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Progenitor Translatome Changes Coordinated by Tsc1 Increase Perception of Wnt Signals to End Nephrogenesis

ABSTRACT: Progenitor Translatome Changes Coordinated by Tsc1 Increase Perception of Wnt Signals to End Nephrogenesis

PROVIDER: PRJNA724992 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR14320904_1.fastq.gz	Fastqsanger.gz
	SRR14320904_2.fastq.gz	Fastqsanger.gz
	SRR14320905_1.fastq.gz	Fastqsanger.gz
	SRR14320905_2.fastq.gz	Fastqsanger.gz

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Progenitor Translatome Changes Coordinated by Tsc1 Increase Perception of Wnt Signals to End Nephrogenesis

Project description:Progenitor Translatome Changes Coordinated by Tsc1 Increase Perception of Wnt Signals to End Nephrogenesis

| PRJNA724990 | ENA

Progenitor Translatome Changes Coordinated by Tsc1 Increase Perception of Wnt Signals to End Nephrogenesis [10x_scRNA-seq]

Project description:Progenitor Translatome Changes Coordinated by Tsc1 Increase Perception of Wnt Signals to End Nephrogenesis [10x_scRNA-seq]

| PRJNA724994 | ENA

Progenitor translatome changes coordinated by Tsc1 increase perception of Wnt signals to end nephrogenesis.

Project description:Mammalian nephron endowment is determined by the coordinated cessation of nephrogenesis in independent niches. Here we report that translatome analysis in Tsc1+/- nephron progenitor cells from mice with elevated nephron numbers reveals how differential translation of Wnt antagonists over agonists tips the balance between self-renewal and differentiation. Wnt agonists are poorly translated in young niches, resulting in an environment with low R-spondin and high Fgf20 promoting self-renewal. In older niches we find increased translation of Wnt agonists, including R-spondin and the signalosome-promoting Tmem59, and low Fgf20, promoting differentiation. This suggests that the tipping point for nephron progenitor exit from the niche is controlled by the gradual increase in stability and possibly clustering of Wnt/Fzd complexes in individual cells, enhancing the response to ureteric bud-derived Wnt9b inputs and driving synchronized differentiation. As predicted by these findings, removing one Rspo3 allele in nephron progenitors delays cessation and increases nephron numbers in vivo.

| S-EPMC8566581 | biostudies-literature

Progenitor Translatome Changes Coordinated by Tsc1 Increase Perception of Wnt Signals to End Nephrogenesis

Project description:This series contains bulk RNA-Seq data dervied from FACS-isolated nephron progenitor cells for transcripts associated with ribosomal protein L10a (TRAP approach)

2021-09-24 | GSE173264 | GEO

Progenitor Translatome Changes Coordinated by Tsc1 Increase Perception of Wnt Signals to End Nephrogenesis

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

2021-09-24 | GSE173266 | GEO

Progenitor Translatome Changes Coordinated by Tsc1 Increase Perception of Wnt Signals to End Nephrogenesis [10x_scRNA-seq]

Project description:This series contains scRNA-Seq data generated using the 10x Genomcis chromium v2 platform for embryonic day 14 and postnatal day 0 mouse kidneys isolated from three different genotypes representing control and elevated nephron number mouse phenotypes.

2021-09-24 | GSE173265 | GEO

Tsc1 promotes the differentiation of memory CD8+ T cells via orchestrating the transcriptional and metabolic programs

Project description:Memory CD8+ T cells are an essential component of protective immunity. Signaling via mechanistic target of rapamycin (mTOR) has been implicated in the regulation of the differentiation of effector and memory T cells. However, little is understood about the mechanisms that control mTOR activity, or the effector pathways regulated by mTOR, in this process. We describe here that tuberous sclerosis 1 (Tsc1), a regulator of mTOR signaling, plays a crucial role in promoting the differentiation and function of memory CD8+ T cells in response to Listeria monocytogenes infection. Mice with specific deletion of Tsc1 in antigen-experienced CD8+ T cells evoked normal effector responses, but were markedly impaired in the generation of memory T cells and their recall responses to antigen re-exposure in a cell-intrinsic manner. Tsc1 deficiency suppressed the generation of memory-precursor effector cells (MPECs) while promoting short-lived effector cell (SLEC) differentiation. Functional genomic analysis indicated that Tsc1 coordinated gene expression programs underlying immune function, transcriptional regulation and cell metabolism. Furthermore, Tsc1 deletion led to excessive mTORC1 activity and dysregulated cellular metabolism including glycolytic and oxidative metabolism. These findings establish a Tsc1-mediated checkpoint in linking immune signaling and cell metabolism to orchestrate memory CD8+ T cell development and function. We used microarrays to explore the gene expression profiles differentially expressed in OVA-specific CD8+ T-cells from wild-type (WT; Tsc1-fl/fl and cre-negative) and Tsc1-/- (Tsc1-fl/fl and Granzyme B-cre-positive) mice

2014-09-20 | E-GEOD-61591 | biostudies-arrayexpress

Transcriptomic analysis of adipocyte Tsc1 knockout mammary glands.

Project description:We report here the adipocyte-specific ablation of Tsc1 and its affects on lactation and mammary gland function. In this dataset, mammary glands from wild-type and adipocyte Tsc1 knockout mice were isolated during lactation and analysed by RNAseq. Deletion of Tsc1 is predicted to activate mTORC1 in both peripheral and mammary adipocytes. This study demonstrates that deletion of Tsc1 in adipocytes changes mammary gland histology, and function resulting in changes to breastmilk composition.

2021-05-28 | GSE175620 | GEO

Tuberous sclerosis complex 1 (Tsc1) enforces quiescence of naive T cells to promote immune homeostasis and function

Project description:The mechanisms that regulate T cell quiescence are poorly understood. We report that tuberous sclerosis complex 1 (Tsc1) establishes a quiescent program in naïve T cells by controlling cell size, cell cycle entry, and responses to T cell receptor stimulation. Loss of quiescence predisposed Tsc1-deficient T cells to apoptosis that depleted conventional T cells and invariant natural killer T cells. Loss of Tsc1 function dampened in vivo immune responses to bacterial infection. Tsc1-deficient T cells exhibited increased mTORC1 but diminished mTORC2 activities, with mTORC1 activation essential for the disruption of immune homeostasis. Therefore, Tsc1-dependent control of mTOR is crucial in establishing naïve T cell quiescence to facilitate adaptive immune function. Naïve CD4 and CD8 T cells from wild-type and Tsc1-deficient mice (in triplicates each group) were stimulated with or without TCR signaling. RNA was analyzed by microarrays. WT/KO for 0 and 4 hr for CD4 (triplicates), and WT/KO for 0 hr for CD8 (duplicates).

2011-07-11 | E-GEOD-29797 | 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

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