MRNA degradation in Mycobacterium smegmatis under aerobic conditions
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ABSTRACT: Transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance. mRNA half-lives were calculated from the decay of signal intensity from T0. Three replicates were sampled before transcription arrest, and after 5 and 10 minutes of mRNA decay for a total of 9 arrays. Five minutes of RNA degradation occurred during the processing of these samples, therefore sample times, indicated in the sample name, represent 0, five, and ten minutes of RNA degradation.
Project description:Transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance. mRNA half-lives were calculated from the decay of signal intensity from T0. Four replicates were sampled after 0, 5 10, 15, 20, and 30 minutes of mRNA decay for a total of 24 arrays.
Project description:After induction of DosR from a tet regulated promoter (uninduced controls were treated with an equivalent ammount of the solvent, DMSO), transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance. mRNA half-lives were calculated from the decay of signal intensity from T0. Three replicates for each condition (DosR induced and uninduced) were sampled after 0, 10, 20, 30, and 60 minutes of mRNA decay for a total of 30 arrays.
Project description:Transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance at 20C (cold) or in 0.2%O2 (hypoxia). mRNA half-lives were calculated from the decay of signal intensity from T0. Three replicates were sampled after 0, 1, 2, and 5 hours of mRNA decay in both cold and hypoxia for a total of 24 arrays.
Project description:This SuperSeries is composed of the following subset Series: GSE36341: mRNA degradation in Mycobacterium tuberculosis under aerobic conditions GSE36342: mRNA degradation in Mycobacterium smegmatis under aerobic conditions GSE36343: mRNA degradation in Mycobacterium tuberculosis during cold and hypoxic stress GSE36344: mRNA degradation in Mycobacterium tuberculosis with DosR ectopically induced Refer to individual Series
Project description:Expression data from hypoxic time course and transcription factor over expression experiments. (Abstract from paper will be appended after publication) Hypoxic time course experiments were done with a minimum of 3 replicates. TFOE are matched to the ChIP-seq experiment done simultaneously. This submission consists of the the gene expression component only.
Project description:Transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance. mRNA half-lives were calculated from the decay of signal intensity from T0.
Project description:Transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance. mRNA half-lives were calculated from the decay of signal intensity from T0.
Project description:Transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance at 20C (cold) or in 0.2%O2 (hypoxia). mRNA half-lives were calculated from the decay of signal intensity from T0.
Project description:After induction of DosR from a tet regulated promoter (uninduced controls were treated with an equivalent ammount of the solvent, DMSO), transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance. mRNA half-lives were calculated from the decay of signal intensity from T0.
Project description:Rifampin causes drug interactions by altering hepatic drug metabolism. Because microRNAs (miRNAs) have been shown to regulate genes involved in drug metabolism, we determined the effect of rifampin on the expression of hepatic miRNAs. Primary human hepatocytes from seven subjects were treated with rifampin, and the expression of miRNA and cytochrome P450 (P450) mRNAs was measured by TaqMan assays and RNA-seq, respectively. Rifampin induced the expression of 10 clinically important and 13 additional P450 genes and repressed the expression of 9 other P450 genes (P < 0.05). Rifampin induced the expression of 33 miRNAs and repressed the expression of 35 miRNAs (P < 0.05). Several of these changes were highly negatively correlated with the rifampin-induced changes in the expression of their predicted target P450 mRNAs, supporting the possibility of miRNA-induced regulation of P450 mRNA expression. In addition, several other miRNA changes were positively correlated with the changes in P450 mRNA expression, suggesting similar regulatory mechanisms. Despite the interindividual variability in the rifampin effects on miRNA expression, principal components analysis clearly separated the rifampin-treated samples from the controls. In conclusion, rifampin treatment alters miRNA expression patterns in human hepatocytes, and some of the changes were correlated with the rifampin-induced changes in expression of the P450 mRNAs they are predicted to target.