Ma Xingyan, Zhang Shebin, Xu Zhenjie, Li Honglin, Xiao Qian, Qiu Feng, Zhang Weizheng, Long Yifei, Zheng Dexiang, Huang Bin, Chen Cha, Lu Yang
Department of Laboratory Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Department of Laboratory Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Front Microbiol. 2020 Jun 3;11:1078. doi: 10.3389/fmicb.2020.01078. eCollection 2020.
The acid tolerance mechanism is important for to resist acidic conditions encountered in mammalian host digestive tract environment. Here, we explored how the LuxR protein SdiA influenced acid tolerance ability in the context of the glutamate- and glutamine-dependent acid resistance system (AR2). First, using a growth and acid shock assay under different acid stresses, we demonstrated that the deletion of in λ or led to impaired growth under the acidic environment of pH 3-6, which was restored by complementary expression of SdiA. Next, transcriptome sequencing and qPCR disclosed that the expression of glutamate decarboxylase W (GadW) and GadY, the key members of the AR2 system, were regulated by SdiA. Further, β-galactosidase reporter assays showed that the promoter activity of and was positively regulated by SdiA. Moreover, qPCR and β-galactosidase reporter assays confirmed that the regulation of SdiA on GadW, but not GadY, could be enhanced by quorum sensing (QS) signal molecules AHLs. Collectively, these data suggest that SdiA plays a crucial role in acid tolerance regulation of . Our findings provide new insights into the important contribution of quorum sensing system AHLs-SdiA to the networks that regulate acid tolerance.
耐酸机制对于抵抗哺乳动物宿主消化道环境中遇到的酸性条件很重要。在此，我们探讨了LuxR蛋白SdiA在谷氨酸和谷氨酰胺依赖性抗酸系统（AR2）背景下如何影响耐酸能力。首先，通过在不同酸胁迫下的生长和酸休克试验，我们证明在λ或中缺失会导致在pH 3 - 6的酸性环境下生长受损，而通过SdiA的互补表达可恢复生长。接下来，转录组测序和qPCR揭示了AR2系统的关键成员谷氨酸脱羧酶W（GadW）和GadY的表达受SdiA调控。此外，β - 半乳糖苷酶报告基因检测表明和的启动子活性受SdiA正调控。而且，qPCR和β - 半乳糖苷酶报告基因检测证实群体感应（QS）信号分子AHLs可增强SdiA对GadW而非GadY的调控。总体而言，这些数据表明SdiA在的耐酸调节中起关键作用。我们的发现为群体感应系统AHLs - SdiA对调节耐酸网络的重要贡献提供了新见解。
