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Transcriptomic analysis of ethanol, DMSO, I-CBP112 and C646 treatment on mouse embryonic fibroblasts (MEFs) during direct cardiac reprogramming

ABSTRACT: Transcriptomic analysis of ethanol, DMSO, I-CBP112 and C646 treatment on mouse embryonic fibroblasts (MEFs) during direct cardiac reprogramming

PROVIDER: PRJNA699894 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13642819_1.fastq.gz	Fastqsanger.gz
	SRR13642819_2.fastq.gz	Fastqsanger.gz
	SRR13642820_1.fastq.gz	Fastqsanger.gz
	SRR13642820_2.fastq.gz	Fastqsanger.gz
	SRR13642821_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of ethanol, DMSO, I-CBP112 and C646 treatment on mouse embryonic fibroblasts (MEFs) during direct cardiac reprogramming

Project description:Direct cardiac reprogramming represents an attractive way of reversing heart damage caused by myocardial infarction. Yet, it is still in pre-clinical stage mainly due to the lack of efficacy with current transdifferentiation protocols. Here, we describe that dimethyl sulfoxide (DMSO) is capable of augmenting direct cardiac reprogramming in vitro. Treatment of Gata4, Hand2, Mef2c and Tbx5 (GHMT) - transduced mouse embryonic fibroblasts (MEFs) with 1% DMSO induced ~5 fold increase in the percentage of Myh6-mCherry+ cells, and significantly increased the global expression of cardiac genes. Transcriptomic studies were carried out to explore the underlying mechanism of how DMSO may enhance cardiac transdifferentiation.

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Transcriptomic analysis of DMSO treatment on mouse embryonic fibroblasts (MEFs) during cardiac transdifferentiation

Project description:Cardiac transdifferentiation represents an attractive way of reversing heart damage caused by myocardial infarction. Yet, it is still in pre-clinical stage mainly due to the lack of efficacy with current transdifferentiation protocols. Here, we describe that dimethyl sulfoxide (DMSO) is capable of augmenting cardiomyocyte transdifferentiation in vitro. Treatment of Gata4, Hand2, Mef2c and Tbx5 (GHMT) - transduced mouse embryonic fibroblasts (MEFs) with 1% DMSO induced ~5 fold increase in the percentage of Myh6-mCherry+ cells, and significantly increased the global expression of cardiac genes. Transcriptomic studies were carried out to explore the underlying mechanism of how DMSO may enhance cardiac transdifferentiation.

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Transcriptomic analysis of DMSO treatment on mouse embryonic fibroblasts (MEFs) during cardiac transdifferentiation

Project description:Transcriptomic analysis of DMSO treatment on mouse embryonic fibroblasts (MEFs) during cardiac transdifferentiation

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Correcting Direct Effects of Ethanol on Translation and Transcription Machinery Confers Ethanol Tolerance in Bacteria [Terminator_Readthrough_RNAseq]

Project description:The molecular mechanisms of ethanol toxicity and tolerance in bacteria, while important for biotechnology and bioenergy applications, remain incompletely understood. Genetic studies have identified potential cellular targets for ethanol and revealed multiple mechanisms of tolerance, but it remains difficult to separate direct and indirect effects of ethanol. We used adaptive evolution to generate spontaneous ethanol-tolerant strains of Escherichia coli, then characterized the mechanisms of toxicity and resistance associated with select mutations. Evolved alleles of metJ, rho, and rpsQ were sufficient to recapitulate much of the observed ethanol tolerance, implicating translation and transcription as key processes affected by ethanol. We found that ethanol induces mistranslation errors during protein synthesis, and that the evolved rpsQ allele protects cells by rendering the ribosome hyper-accurate. Ribosome profiling and RNAseq analyses of the ethanol-tolerant strain versus the wild type established that ethanol negatively affects transcriptional and translational processivity. Ethanol-stressed cells exhibited ribosomal stalling at internal AUG codons, which may be ameliorated by the adaptive inactivation of the MetJ repressor of methionine biosynthesis genes. Ethanol also caused aberrant intragenic transcription termination for mRNAs with low ribosome density, which was reduced in a strain with the adaptive rho mutation. Furthermore, ethanol inhibited transcript elongation by RNA polymerase in vitro. We propose that ethanol-induced inhibition and uncoupling of mRNA and protein synthesis are major contributors to ethanol toxicity in E. coli, and that adaptive mutations in metJ, rho, and rpsQ protect central dogma processes in the presence of ethanol.

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Gene expression profiles in TICAM1 knockout and wild-type MEFs

Project description:TICAM1 knockout and wild-type (TICAM1 knockout MEFs with restored TICAM1 expression) MEFs were treated by c-di-GMP or DMSO for 4 hours. Total RNA was analyzed via Illumina Mouse Ref-8 V2. Changes in gene induction, especially of interferon-stimulated genes, between c-di-GMP and DMSO treated cells were examined.

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