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RNA deep sequencing data of the whole transcriptomes of the aa3 mutant, aa3 mprA double mutant, and aa3 rel double mutant strains of Mycobacterium smegmatis MC2 155

ABSTRACT: RNA deep sequencing data of the whole transcriptomes of the aa3 mutant, aa3 mprA double mutant, and aa3 rel double mutant strains of Mycobacterium smegmatis MC2 155

PROVIDER: PRJNA1109406 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28972300_1.fastq.gz	Fastqsanger.gz
	SRR28972300_2.fastq.gz	Fastqsanger.gz
	SRR28972301_1.fastq.gz	Fastqsanger.gz
	SRR28972301_2.fastq.gz	Fastqsanger.gz
	SRR28972302_1.fastq.gz	Fastqsanger.gz

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RNA deep sequencing data of the whole transcriptomes of the aa3 mutant, aa3 mprA double mutant, and aa3 rel double mutant strains of Mycobacterium smegmatis MC2 155

Project description:To identify the effect of additional deletion of rel and mprA in the aa3 mutant strain lacking the aa3 cytochrome c oxidase of the respiratory electron transport chain of Mycobacterium smegmatis MC2 155, we constructed the aa3 rel double mutant and aa3 mprA double mutant and profiled the transcriptomes of the aa3 mutant, aa3 mprA double mutant and aa3 rel double mutant strains. Our comparative RNA sequencing analysis revealed that expression of most ribosomal proteins was induced in the aa3 rel double mutant and aa3 mprA double mutant relative to the aa3 mutant.

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Project description:'The REL gene, encoding the NF-κB subunit c-Rel, is frequently amplified in B-cell lymphoma and functions as a tumour promoting transcription factor. Here we report the surprising result that c-rel -/- mice display significantly earlier lymphomagenesis in the c-Myc driven, Eμ-Myc model of B-cell lymphoma. c-Rel loss also led to earlier onset of disease in a separate TCL1-Tg driven lymphoma model. Tumour reimplantation experiments indicated that this is an effect intrinsic to the Eμ-Myc lymphoma cells but, counter-intuitively, c-rel -/- Eμ-Myc lymphoma cells were more sensitive to apoptotic stimuli. To learn more about why loss of c-Rel led to earlier onset of disease, microarray gene expression analysis was performed on B-cells from 4-week old, wild type and c-rel -/- Eμ-Myc mice. Extensive changes in gene expression were not seen at this age but among those transcripts significantly downregulated by the loss of c-Rel was the B-cell tumour suppressor BTB and CNC homology 2 (Bach2). Q-PCR and western blot analysis confirmed loss of Bach2 in c-Rel mutant Eμ-Myc tumours at both 4 weeks and the terminal stages of disease. Moreover Bach2 expression was also downregulated in c-rel -/- TCL1-Tg mice and RelA Thr505Ala mutant Eμ-Myc mice. Analysis of wild type Eμ-Myc mice demonstrated that the population expressing low levels of Bach2 exhibited the earlier onset of lymphoma seen in c-rel-/- mice. Confirming the relevance of these findings to human disease, analysis of ChIP-Seq data revealed that Bach2 is a c-Rel and NF-κB target gene in transformed human B-cells, while treatment of Burkitt''s lymphoma cells with inhibitors of the NF-κB/IKK pathway or deletion of c-Rel or RelA resulted in loss of Bach2 expression. This data reveals a surprising tumour suppressor role for c-Rel in lymphoma development explained by regulation of Bach2 expression, underlining the context dependent complexity of NF-κB signalling in cancer.'

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