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A conserved cytosine-rich sRNA interacting with mycobacterial ribosome and mediate rifampicin phenotypic resistance

ABSTRACT: A conserved cytosine-rich sRNA interacting with mycobacterial ribosome and mediate rifampicin phenotypic resistance

PROVIDER: PRJNA630594 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11699715_1.fastq.gz	Fastqsanger.gz
	SRR11699715_2.fastq.gz	Fastqsanger.gz
	SRR11699716_1.fastq.gz	Fastqsanger.gz
	SRR11699716_2.fastq.gz	Fastqsanger.gz
	SRR11699717_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

A conserved cytosine-rich sRNA interacting with mycobacterial ribosome and mediate rifampicin phenotypic resistance

Project description:NOT PROVIDED; REQUESTED

2020-05-07 | GSE149937 | GEO

Transcription profiling by array of Rifampicin-induced transcriptome response in rifampicin-resistant Mycobacterium tuberculosis

Project description:Tuberculosis (TB) is still a major life-threatening infectious disease, within which especially the rise of multidrug resistant TB (MDR-TB) is currently worrying. This study focuses on mechanisms of development of rifampicin resistance, since rifampicin seems to play an important role in the development of MDR-TB. To provide further insight in rifampicin resistance, we performed a genome-wide transcriptional profile analysis for Mycobacterium tuberculosis (M. tuberculosis) using microarray technology and qRT-PCR analysis. We exposed a rifampicin-susceptible H37Rv wild type (H37Rv-WT) and a rifampicin-resistant progeny H37Rv strain with a H526Y mutation in the rpoB gene (H37Rv-H526Y) to several concentrations of rifampicin, to define the effect of rifampicin on the transcription profile. Our study showed that there are resistance-dependant differences in response between both M. tuberculosis strains. Gene clusters associated with efflux, transport and virulence were altered in the rifampicin-resistant H37Rv mutant compared to the rifampicin-susceptible H37Rv-WT strain after exposure to rifampicin. We conclude that the small gene cluster Rv0559c-Rv0560c in the H37Rv-H526Y strain was remarkably up-regulated in the microarray analysis and qRT-PCR results and appeared to be dependent on rifampicin concentration and time of exposure. Therefore this study suggests that Rv0559c and Rv0560c play a pivotal role in rifampicin resistance of M. tuberculosis. Further investigation of Rv0559c and Rv0560c is needed to reveal function and mechanism of both genes that were triggered upon rifampicin exposure. [Data is also available from http://bugs.sgul.ac.uk/E-BUGS-139]

2013-04-21 | E-BUGS-139 | biostudies-arrayexpress

Molecular insights into RNA polymerase recycling by mycobacterial HelD

Project description:Mycobacterial HelD is a transcription factor that binds RNA polymerase (RNAP) and thereby rescues it from stalled transcription complexes. HelD also protects RNAP against the antibiotic rifampicin. HelD, however, must be released from the rescued RNAP to participate in the next round of the transcription cycle. The exact mechanism of this release is unknown. Here we show that HelD from Mycobacterium smegmatis can form a complex with RNAP, together with σA primary sigma factor, and RbpA, but not CarD, transcription factors. Using cryo-EM, we solved a series of RNAP-σA-RbpA-HelD structures with or without promoter DNA. These snapshots capture the involvement of HelD in transcription initiation, describes mechanistic aspects of HelD release, and its protective effect against rifampicin. Biochemical evidence supports these findings, defines the role of ATP binding/hydrolysis to/by HelD in the process, and functionally confirms the rifampicin-protective effect of HelD. Taken together, HelD assists an alternative pathway of transcription initiation.

2024-10-08 | PXD046632 | Pride

Rifampicin-mouse liver proteomics

Project description:Tuberculosis is one of top causes of death among curable infectious diseases; it is an airborne infectious disease that kills 2 million people worldwide. Anti-tuberculosis drug-induced liver injury is the primary cause of drug-induced liver injury (DILI). Rifampicin is one of the most common anti-tuberculosis therapies and has well-known hepatotoxicity. To understand the mechanism of rifampicin-induced liver injury, we performed a global proteomic analysis of liver proteins by LC-MS/MS in a mouse model after the oral administration of 177 and 442.5 mg/kg rifampicin (LD10 and LD25) for 14 days. Based on the biochemical parameters in the plasma after rifampicin treatment, the hepatotoxic effect of rifampicin in the mouse liver was defined as a mixed liver injury. In the present study, we identified 1,101 proteins and quantified 1,038 proteins. A total of 29 and 40 proteins were up-regulated and 27 and 118 proteins were down-regulated in response to 177 and 442.5 mg/kg rifampicin, respectively.

2017-07-10 | PXD006313 | Pride

Caulobacter crescentus mRNA half-lives by rifampicin transcription shutoff

Project description:mRNA half-life profiling in the bacterium Caulobacter crescentus was preformed by shutting of transcription with the antibiotic rifampicin, and following mRNA abundance at 1, 2, 4, 8, and 15 minutes post rifampicin. All RNA measurements were performed on cells grown to mid-log in M2G minimal growth medium. Two biological replicates time coursees were collected from independent starter cultures.

2020-09-04 | GSE157432 | GEO

In vivo gene expression analysis of C elegans in response to rifampicin

Project description:We have discovered rifampicin as a glycation inhibitor, which increases life span in C elegans. In order to understand the mechanism of rifampicin action, microarray analysis was performed to study the changes in gene expression brought about by the drug.

2014-12-31 | GSE45292 | GEO

Mycobacterial communities in pulmonary NTM

Project description:Profiling Mycobacterial Communities in Pulmonary Nontuberculous Mycobacterial Disease

| PRJEB22153 | ENA

Rifampicin test as a predictor of Irinotecan toxicity in metastatic colorectal cancer.

Project description:Interventions: The patients with metastatic colorectal cancer being considered for Irinotecan treatment will take single 900 mg dose of oral rifampicin. Bilirubin levels will be measured after 4 hours. The patients will go on to have standard Irinotecan treatment. There will be at least 48 hours interval between rifampicin ingestion and irinotecan treatment. They will be monitored for toxicities especially diarrhoea and neutropenia after cycle 1 irinotecan. A correlation will be done between rise in bilirubin and toxicities. Both the intervention- rifampicin intake and irinotecan administration will be on a single day only 2 days apart. Patients will be monitored for 3 weeks after irinotecan dose for toxicities. Blood will also be analysed for UGT 1A1 polymorphism and correlated with toxicities and rise in bilirubin. Primary outcome(s): To determine if rifampicin induced hyperbilirubinemia can predict irinotecan toxicity.[Measured on day 21 after irinotecan dose.] Study Design: Purpose: Diagnosis; Allocation: Non-randomised trial; Masking: Open (masking not used);Assignment: Single group;Type of endpoint: Safety

| 2453055 | ecrin-mdr-crc

Atorvastatin, rosuvastatin and rifampicin effect on human primary hepatocyte transcriptome

Project description:This SuperSeries is composed of the following subset Series: GSE24186: Atorvastatin, rosuvastatin and rifampicin effect on human primary hepatocyte transcriptome [Steroltalk platform] GSE24187: Atorvastatin, rosuvastatin and rifampicin effect on human primary hepatocyte transcriptome [Affymetrix platform] Refer to individual Series

2011-09-04 | E-GEOD-24188 | biostudies-arrayexpress

The effect of rifampicin on human mononuclear cell gene expression

Project description:The aim of the study was to elucidate the effects of pregnane receptor X (PXR) activation by rifampicin on the mononuclear cell gene expression in vivo.

2020-03-23 | GSE108100 | GEO

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