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Ontology highlight
ABSTRACT:
PROVIDER: PRJEB55124 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR10025257_1.fastq.gz | Fastqsanger.gz | |||
| ERR10025257_2.fastq.gz | Fastqsanger.gz | |||
| ERR10025258_1.fastq.gz | Fastqsanger.gz | |||
| ERR10025258_2.fastq.gz | Fastqsanger.gz | |||
| ERR10025259_1.fastq.gz | Fastqsanger.gz |
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Project description:Streptococcus suis is an important emerging worldwide pig pathogen and zoonotic agent with rapid evolution of virulence and drug resistance. Licochalcone A, used in traditional Chinese medicine, exhibits antimicrobial, antioxidant and anti-inflammatory activities. Herein, a whole-genome DNA microarray was used to investigate the global transcriptional regulation of Streptococcus suis 05ZYH33 treated by subinhibitory concentration of licochalcone A. 132 genes were differentially regulated upon liochalcone A treatment, including 78 genes up-regulated and 54 genes down-regulated which included many central biological functions such as metabolism, transcription and translation. We tried to investigate the antimicrobial mechanism of licochalcone A in the aspect of bacterial cell cycle control. Our analysis indicated that licochalcone A might inhibit the growth of S. suis by controlling the replication initiation and cell division through amino acid metabolism.
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Project description:Two-component regulatory systems (TCS) are one of the most widespread mechanism that bacteria use to sense and respond to environmental changes. In Streptococcus pneumoniae, a total of 13 TCS and one orphan response regulator have been identified and many of them have been linked to pathogenicity. Notably, TCS01 strongly contributed to pneumococcal virulence in several infection models. However, it remains one of the least studied TCS in pneumococci and its functional role is still unclear. In this study, we demonstrate that TCS01 upregulates a BceAB-type ATP-Binding Cassette (ABC) transporter that mediates resistance to several antimicrobial peptides targeting lipid II. Even though Tcs01 and BceAB genes are localized far apart from each other in the genome, disruption of either of them equally sensitized the bacterium to the same antimicrobial peptides. Although it is still poorly understood how S. pneumoniae can switch from a harmless colonizer of the human nasopharynx to a serious pathogen causing a variety of diseases, TCS01 likely contributes to the physiopathology of this organism by cooperating with a BceAB-type transporter to sense and induce resistance to antimicrobial peptides encountered in the human host.
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