Regulation of sialidase production in clostridium perfringens by the orphan sensor histidine kinase ReeS
Ontology highlight
ABSTRACT:
ORGANISM(S): Clostridium perfringens str. 13
PROVIDER: GSE36786 | GEO | 2013/08/31
SECONDARY ACCESSION(S): PRJNA156741
REPOSITORIES: GEO
Similar Datasets
Project description:ReeS, previously named as CPE1512, was originally annotated as the only hybrid sensor histidine kinase/response regulator in Clostridium perfringens. Further evidence suggests that ReeS is more likely to function as an orphan sensor histidine kinase. A reeS deletion mutant was constructed and the transcriptome analysed using microarrays. Total RNA was isolated from the reeS mutant and the wild-type control cells during exponential phase growth. Gene expression levels were compared between the reeS mutant and wild-type strain 13
2013-08-31 | E-GEOD-36786 | biostudies-arrayexpress
Project description:Regulation of sialidase production in clostridium perfringens by the orphan sensor histidine kinase ReeS
| PRJNA156741 | ENA
Project description:Colistin-resistance mediated by PhoQ sensor histidine kinase mutagenesis in a clinical Enterobacter cloacae
| PRJEB73581 | ENA
Project description:Purpose: RNA-Seq has become a powerful tool for investigating transcriptional profiles in gene expression analysis, which would help to reveal the molecular mechanism of Clostridium perfringens type C infecting the piglets. In this study, we analyzed the transcriptome profiles of the spleen of piglets caused by Clostridium perfringens type Cens type C. Methods: 30 normal 7-day-old piglets (Y x L), without infecting Clostridium perfringens type C, Escherichia coli and Salmonella, were selected as experimental subjects. 25 piglets were randomly selected as the experimental group, which were disposed once a day for 5 days. Each piglet was dosed with 1 ml of bouillon culture-medium inoculated Clostridium perfringens type C at 37℃ for 16h, which approximate to 1 x109 CFU per ml. Then, 5 piglets were randomly selected as the control group (SC), which were taken the equal volume medium for 5 days.Based on total diarrhea scores, 25 piglets were ranked from high to low. The top and last five piglet were considered as sensitive group (SS) and resistant group (SR), respectively. Finally, spleen were collected and sequenced for lncRNA and mRNA. Results: RNA libraries constructed from spleen of piglets caused by Clostridium perfringens type C were sequenced. A total of 1,450,292,484 clean reads were generated. Among them, 2056 novel lncRNA transcripts corresponding to 1561 lncRNA genes were identified, including 1811 intergenic lncRNAs and 245 anti-sense lncRNAs. The identified spleen lncRNAs shared some characteristics, such as fewer exons and shorter length, with the lncRNAs in other animal. Notably, in pairwise comparisons between the libraries of spleen tissue at the different group, a total of 247 lncRNA and 2170 mRNA were differentially expressed (P < 0.05). Function analyses indicated that these differentially expressed lncRNAs and mRNAs play roles in defensing Clostridium perfringens type C, which were enriched in immune-related biological processes, such as the antigen processing and presentation, TNF signaling pathway, NF-kappa B signaling pathway, B cell receptor signaling pathway and MAPK signaling pathway. Conclusions: This study provides the information of spleen-related lncRNAs in swine diarrhea with Clostridium perfringens type C. We also analyzed all lncRNA’s genomic feature and expression. Bioinformatic analysis indicates that some lncRNAs participated in important biological processes associated with defeasing Clostridium perfringens type C, such as antigen processing and presentation, the MHC protein complex and regulation of autophagy.
