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Transcriptome of Drosophila S2 cells stressed upon amino-acid starvation in KRB (Krebs Ringer Bicarbonate)

ABSTRACT: Transcriptome of Drosophila S2 cells stressed upon amino-acid starvation in KRB (Krebs Ringer Bicarbonate)

PROVIDER: PRJNA601750 | ENA |

REPOSITORIES: ENA

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Transcriptome of Drosophila S2 cells stressed upon amino-acid starvation in KRB (Krebs Ringer Bicarbonate)

Project description:The phase separation of the non-membrane bound Sec bodies occurs in Drosophila S2 cells by coalescence of components of the ER exit sites under the stress of amino-acid starvation. Here we provide the comparison of the gene expression profiles of S2 cells grown in full medium (Schneider's) and S2 cells upon of amino-acid starvation in KRB

2020-01-17 | GSE143810 | GEO

Transcriptional response to single amino acid starvation in HeLa cells

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APEX2 labeling of Sec bodies in S2 cells

Project description:APEX2 was tagged to Sec24AB protein in S2 cells. Biotinylation was triggeredin resting cells and amino acid starved cells for comparative analyses of Sec24AB interactome. Sec24AB is localised to Sec bodies during starvation, thereby allowing the identification of protein components in Sec bodies.

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AmpliSeq Data of WT and SLC38A10 knockout primary cortex cells in amino acid starvation and refed conditions

Project description:Samples-WT Basal condition primary cortex cells; WT B27 Starved-Primary cortex cells starved overnight without B27 supplement media. WT AA Starved-Primary cortex cell starved without amino acid for 2 hours. WT AA Refed-Primary cortex cell refed for 1 hour after amino acid starvation. KO Basal-SLC38 Knockout Primary cortex cells starved overnight without B27 supplement media. KO B27 Starved-SLC38 Knockout Primary cortex cell starved without amino acid for 2 hours. KO AA starved-SLC38 Knockout Primary cortex cell refed for 1 hour after amino acid starvation. KO AA Refed-SLC38 Knockout Primary cortex cell refed for 1 hour after amino acid starvation.

2021-06-03 | E-MTAB-10413 | biostudies-arrayexpress

Ribosome profiling and parallel RNA-seq of S. pombe cells subject to amino acid starvation

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The nutrient-sensing GCN2 signaling pathway is essential for circadian clock function by regulating histone acetylation under amino acid starvation

Project description:Circadian clocks are evolved to adapt to the daily environment changes under different conditions. The ability to maintain circadian clock functions in response to various stress and perturbations is important for organismal fitness. Here, we show that the nutrient sensing GCN2 signaling pathway is required for robust circadian clock function under amino acid starvation in Neurospora. The deletion of GCN2 pathway components disrupts rhythmic transcription of clock gene frq by suppressing WC complex binding at the frq promoter due to its reduced histone H3 acetylation levels. Under amino acid starvation, the activation of GCN2 kinase and its downstream transcription factor CPC-1 establish a proper chromatin state at the frq promoter by recruiting the histone acetyltransferase GCN-5. The arrhythmic phenotype of the GCN2 kinase mutants under amino acid starvation can be rescued by inhibiting histone deacetylation. Finally, genome-wide transcriptional analysis indicates that the GCN2 signaling pathway maintains robust rhythmic expression of metabolic genes under amino acid starvation. Together, these results uncover an essential role of GCN2 signaling pathway in maintaining robust circadian clock function in response to amino acid starvation and the importance of histone acetylation at the frq locus in rhythmic gene expression.

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Transcriptional response to single amino acid starvation in HEK293T cells

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Transcriptional response to single amino acid starvation in HeLa cells

Project description:Transcriptional response to single amino acid starvation in HeLa cells

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Expression profiling of E.coli K-12 wild-type vs. delta dksA cells upon amino acid starvation

Project description:Actively dividing cells perform robust and accurate DNA replication during fluctuating nutrient availability, yet factors that prevent disruption of replication remain largely unknown. Here we report that DksA, a nutrient-responsive transcription factor, ensures replication completion in Escherichia coli. In the absence of DksA, replication is rapidly arrested upon amino acid starvation. This replication arrest occurs independently of exogenous DNA damage, yet it induces the DNA damage response and recruits the main recombination protein RecA. This microarray experiment compares the transcriptional responses to amino acid starvation in wild-type and delta dksA cells. The SOS-regulated genes are highly induced in delta dksA cells.

2010-06-01 | GSE19742 | GEO

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