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Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [chipseq]

ABSTRACT: Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [chipseq]

PROVIDER: PRJNA1137060 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29869238.fastq.gz	Fastqsanger.gz
	SRR29869239.fastq.gz	Fastqsanger.gz
	SRR29869240.fastq.gz	Fastqsanger.gz
	SRR29869241.fastq.gz	Fastqsanger.gz
	SRR29869242.fastq.gz	Fastqsanger.gz

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Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [chipseq]

Project description:Depletion of growth factors and nutrients induces cellular quiescence, which often accompanies transcriptional silencing and chromatin compaction. Paradoxically, such depletion occurs in pathological microenvironments in which fibroblasts are activated to orchestrate tissue remodeling. The relationship between fibroblast activation and growth factor and nutrient depletion remains unclear. Here, we report that serum depletion in cell culture, a model for growth factor and nutrient depletions, extensively activates transcription in fibroblasts, despite inducing quiescence. Activated genes were enriched for extracellular matrix (ECM) structural components and proteases. The ECM-related transcription accompanied activation of putative distal enhancers, but not promoters. The activated putative enhancers were enriched for non-coding variants associated with inflammatory bowel disease (IBD) risk, suggesting an alteration in the ECM remodeling gene regulatory network in IBD. This study implicates nutrient and growth factor depletion in activating the ECM remodeling gene program in fibroblasts, challenging the prevailing view linking such depletion to transcriptional dormancy.

2025-06-01 | GSE272507 | GEO

Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [bruseq]

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Starvation activates ECM-remodeling gene transcription and putative enhancers in fibroblasts despite inducing quiescence

Project description:Starvation activates ECM-remodeling gene transcription and putative enhancers in fibroblasts despite inducing quiescence

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Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [bruseq]

Project description:Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [bruseq]

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Starvation activates ECM-remodeling gene transcription and putative enhancers in fibroblasts despite inducing quiescence

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Serum starvation induces quiescence in ovarian cancer

Project description:While prior work in muscle cells indicates that metabolic reprogramming is associated with quiescence, whether metabolic changes occur in cancer to drive quiescence is unclear. We found that the metabolic enzyme ACSS2 is highly upregulated in quiescent ovarian cancer cells and overexpresssion of ACSS2 induces ovarian cancer quiescence.

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Parallel proteomics and phosphoproteomics defines starvation signal specific processes in cell quiescence

Project description:Cells arrest growth and enter a quiescent state upon nutrient deprivation. However, the molecular processes by which cells respond to different starvation signals to regulate exit from the cell division cycle and initiation of quiescence remains poorly understood. To study the role of protein expression and signaling in quiescence we combined temporal profiling of the proteome and phosphoproteome using stable isotope labeling with amino acids in cell culture (SILAC) in Saccharomyces cerevisiae (budding yeast). We find that carbon and phosphorus starvation signals activate quiescence through largely distinct proteome and phosphoproteome remodeling. However, increased expression of mitochondrial proteins is essential for quiescence establishment in response to both starvation signals. Whereas the quiescent proteome is established within 6 hours of starvation the quiescent phosphoproteome undergoes continuous changes for at least 30 hours following initial starvation. Deletion of the putative quiescence regulator RIM15, which encodes a serine-threonine kinase, results in reduced survival of cells starved for phosphorus and nitrogen, but not carbon. However, we identified common protein phosphorylation roles for RIM15 in quiescence that are enriched for RNA metabolism and translation. We also find evidence for RIM15-mediated phosphorylation of some targets, including IGO1, prior to starvation consistent with a functional role for RIM15 beyond quiescence regulation. Finally, we find evidence for widespread catabolism of amino acids in response to nitrogen starvation, indicating widespread amino acid recycling via salvage pathways in conditions lacking environmental nitrogen. Our study defines an expanded quiescent proteome and phosphoproteome in yeast, and highlights the multiple coordinated molecular processes at the level of protein expression that are required for quiescence.

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Serum starvation induces quiescence in ovarian cancer

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ECM-dependent gene expression in normal and tumor-derived mammary organoids

Project description:A critical step in metastasis is cancer cell dissemination. Dissemination and metastasis are associated with specific genetic changes and changes in extracellular matrix (ECM), but how these changes interact to enable dissemination remains unclear. Here we tested the importance of ECM to dissemination in both normal and malignant mammary epithelium. By time-lapse imaging, we observed collective invasion and dissemination directly in 3D culture. Our results reveal that the pattern of epithelial migration and local dissemination are constrained by the local ECM microenvironment. To identify RNA expression changes that could regulate these changes in cell behavior, we conducted whole genome RNA expression profiling from normal and malignant mammary epithelium in 3D culture. We collected RNA from normal and malignant epithelium during active growth at 4 days in culture in either Matrigel or collagen I. We hybridized the resulting RNA to Agilent single color microarrays with a minimum of three biologically independent microarray replicates per condition. We observed significant gene expression differences between normal and malignant epithelium, even when cultured in the same ECM. In contrast, the ECM microenvironment had a relatively small impact on RNA expression, despite its large effects on migratory strategy and local dissemination. Gene expression was measured in normal and malignant mammary epithelial fragments cultured in one of two 3D matrices (laminin-rich basement membrane gel or collagen I) and collected at day 4, which we observed to have peak invasion and dissemination. At least three independent experiments were performed at each time using different mice for each experiment.

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