2018-11-01 | GSE105797 | GEO
Project description:Purpose: The purpose of this study is to clarify the response of Clostridium perfringens ATCC 13124 to host polysaccharide. Methods: Clostridium perfringens ATCC 13124 cells were cultured anaerobically in a medium containing Minimal medium-like condition Poor + medium, medium in which hyaluronic acid or mucin was added to Poor + medium. Total RNA was extracted from bacterial cells by the Hot-Phenol method. Samples for RNA-seq were prepared according to the Illmina protocol available from the manufacturer. Array leads passed through quality filters were analyzed at the transcript isoform level using bowtie v 1.1.2. Results: Using the optimized data analysis workflow, we mapped about 50 million sequence leads per sample to the whole genome of Clostridium perfringens ATCC 13124. In addition, 2735 transcripts in C. perfringens ATCC 13124 were identified using a Bowtie aligner. Lead counts per genome were extracted from known gene annotations using the HTSeq program.
2024-07-29 | GSE240236 | GEO
Project description:Clostridium perfringens is ubiquitous in nature and is often found as a commensal of the human and animal gastrointestinal tract. It is the primary etiological agent of clostridial myonecrosis, or gas gangrene, a serious infection that results in extensive tissue necrosis due to the action of one or more potent extracellular toxins. ?-toxin and perfringolysin O are the major extracellular toxins involved in the pathogenesis of gas gangrene, but histotoxic strains of C. perfringens, such as strain 13, also produce many degradative enzymes such as collagenases, hyaluronidases, sialidases and the cysteine protease, ?-clostripain. The production of many of these toxins is regulated either directly or indirectly by the global VirSR two-component signal transduction system. By isolating a chromosomal mutant and carrying out microarray analysis we have identified an orphan sensor histidine kinase, which we have named ReeS (regulator of extracellular enzymes sensor). Expression of the sialidase genes nanI and nanJ was down-regulated in a reeS mutant. Since complementation with the wild-type reeS gene restored nanI and nanJ expression to wild-type levels, as shown by quantitative reverse transcription-PCR and sialidase assays we concluded that ReeS positively regulates the expression of these sialidase genes. However, mutation of the reeS gene had no significant effect on virulence in the mouse myonecrosis model. Sialidase production in C. perfringens has been previously shown to be regulated by both the VirSR system and RevR. In this report, we have analyzed a previously unknown sensor histidine kinase, ReeS, and have shown that it also is involved in controlling the expression of sialidase genes, adding further complexity to the regulatory network that controls sialidase production in C. perfringens.
| S-EPMC3762733 | biostudies-literature
Project description:Purpose: RNA-Seq has become a powerful tool for investigating transcriptional profiles in gene expression analysis, which would help to reveal the molecular mechanism of Clostridium perfringens type C infecting the piglets. In this study, we analyzed miRNA profiles of the ileum of piglets caused by Clostridium perfringens type C. Methods: 30 normal 7-day-old piglets (Y x L), without infecting Clostridium perfringens type C, Escherichia coli and Salmonella, were selected as experimental subjects. 25 piglets were randomly selected as the experimental group, which were disposed once a day for 5 days. Each piglet was dosed with 1 ml of bouillon culture-medium inoculated Clostridium perfringens type C at 37℃ for 16h, which approximate to 1 x10e9 CFU per ml. Then, 5 piglets were randomly selected as the control group (IC), which were taken the equal volume medium for 5 days.Based on total diarrhea scores, 25 piglets were ranked from high to low. The top and last five piglet were considered as sensitive group (IS) and resistant group (IR), respectively. Finally, ileum were collected and sequenced for miRNA. Result: 53 differentially expressed miRNAs were found. KEGG pathway analysis for target genes revealed that these miRNAs were involved in ErbB signaling pathway, MAPK signaling pathway, Jak-STAT signaling pathway and Wnt signaling pathway. The expression correlation analysis between miRNAs and target genes revealed that the expression of miR-7134-5p had negative correlation with target NFATC4, miR-500 had negative correlation with target ELK1, HSPA2 and IL7R, and miR-92b-3p had negative correlation with target CLCF1 in ileum of IR vs IS group, suggesting that miR-7134-5p targeting to NFATC4, miR-500 targeting to ELK1, HSPA2 and IL7R, and miR-92b-3p targeting to CLCF1 were probably involved in piglet resisting C. perfringens type C. Conclusions: The results will provide value resources for better understanding of the genetic basis of C. perfringens type C resistance in piglet and lays a new foundation for identifying novel markers of C. perfringens type C resistance
