ScRNA-seq analysis of skin CD45+ cells mice where Tsc2 is deleted in CD11c-expressing cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1054187 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27276263.fastq.gz | Fastqsanger.gz | |||
| SRR27276264.fastq.gz | Fastqsanger.gz | |||
| SRR27276265.fastq.gz | Fastqsanger.gz | |||
| SRR27276266.fastq.gz | Fastqsanger.gz | |||
| SRR27276267_1.fastq.gz | Fastqsanger.gz |
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Project description:RNA-seq analysis of FACS-sorted control and Tsc2-deleted nociceptors
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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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Project description:scRNA-seq analysis of duodenum CD68+ macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells
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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.
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Project description:Microglia, the parenchymal macrophage of the central nervous system serve crucial remodeling functions throughout development in response to developmental cues. Microglia are transcriptionally heterogenous, suggesting that distinct microglial states confer distinct roles. Currently, little is known about how dynamic these states are, the cues that promote them, or how they impact microglial function. In the developing retina, we previously found a significant proportion of microglia that express CD11c (Integrin αX, complement receptor 4, Itgax). which has also been reported in other developmental and disease contexts. Here, we sought to understand the regulation and function of CD11c+ microglia by examining the developmental contexts and dynamics for the emergence of CD11c+ microglia. We find that microglial CD11c expression tracks with prominent waves of neuronal apoptosis in postnatal retina. Using genetic fate mapping, we provide evidence that microglia transition out of the CD11c state to return to homeostasis. We show that CD11c+ microglia have elevated lysosomal content and contribute to the clearance of apoptotic neurons, and found that acquisition of CD11c expression is, in part, dependent upon the TAM receptor Axl. Using selective ablation, we find similar effects on apoptotic cell clearance with depletion of CD11c+ versus non-CD11c microglia, suggesting that CD11c+ microglia are not uniquely critical for phagocytic clearance. Together, our data suggests CD11c+ microglia are a transient state induced in response to developmental apoptosis rather than a specialized subset mediating phagocytic elimination.
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Project description:Transcriptome analysis of dentritic cells from the spleen (CD11c+) or MLN (CD11c+CD103+) of mice with DC-specific deletion of TGFBR2 gene, or their control littermates. TRGFR2 gene was deleted in dendritic cells using Cre/lox approach. Mice with this deletion develop spontaneous multi-organ autoimmune inflammation and die by 15 weeks of age. Splenic CD11c+ Dc were isolated by magetic cell sorting. MLN CD11c+CD103+ DC were flow sorted. RNA was isolated using RNAqueous-Micro kit (Ambion) and analyzed using Affymetrix Mouse Exon 1.0 ST Array
2012-07-25 | E-GEOD-39651 | biostudies-arrayexpress
Project description:Transcriptome analysis of dentritic cells from the spleen (CD11c+) or MLN (CD11c+CD103+) of mice with DC-specific deletion of TGFBR2 gene, or their control littermates. TRGFR2 gene was deleted in dendritic cells using Cre/lox approach. Mice with this deletion develop spontaneous multi-organ autoimmune inflammation and die by 15 weeks of age.
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