题

群体感应 N-酰基高丝氨酸内酯-SdiA 通过抑制 tra 表达来抑制大肠杆菌-铜绿假单胞菌缀合

DOI:
10.3389/fcimb.2017.00007
复制
发表时间:
2017
影响因子:
5.7
通讯作者:
Chen C
Chen C
中科院分区:
医学2区
文献类型:
--
作者:
Lu Y;Zeng J;Wu B;E S;Wang L;Cai R;Zhang N;Li Y;Huang X;Huang B;Chen C

文献摘要

被引文献

相似文献

接合作用是水平基因转移的关键机制,在细菌进化,尤其是在抗生素耐药性方面发挥着重要作用。然而,关于供体细胞和受体细胞在接合调控中的作用却知之甚少。在此,我们利用大肠杆菌(SM10λπ) - 铜绿假单胞菌(PAO1)接合模型,证明了PAO1中与群体感应信号N - 酰基高丝氨酸内酯(AHLs)生成相关的lasI/rhlI基因缺失,或者供体SM10λπ中AHLs受体SdiA的缺失,均能促进接合作用。当使用另一种不产生AHLs的大肠杆菌菌株EC600作为受体细胞时,供体SM10λπ中sdiA的缺失几乎不影响接合作用。更重要的是,在存在外源AHLs的情况下,SM10λπ与EC600之间的接合效率显著降低,而SM10λπ中sdiA的缺失则减弱了AHLs对接合的抑制作用。这些数据表明AHLs - SdiA化学信号传导具有抑制接合的功能。进一步的生物信息学分析、β - 半乳糖苷酶报告系统以及电泳迁移率变动分析确定了SdiA在traI基因启动子区域的结合位点。此外,在SM10λπ与PAO1共培养系统中,lasI/rhlI或sdiA的缺失促进了traI mRNA的表达,而AHLs则消除了这种促进作用。总体而言,我们的研究结果为群体感应系统AHLs - SdiA对调控接合网络的重要贡献提供了新的见解。
Conjugation is a key mechanism for horizontal gene transfer and plays an important role in bacterial evolution, especially with respect to antibiotic resistance. However, little is known about the role of donor and recipient cells in regulation of conjugation. Here, using an Escherichia coli (SM10λπ)-Pseudomonas aeruginosa (PAO1) conjugation model, we demonstrated that deficiency of lasI/rhlI, genes associated with generation of the quorum sensing signals N-acyl homoserine lactones (AHLs) in PAO1, or deletion of the AHLs receptor SdiA in the donor SM10λπ both facilitated conjugation. When using another AHLs-non-producing E. coli strain EC600 as recipient cells, deficiency of sdiA in donor SM10λπ hardly affect the conjugation. More importantly, in the presence of exogenous AHLs, the conjugation efficiency between SM10λπ and EC600 was dramatically decreased, while deficiency of sdiA in SM10λπ attenuated AHLs-inhibited conjugation. These data suggest the conjugation suppression function of AHLs-SdiA chemical signaling. Further bioinformatics analysis, β-galactosidase reporter system and electrophoretic mobility shift assays characterized the binding site of SdiA on the promoter region of traI gene. Furthermore, deletion of lasI/rhlI or sdiA promoted traI mRNA expression in SM10λπ and PAO1 co-culture system, which was abrogated by AHLs. Collectively, our results provide new insight into an important contribution of quorum sensing system AHLs-SdiA to the networks that regulate conjugation.