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Bulk RNA sequencing of mouse embryonic fibroblasts in autophagy processes

ABSTRACT: Bulk RNA sequencing of mouse embryonic fibroblasts in autophagy processes

PROVIDER: PRJNA822101 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18579833_1.fastq.gz	Fastqsanger.gz
	SRR18579833_2.fastq.gz	Fastqsanger.gz
	SRR18579834_1.fastq.gz	Fastqsanger.gz
	SRR18579834_2.fastq.gz	Fastqsanger.gz
	SRR18579835_1.fastq.gz	Fastqsanger.gz

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Bulk RNA sequencing of mouse embryonic fibroblasts in autophagy processes

Project description:Autophagy, a catabolic process to remove unnecessary or dysfunctional cells, is triggered by various signals including nutrient starvation. Depending on the type of the nutrient deficiency, diverse sensing mechanisms and pathways are used for autophagy, suggesting subsequent nutrient dependent transcriptional regulation. Still, however, our knowledge about nutrient specific transcriptional regulation during autophagy is limited. To understand nutrient type dependent transcriptional mechanisms during autophagy, we performed single cell RNA sequencing (scRNAseq) for the mouse embryonic fibroblasts (MEFs) before and after applying glucose- (GS) as well as amino acid starvation (AAS). Trajectory analysis using scRNAseq identified sequential induction of potential transcriptional regulators for each deficiency condition. Gene regulatory rules inferred using TENET newly identified CCAAT/enhancer binding protein γ (C/EBPγ) regulates autophagy processes specifically to AAS condition. Strikingly, knockdown of C/EBPγ attenuated the autophagic process only in the AAS condition. Cell biological and biochemical studies validated that C/EBPγ plays a switching role for ATF4 to activate autophagy genes under AAS, but not under GS. Together, our data identified C/EBPγ as a previously unidentified key regulator under amino acid starvation-induced autophagy.

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Mouse embryonic fibroblasts in autophagy processes

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

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Bulk mRNA sequencing of wildtype (WT) and mutator mouse embryonic fibroblasts (MEFs)

Project description:Bulk mRNA sequencing of wildtype (WT) and mutator mouse embryonic fibroblasts (MEFs)

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Bulk ATAC-seq data of fibroblasts from healthy mouse tissues

Project description:Bulk ATAC-seq was performed on fibroblasts from 8 different healthy mouse tissues such as bone, epididymal and inguinal fat pads, omentum, liver, lung and lymph node. This data was used to examine tissue specific chromatin landscapes in fibroblasts.

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T-cell intracellular antigen (TIA) proteins deficiency in murine embryonic fibroblasts alters cell cycle progression and induces autophagy

Project description:Background: Mice lacking either T-cell intracellular antigen 1 (TIA1) or TIA1-related/like protein (TIAR/TIAL1) show high rates of embryonic lethality, suggesting a relevant role for these proteins during embryonic development. However, intrinsic molecular and cellular consequences of either TIA1 or TIAR deficiency remain poorly defined. Results: By using genome-wide expression profiling approach, we demonstrate that either TIA1 or TIAR inactivation broadly alter normal development-associated signaling pathways in murine embryonic fibroblasts (MEF). Indeed, these analyses highlighted alterations of cytokine-cytokine and ECM-receptor interactions and Wnt, MAPK, TGF-beta dependent signaling pathways. Consistent with these results, TIA1 and TIAR knockout (KO) MEF show reduced rates of cell proliferation, cell cycle progression delay and increased cell size. Furthermore, TIA-proteins deficiency also caused metabolic deficiencies, increased ROS levels and DNA damage, promoting a gentle rise of cell death. Concomitantly, high rates of autophagy were detected in both TIA1 and TIAR KO MEF with induction of the formation of autophagosomes, as evidenced by the up-regulation of the LC3B protein, and autolysosomes, measured by colocalization of LC3B and LAMP1, as a survival mechanism attempt. Conclusions: Taken together, these observations support that TIA proteins orchestrate a transcriptome programme to activate specific developmental decisions. This program is likely to contribute to mouse physiology starting at early stages of the embryonic development. TIA1/TIAR might function as cell sensors to maintain homeostasis and promote adaptation/survival responses to developmental stress. Two independent replicates were performed for each experimental condition and hybridized to Agilent SurePrint G3 Mouse 8x60 microarrays.

2014-11-05 | E-GEOD-43077 | biostudies-arrayexpress

Expression data from mouse embryonic fibroblasts

Project description:Expression data from mouse embryonic fibroblasts

| PRJNA768829 | ENA