2022-04-24 | GSE130471 | GEO
Project description:Purpose: RNA-Seq has become a powerful tool for investigating transcriptional profiles in gene expression analysis, which would help to reveal the molecular mechanism of Clostridium perfringens type C infecting the piglets. In this study, we analyzed miRNA profiles of the spleen of piglets caused by Clostridium perfringens type C. Methods: 30 normal 7-day-old piglets (Y x L), without infecting Clostridium perfringens type C, Escherichia coli and Salmonella, were selected as experimental subjects. 25 piglets were randomly selected as the experimental group, which were disposed once a day for 5 days. Each piglet was dosed with 1 ml of bouillon culture-medium inoculated Clostridium perfringens type C at 37℃ for 16h, which approximate to 1 x109 CFU per ml. Then, 5 piglets were randomly selected as the control group (SC), which were taken the equal volume medium for 5 days.Based on total diarrhea scores, 25 piglets were ranked from high to low. The top and last five piglet were considered as sensitive group (SS) and resistant group (SR), respectively. Finally, spleen were collected and sequenced for miRNA. Result: 88 differentially expressed miRNAs were found. KEGG pathway analysis for target genes revealed that these miRNAs were involved in MAPK signaling pathway, mTOR signaling pathway, FoxO signaling pathway, p53 signaling pathway and ECM-receptor interaction. And 4 miRNAs (miR-133b, miR-532-3p, miR-339-5p and miR-331-3p) of closely related to piglets resistance to C. perfringens type C were obtained. The expression correlation analysis between these miRNAs and target genes revealed that the expression of miR-133b and miR-532-3p had negative correlation with their target NFATC4, miR-339-5p had negative correlation with target HTRA3, and miR-339-5p and miR-331-3p had negative correlation with target TNFAIP8L2 in spleen, suggesting that miR-133b and miR-532-3p targeting to NFATC4, miR-339-5p targeting to HTRA3, and miR-339-5p and miR-331-3p targeting to TNFAIP8L2 were probably involved in piglet resisting C. perfringens type C. Conclusions:The results will provide value resources for better understanding of the genetic basis of C. perfringens type C resistance in piglet and lays a new foundation for identifying novel markers of C. perfringens type C resistance.
2020-06-04 | GSE145302 | GEO
Project description:RevR is a putative orphan response regulator with a high degree of similarity to YycF from Bacilus subtilis and PhoB from Clostridium kluyveri. A revR deletion mutant of C. perfringens strain 13 was generated and the transcriptome analysed using microarrays.
2011-01-17 | GSE26508 | GEO
Project description:Clostridium acetobutylicum has been extensively exploited to produce biofuels and solvents and its biofilm could dramatically improve its productivities. However, genetic control of C. acetobutylicum biofilm has not been dissected so far. Here, a total of 24 disruptants were finally obtained over several years of attempts. Biofilm formation and physiological phenotypes were characterized for these disruptants and most of them showed robust biofilm formation still, or showed both impaired biofilm formation and cell growth. Only a mutant with a disputed histidine kinase gene (CA_C2730, designated bfcK in this study) abolished biofilm formation without impaired cell growth or solvent production. Phosphoproteomic analysis revealed that bfcK could control C. acetobutylicum flagellar motility at both translational and post-translational (protein phosphorylation) levels. The bfcK also showed apparent regulation of a serine/threonine protein kinase (encoded by CA_C0404) which was involved in protein secretion. Based on these findings, possible bfcK-based mechanisms for biofilm formation in C. acetobutylicum were proposed.
2021-07-30 | PXD021161 | Pride