RNase Y of Bacillus subtilis is a key member of the degradosome and important for bulk mRNA turnover. In contrast to B. subtilis, the RNase Y homologue (rny/cvfA) of Staphylococcus aureus is not essential for growth. Here we found that RNase Y plays a major role in virulence gene regulation. Accordingly, rny deletion mutants demonstrated impaired virulence in a murine bacteraemia model. RNase Y is important for the processing and stabilisation of the immature transcript of the global virulence regulator system SaePQRS. Moreover, RNase Y is involved in the activation of virulence gene expression at the promoter level. This control is independent of both the virulence regulator agr and the saePQRS processing and may be mediated by small RNAs some of which were shown to be degraded by RNase Y. Besides this regulatory effect, mRNA levels of several operons were significantly increased in the rny mutant and the half-life of one of these operons was shown to be extremely extended. However, the half-life of many mRNA species was not significantly altered. Thus, RNase Y in S. aureus influences mRNA expression in a tightly controlled regulatory manner and is essential for coordinated activation of virulence genes.
RNase Y of Staphylococcus aureus and its role in the activation of virulence genes.
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View SamplesDataset of IL-12+IL-18 trated and Yersinia enterocolitica infected C57BL/6 NK cells
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The Methyl-CpG-Binding Protein Mbd2 Regulates Susceptibility to Experimental Colitis via Control of CD11c<sup>+</sup> Cells and Colonic Epithelium.
Specimen part
View SamplesMice deficient in MBD2 (Mbd2-/-) were treated with 2% dextran sulfate sodium or normal drinking water for 6 continuous days. A single cell suspension of colon lamina propria and epithelium was isolated, with monocytes (CD11b+ Ly6CHi, MHC-II+/-), macrophages (CD11b+ Ly6C-MHC-II+), cDC2s (CD11b- CD11c+ CD103+) and epithelial cells (CD45- EpCAM+) purified by FACS.
The Methyl-CpG-Binding Protein Mbd2 Regulates Susceptibility to Experimental Colitis via Control of CD11c<sup>+</sup> Cells and Colonic Epithelium.
Specimen part
View SamplesT follicular helper cells (TFH) are heterogenic population of CD4+ T cells, expressing CXCR5+ and PD-1+ on their surface. Their role is linked to supporting formation of germinal centres (GC) and these cells are thought to express high levels of PD-1 marker. Two models of immunisation were used to investigate the role of PD-1 low TFH. In Salmonella enterica infection high frequency of T follicular helper cells expressing low levels of PD-1 surface molecule are observed within first week of infection but GC do not appear until much a later stage (week 7-8). Sheep red blood cell immunisation (SRBC) gives rise to both TFH and GC B cells within first week of response and these TFH express low to high level of PD-1 molecule.
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Sex, Specimen part
View SamplesMice deficient in MBD2 (Mbd2-/-) were treated with 2% dextran sulfate sodium or normal drinking water for 6 continuous days. A single cell suspension of colon lamina propria and epithelium was isolated, with monocytes (CD11b+ Ly6CHi, MHC-II+/-), macrophages (CD11b+ Ly6C-MHC-II+), cDC2s (CD11b- CD11c+ CD103+) and epithelial cells (CD45- EpCAM+) purified by FACS.
The Methyl-CpG-Binding Protein Mbd2 Regulates Susceptibility to Experimental Colitis via Control of CD11c<sup>+</sup> Cells and Colonic Epithelium.
Specimen part
View SamplesIn the current study, we investigated the collective roles of protein tyrosine phosphatases (PTPs) and histone deacetylases (HDACs) on regulation of IRG expression in human choriocarcinoma cells by genome-wide transcriptional profiling. Logic-rules were optimized to derive rules governing gene expression patterns observed upon different combinations of treatment with PTP and HDAC inhibitors. The data reveal that IRGs can be divided into distinct subsets that are differentially modulated by co-treatment of Jar cells with IFN-? and PTP versus HDAC inhibitors, respectively. Furthermore, promoter analysis of the genes governed by the rules identifies transcription factor binding sites associated with the different gene subsets. Thus, the regulatory modes identified in this study provide insights into the complex regulation of inflammatory pathways at the fetal-maternal interface, as well as mechanisms that choriocarcinoma cells may utilize to promote their survival.
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Sex, Specimen part, Cell line, Treatment
View SamplesRetinoic acid-inducible gene-I (RIG-I) is a cytosolic pathogen recognition receptor that initiates the innate immune response against many RNA viruses. RIG-I also has been shown to sense some DNA viruses, and host RNA polymerase III (RNA Pol III), a cytosolic DNA sensor, converts cytosolic AT-rich DNA into RNA to be sensed by RIG-I. We previously showed that the RIG-I restricts Kaposi Sarcoma-associated herpesvirus (KSHV) reactivation (J Virol. 2014 May;88(10):5778-87). In this study, we report that KSHV stimulates the RIG-I signaling pathway in an RNA Pol III-independent manner and subsequently induces type I IFN responses. Knockdown or inhibition of RNA Pol-III had no effect on IFN-ß induction by KSHV. By using CLIP (Cross-Linking and Immunoprecipitation) and RNA deep sequencing technologies, we identified multiple KSHV regions that give rise to RNA fragments binding to RIG-I, such as ORF810420-10496, ORF6411058-110675, Repeat region (LIR1)119059-119204, and ORF2543561-43650. The sequence dissimilarity between these fragments suggests that RIG-I detects a particular structure rather than a specific sequence motif. Synthesized ORF810420-10496 RNA stimulated RIG-I-dependent but RNA Pol III-independent IFN-ß signaling. In summary, some KSHV viral RNAs are sensed by RIG-I in an RNA Pol III-independent manner.
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Sex, Specimen part, Disease, Cell line, Treatment, Race
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Sex, Age, Specimen part, Disease, Cell line, Treatment
View SamplesFresh splenic Treg cells (CD4+CD25+YFP+) were isolated from 6-week-old Senp3+/+Foxp3-Cre and Senp3fl/flFoxp3-Cre mice and stimulated with anti-CD3 and anti-CD28 for 24 hours. Activated Treg cells were used for total RNA isolation with TRIzol and subjected to RNA-sequencing.
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Sex, Specimen part, Cell line, Treatment
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