Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The small RNA Teg41 Regulates Expression of the alpha Phenol Soluble Modulins and is Required for Virulence in Staphylococcus aureus

ABSTRACT: The small RNA Teg41 Regulates Expression of the alpha Phenol Soluble Modulins and is Required for Virulence in Staphylococcus aureus

PROVIDER: PRJNA423193 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

The small RNA Teg41 Regulates Expression of the alpha Phenol Soluble Modulins and is Required for Virulence in Staphylococcus aureus

Project description:Small RNAs (sRNAs) remain an understudied class of regulatory molecules in bacteria. Hundreds of sRNAs have been identified in the major human pathogen Staphylococcus aureus; however, only a few have been characterized in detail. In this study we investigate the role of the sRNA Teg41 in S. aureus virulence. We demonstrate that Teg41, an sRNA divergently transcribed from the locus that encodes the cytolytic alpha phenol soluble modulin (αPSM) peptides, plays a critical role in αPSM production. Overproduction of Teg41 leads to an increase in αPSM levels and a corresponding increase in hemolytic activity from S. aureus cells and cell-free culture supernatants. We demonstrate that the increase in αPSM production is post-transcriptional, as expression of the αPSM transcript is unaltered upon Teg41 overproduction. To identify regions of Teg41 important for its function we performed an in silico RNA:RNA interaction analysis which predicted an interaction between the 3’ end of Teg41 and the αPSM transcript. Deleting a 24-nucleotide region from the S. aureus genome, corresponding to the 3’ end of Teg41, led to a 10-fold reduction in αPSM-dependent hemolytic activity and attenuation of virulence in a murine abscess model of infection. Together these results demonstrate, for the first time, post-transcriptional regulation of the αPSM peptides by an sRNA in S. aureus.

2019-01-01 | GSE108336 | GEO

Effect of S. epidermidis phenol-soluble modulins on primary human keratinocytes.

Project description:To investigate the effect of synthetic phenol-soluble modulins (PSMs) secreted by S. epidermidis on primary keratinocytes. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.

2023-01-01 | GSE209653 | GEO

Effect of S. epidermidis phenol-soluble modulins on murine dorsal skin (24h)

Project description:To investigate the effect of both S. epidermidis phenol-soluble modulins (PSMs) and EcpA genetic knockouts on murine back skin. We then performed gene expression profiling analysis using data obtained from RNA-seq of 5 conditions (n=3 per condition).

2023-07-01 | GSE210046 | GEO

Identification of post-translational modifications on soluble alpha-Syn purified from various alpha-Synucleinopathies

Project description:LC-MS/MS analyses were performed on soluble alpha-Syn purified from PD and various alpha-Synucleinopathies to systematically explore the landscape of post-translational modifications (PTMs) on soluble alpha-Syn, leading to the identification of a large number of novel alpha-Syn PTMs.

2022-10-30 | MSV000090618 | MassIVE

The Small RNA Teg41 Regulates Expression of the Alpha Phenol-Soluble Modulins and Is Required for Virulence in Staphylococcus aureus.

Project description: Not available

| S-EPMC6428751 | biostudies-literature

Identification of post-translational modifications on soluble alpha-Synuclein purified from various alpha-Synucleinopathies by LC-MSMS

2023-02-02 | PXD037994 | Pride

phenol degrading consortium

Project description:Phenol bioremediation from groundwater

| PRJNA741716 | ENA

Project description:The small RNA Teg41 regulates expression of the alpha Phenol Soluble Modulins (αPSMs) and is required for virulence in Staphylococcus aureus

| PRJNA445980 | ENA

Phenol-soluble modulins--critical determinants of staphylococcal virulence.

Project description: Not available

| S-EPMC4072763 | biostudies-literature

Microglia infection of Listeria monocytogenes is regulated by ActA virulence factor and TNF-α.

Project description:Cerebral listeriosis is characterized by neuronal apoptosis and microglial cell activation, but little is known about the bacterial virulence factors involved in this process and how bacterial dissemination is controlled. Here, we show that the cellular target of Listeria monocytogenes (LM) in murine hippocampal cultures is microglia rather than neurons or other glial cells, which are rarely infected. This in vitro model served to demonstrate that infected microglial cells release a soluble factor to the medium responsible for neuronal apoptosis. We investigated the production of this factor in a well-established murine microglia cell model BV2 cells, and compared with J-774 macrophage cells after infection with different LM bacterial mutants. Our purpose was to study in both cell types parameters such as the listericidal capacities, pro-inflammatory cytokines released, and bacterial factors involved in the intracellular cycle. Our data reveal that microglia shows unique features to handle a LM infection. Microglia is three times more permissive for LM intracellular growth than murine macrophages; while producing five times higher levels of pro-inflammatory cytokines IL-6, MCP-1 and TNF-α than macrophages. Using different LM mutants (i.e., LMWT, LM∆LLO, LM∆ActA or LM∆plcB) we conclude that LLO and ActA are not involved in LM proliferation within microglia cells, while they are required for survival within macrophages. Moreover, ActA controls TNF-α production, a cytokine involved in neural apoptosis. Transcriptional differential response of microglia infected with different LM mutants reflected ActA controls the TNF-a signaling pathway through out molecules and chemokines involved in this pathway such as NFkβ, MAPK-1, Ccl2, Ccl3, Ccl4 and CxCl10.

2011-10-03 | GSE32505 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data