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RNA-seq analysis of sorted duodenum epithelial cells and duodenum lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

ABSTRACT: RNA-seq analysis of sorted duodenum epithelial cells and duodenum lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

PROVIDER: PRJNA807361 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18042600.fastq.gz	Fastqsanger.gz
	SRR18042601.fastq.gz	Fastqsanger.gz
	SRR18042602.fastq.gz	Fastqsanger.gz
	SRR18042603.fastq.gz	Fastqsanger.gz
	SRR18042604.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of sorted duodenum epithelial cells and duodenum lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:Iron is an essential cellular and important for many physiological functions including erythropoiesis and host defense. It is taken up from the diet in the duodenum, the first part of the small intestine by enterocytes and loaded onto transferrin, the main iron transport molecules in the circulation. Macrophages are ancient sentinel cells that are implicated in all steps of systemic iron metabolism except duodenal iron import. By assessing mice that harbor a macrophage-specific deletion of the tuberous sclerosis complex 2 (Tsc2), a negative regulator of mTORC1, we found that these mice possessed various defects in iron metabolism including defective steady state erythropoiesis and a highly reduced saturation of transferrin with iron. This iron-deficiency phenotype was caused by a block of iron import from the duodenal epithelial cells into the circulation. Activation of mTORC1 in villous duodenal CD68+ macrophages induced expression of serine proteases and promoted local degradation of the major iron transport molecule transferrin, whereas depletion of macrophages in mice increased transferrin levels in the duodenal villi. Inhibition of serine protease activity restored transferrin levels in the Tsc2-deficient mice. Physiologically, transferrin levels were regulated in the villi during Citrobacter rodentium infection in mice. These data show that transferrin is controlled locally in the duodenum and establish macrophages as regulators of duodenal iron uptake.

2023-06-08 | GSE196815 | GEO

scRNA-seq analysis of duodenum CD68+ macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:scRNA-seq analysis of duodenum CD68+ macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

| PRJNA809313 | ENA

scRNA-seq analysis of duodenum CD68+ macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:Iron is an essential cellular trace element and important for many physiological functions including erythropoiesis and host defense. It is taken up from the diet in the duodenum, the first part of the small intestine by enterocytes and loaded onto transferrin, the main iron transport molecules in the circulation. Macrophages are ancient sentinel cells that are implicated in all steps of systemic iron metabolism except duodenal iron import. By assessing mice that harbor a macrophage-specific deletion of the tuberous sclerosis complex 2 (Tsc2), a negative regulator of mTORC1, we found that these mice possessed various defects in iron metabolism including defective steady state erythropoiesis and a highly reduced saturation of transferrin with iron. This iron-deficiency phenotype was caused by a block of iron import from the duodenal epithelial cells into the circulation. Activation of mTORC1 in villous duodenal CD68+ macrophages induced expression of serine proteases and promoted local degradation of the major iron transport molecule transferrin, whereas depletion of macrophages in mice increased transferrin levels in the duodenal villi. Inhibition of serine protease activity restored transferrin levels in the Tsc2-deficient mice. Physiologically, transferrin levels were regulated in the villi during Citrobacter rodentium infection in mice. These data show that transferrin is controlled locally in the duodenum and establish macrophages as regulators of duodenal iron uptake.

2023-06-08 | GSE197175 | GEO

RNA-seq analysis of sorted colon epithelial cells and colon lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:RNA-seq analysis of sorted colon epithelial cells and colon lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

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RNA-seq analysis of FACS-sorted control and Tsc2-deleted nociceptors

Project description:RNA-seq analysis of FACS-sorted control and Tsc2-deleted nociceptors

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RNA-seq analysis of FACS-sorted control and Tsc2-deleted nociceptors

Project description:The goals of this study are to compare the transcriptomes of control heterozygous and Tuberous sclerosis 2 (Tsc2) homozygous nociceptors that have been enriched by fluorescence-associated cell sorting (FACS) with the aim of identifying differences in genes associated with sensory behavior. Nav1.8-Cre transgenic mice were used to delete Tsc2 as well as express Green fluorescent protein from the Rosa26 locus. Tsc2 deletion constitutively activates mTORC1 signaling cell autonomously. Dissociated dorsal root ganglia from adult mice were FACS-sorted for GFP and analyzed by RNA-seq. We find that a number of sensory behavior associated genes are affected by Tsc2 deletion including Calca, Ntrk1, Mrgpra3, and Nppb. Additionally, profiling of ion channel expression showed a reduction in almost half of expressed sodium, potassium and calcium channel as well as G-protein coupled receptors. Other categories of genes such as transcription factors and ligand-gated ion channels contained an even numbers of up- and downregulated genes with many that did not change as a result of Tsc2 deletion. In addition, expression of most marker genes enriched in Isolectin B4 (IB4) negative neurons were strongly reduced in Tsc2 mutant nociceptors, consistent with reduced sensitivity to heat, which is a modality related to these neurons. We conclude Tsc2 deletion and consequent mTORC1 activation alters gene expression of nociceptors resulting in altered sensory thresholds.

2018-04-01 | GSE112499 | GEO

Gene expression profiling of mT/mG;Lyz2.Cre vs IKKbetaf/f;Lyz2.Cre mouse bone marrow derived macrophages

Project description:Gene expresion comparison between tomato Lyz2 Cre and IKKbeta flox/flox Lyz2 Cre bone marrow derived macrophages

2019-06-28 | GSE94880 | GEO

RNA-seq of depdc5-/-, tsc2-/-, depdc5-/- x tsc2-/- and wildtype zebrafish larvae

Project description:Transcriptome analysis of the heads of 5 dpf epdc5-/-, tsc2-/-, depdc5-/- x tsc2-/- and wildtype zebrafish larvae to provide insights into the neuropathological processes underlying the observed epileptic phenotype in sv2a-/- zebrafish larvae.

2022-09-12 | E-MTAB-11776 | biostudies-arrayexpress

Drosophila S2R+ / TSC1 / TSC2 mutant phosphoproteomics

Project description:The tuberous sclerosis complex (TSC) family of tumor suppressors, TSC1 and TSC2, function together in an evolutionarily conserved protein complex that is a point of convergence for major cell signaling pathways that regulate mTOR complex 1 (mTORC1). Mutation or aberrant inhibition of the TSC complex is common in various human tumor syndromes and cancers. The discovery of novel therapeutic strategies to selectively target cells with functional loss of this complex is therefore of substantial clinical relevance to TSC and sporadic cancers. We developed a CRISPR-based method to generate homogenous mutant Drosophila cell lines. By combining TSC1 and TSC2 mutant cell lines with RNAi screens against all kinases and phosphatases, we identified synthetic interactions with TSC1 and TSC2. Knockdown of three candidate genes (mRNA-cap, Pitslre and CycT; orthologs of RNGTT, CDK11 and CCNT1 in humans) reduced the population growth rate of both Drosophila TSC1 and TSC2 mutant cells but not that of wild-type cells. Moreover, knockdown of all three genes displayed similar selective effects in mammalian TSC2-deficient cell lines, including human tumor-derived cells, illustrating the power of this cross species screening strategy to identify potential drug targets.

2018-10-24 | PXD002670 | Pride

Tsc2 coordinates differentiation

Project description:Tsc2 coordinates differentiation

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