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Global analysis of gene expression changes following LINE1 inhibition [III]

ABSTRACT: Global analysis of gene expression changes following LINE1 inhibition [III]

PROVIDER: PRJNA437623 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6821750.fastq.gz	Fastqsanger.gz
	SRR6821751.fastq.gz	Fastqsanger.gz
	SRR6821742.fastq.gz	Fastqsanger.gz
	SRR6821752.fastq.gz	Fastqsanger.gz
	SRR6821743.fastq.gz	Fastqsanger.gz

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Global analysis of gene expression changes following LINE1 inhibition

Project description:Global analysis of gene expression changes following LINE1 inhibition

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Global analysis of gene expression changes following LINE1 inhibition [III]

Project description:Transposable elements make up nearly half of mammalian genomes, yet are generally described as ‘junk DNA’ or genome parasites. The LINE1 retrotransposon is the most abundant class and is thought to be deleterious for cells, but it is paradoxically expressed at high levels during early development. Here, we report that LINE1 plays essential roles in mouse embryonic stem (ES) cells and pre-implantation embryos. In ES cells, LINE1 acts as a nuclear RNA scaffold that recruits Nucleolin and Kap1/Trim28 to repress Dux, the master activator of a gene expression program specific to the 2-cell stage. In parallel, LINE1 RNA mediates binding of Nucleolin and Kap1 to rDNA, thereby promoting rRNA synthesis and ES cell self-renewal. In embryos, LINE1 RNA is required for silencing of Dux, proper synthesis of rRNA and exit from the 2-cell stage. These results reveal an essential partnership between nuclear LINE1 RNA and chromatin factors in the regulation of transcription, developmental potency and ES cell self-renewal.

2018-06-30 | GSE111633 | GEO

Global analysis of gene expression changes following LINE1 inhibition [II]

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2018-06-30 | GSE100937 | GEO

MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing

Project description:This SuperSeries is composed of the following subset Series: GSE32180: MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing [microarray] GSE32184: MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing [deep sequencing] Refer to individual Series

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CHK1 inhibition following gemcitabine treatment

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Global analysis of gene expression changes following LINE1 inhibition

Project description:This SuperSeries is composed of the SubSeries listed below.

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Effect of mitochEffect of mitochondrial complex III chronic inhibition on mitochondrial proteomic landscapeondrial complex III chronic inhibition on mitochondrial proteomic landscape

Project description:The mitochondria play a vital role in controlling cell metabolism and regulating crucial cellular outcomes. We previously demonstrated that chronic inhibition of the mitochondrial complex III in rats by Antimycin A (AA) induced pulmonary vasoconstriction. On the metabolic level, AA-induced mitochondrial dysfunction resulted in a glycolytic shift that was reported as the primary contributor to pulmonary hypertension pathogenesis. However, the regulatory proteins driving this metabolic shift with complex III inhibition are yet to be explored. Therefore, to delineate the mechanisms, we followed the rat lung mitochondrial proteomics. Rats treated with the complex III inhibitor, Antimycin-A for up to 24 days, showed a disturbed mitochondrial proteome with significant changes in 28 proteins (p<0.05). We observe a time-dependent decrease in the expression of key proteins that regulate fatty acid oxidation, the tricarboxylic acid cycle, electron transport chain, and amino acid metabolism, indicating diminished mitochondrial function. We also found a significant dysregulation in proteins that control protein import, and the clearance and detoxification of oxidatively damaged peptides via proteolysis and mitophagy. This could lead to the onset of mitochondrial toxicity due to the misfolded protein's stress. We conclude that chronic inhibition of the mitochondrial complex III attenuates mitochondrial function by disruption of global mitochondrial metabolism. This potentially aggravates cellular proliferation by initiating a glycolytic switch and thereby leading to pulmonary hypertension.

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