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NELF-A controls Drosophila healthspan by regulating heat-shock protein-mediated cellular protection and heterochromatin maintenance [RNA-seq]

ABSTRACT: Comparison of differentially expressed genes in Day 50 adult heterozygous NELF-A*/+ mutant (BX) and control sibling (Sib) fly heads (2 replicates).

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE155939 | GEO | 2020/11/30

REPOSITORIES: GEO

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NELF-A controls Drosophila healthspan by regulating heat-shock protein-mediated cellular protection and heterochromatin maintenance [ChIP-seq]

Project description:Comparison of differential H3K9me2 enrichment in Day 50 adult heterozygous NELF-A*/+ mutant (BX) and control sibling (Sib) fly heads (2 biological replicates).

2020-11-30 | GSE155938 | GEO

NELF-A controls Drosophila healthspan by regulating heat-shock protein-mediated cellular protection and heterochromatin maintenance

Project description:Epigenetic alteration is a hallmark of aging, but it remains unclear if perturbation of transcription machineries may affect longevity. NELF-mediated pausing of RNA polymerase II (RNAPII) constitutes an important step in transcription regulation. We found that halving NELF-A level in heterozygous mutants or via neuronal-specific depletion of NELF-A improves locomotor activity, stress resistance and lifespan of Drosophila significantly. Mechanistically, lower NELF-A releases paused RNAPII to facilitate productive transcription of the heat-shock protein (Hsp) genes. Elevated HSPs attenuate the level of protein aggregation, reactive oxidative species, DNA damage and systemic inflammation in the brains of NELF-A depleted flies. This protection is conserved in human cells where NELF-A depletion confers improved resistance against oxidative stress. Reduced oxidative DNA damage allows the maintenance of H3K9me2-enriched heterochromatin, which represses the activation of specific retrotransposons during aging. Therefore, by regulating transcription of Hsp genes in the brains, NELF-A controls multiple aspects of aging in Drosophila.

2020-11-30 | GSE155940 | GEO

NELF-A controls Drosophila healthspan by regulating heat-shock protein-mediated cellular protection and heterochromatin maintenance.

Project description: Not available

| S-EPMC8135010 | biostudies-literature

NELF-A controls Drosophila healthspan by regulating heat-shock protein-mediated cellular protection and heterochromatin maintenance

Project description:NELF-A controls Drosophila healthspan by regulating heat-shock protein-mediated cellular protection and heterochromatin maintenance

| PRJNA656115 | ENA

NELF-A controls Drosophila healthspan by regulating heat-shock protein-mediated cellular protection and heterochromatin maintenance [ChIP-seq]

Project description:NELF-A controls Drosophila healthspan by regulating heat-shock protein-mediated cellular protection and heterochromatin maintenance [ChIP-seq]

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NELF-A controls Drosophila healthspan by regulating heat-shock protein-mediated cellular protection and heterochromatin maintenance [RNA-seq]

Project description:NELF-A controls Drosophila healthspan by regulating heat-shock protein-mediated cellular protection and heterochromatin maintenance [RNA-seq]

| PRJNA656368 | ENA

NELF-dependent transcription activation

Project description:Jurkat T-cells were latently infected with a defective HIV provirus carrying a GFP reporer gene. The cells were superinfected with a lentiviral vector expressing shRNA to NELF-E. The impact of NELF-depletion on RNAP II distribution on cellular genes and the HIV provirus was measured by ChIP-Seq. Data sets contained between 45 and 56 million mapped reads Four samples were compared: Control shRNA, NELF-E shRNA, Control shRNA plus TNF-a, NELF-E shRNA plus TNF-a.

2014-03-26 | E-GEOD-47481 | biostudies-arrayexpress

NELF-A phosphorylation site identification

Project description:NELF-A phosphorylation by P-TEFb is a key event in the pausing release. We conduct IMAC-LC-MS-MS to identified NELF-A phosphorylation site by activation P-TEFb kinase.

2016-03-23 | PXD003433 | Pride

Heart tissue from Nelf-b CreER mice

Project description:Negative elongation factor (NELF) is known to enforce promoter-proximal pausing of RNA polymerase II (Pol II), a pervasive phenomenon observed across multicellular genomes. However, the physiological impact of NELF on tissue homeostasis remains unclear. Here we show for the first time that whole-body conditional deletion of the B subunit of NELF (NELF-B) in adult mice results in cardiomyopathy and impaired response to cardiac stress. Tissue-specific knockout of NELF-B confirms its cell-autonomous function in cardiomyocytes. NELF directly supports transcription of those genes encoding rate-limiting enzymes in fatty acid oxidation and the tricarboxylic acid (TCA) cycle. NELF also shares extensively transcriptional target genes with peroxisome proliferator-activated receptors alpha (PPARalpha), a master regulator of energy metabolism in myocardium. Mechanistically, NELF helps stablize the transcription initation complex at the metabolism-related genes. Our findings strongly indicate that NELF is part of the PPARalpha-mediated transcription regulatory network that maintains metabolic homeostasis in cardiomyocytes. 3 Nelf-b f/f and 3 Nelf-b f/f; CreER female mice were injected with Tamoxifen at 8 wk old. Heart tissue were harvested at 20 wks old and used for RNA preparation.

2014-03-01 | E-GEOD-54372 | biostudies-arrayexpress

Chromatin immunoprecipitation of Drosophila Schneider 2 cells using NELF-E and NELF-B antibodies

Project description:ChIP-chip analysis of GAGA factor and NELF in Drosophila S2 cells

2008-04-04 | E-MEXP-1547 | biostudies-arrayexpress