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Tsc2 coordinates differentiation [bulkRNA-seq]

ABSTRACT: Tsc2 coordinates differentiation [bulkRNA-seq]

PROVIDER: PRJNA954865 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24149307_1.fastq.gz	Fastqsanger.gz
	SRR24149307_2.fastq.gz	Fastqsanger.gz
	SRR24149308_1.fastq.gz	Fastqsanger.gz
	SRR24149308_2.fastq.gz	Fastqsanger.gz
	SRR24149309_1.fastq.gz	Fastqsanger.gz

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Project description:Multipotent neural stem cells (NSCs) that reside within the ventricular-subventricular zone (V-SVZ) of the brain generate a variety of cell types. Here we provide transcriptomes of NSCs that have lost Tsc2 as occurs in the neurodevelopmental disorder Tuberous Sclerosis Complex (TSC).

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Tsc2 coordinates differentiation

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Project description:Multipotent neural stem cells (NSCs) that reside within the ventricular-subventricular zone (V-SVZ) of the brain generate a variety of cell types. Here we provide transcriptomes of cells that have lost Tsc2 as occurs in the neurodevelopmental disorder Tuberous Sclerosis Complex (TSC).

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

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<i>Tsc2</i> coordinates neuroprogenitor differentiation.

Project description:Neural stem cells (NSCs) of the ventricular-subventricular zone (V-SVZ) generate numerous cell types. The uncoupling of mRNA transcript availability and translation occurs during the progression from stem to differentiated states. The mTORC1 kinase pathway acutely controls proteins that regulate mRNA translation. Inhibiting mTORC1 during differentiation is hypothesized to be critical for brain development since somatic mutations of mTORC1 regulators perturb brain architecture. Inactivating mutations of TSC1 or TSC2 genes cause tuberous sclerosis complex (TSC). TSC patients have growths near the striatum and ventricles. Here, it is demonstrated that V-SVZ NSC Tsc2 inactivation causes striatal hamartomas. Tsc2 removal altered translation factors, translatomes, and translational efficiency. Single nuclei RNA sequencing following in vivo loss of Tsc2 revealed changes in NSC activation states. The inability to decouple mRNA transcript availability and translation delayed differentiation leading to the retention of immature phenotypes in hamartomas. Taken together, Tsc2 is required for translational repression and differentiation.

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

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

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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.

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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.

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