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Mouse E14.5 Ret+ mechanoreceptors vs. laser captured spinal cord dorsal column midline cells

ABSTRACT: Mouse E14.5 Ret+ mechanoreceptors vs. laser captured spinal cord dorsal column midline cells

PROVIDER: PRJNA470524 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7135004_1.fastq.gz	Fastqsanger.gz
	SRR7135004_2.fastq.gz	Fastqsanger.gz
	SRR7135005_1.fastq.gz	Fastqsanger.gz
	SRR7135005_2.fastq.gz	Fastqsanger.gz
	SRR7135006_1.fastq.gz	Fastqsanger.gz

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Mouse E14.5 Ret+ mechanoreceptors vs. laser captured spinal cord dorsal column midline cells

Project description:Our study examined a population of radial glial-like cells (RGLCs) in the dorsal spinal cord midline that we showed provide long-distance growth support for longitudinal rapidly adapting (RA) mechanoreceptor axons during development of spinal cord dorsal column. To evaluate potential molecular markers of these cells, we isolated the RGLCs using hematoxylin and eosin staining to visualize the cell bodies in the dorsal column midline from E14.5 mouse embryos, and used laser capture microdissection for each sample ("LCM"). To compare transcript expression to the adjacent RA mechanoreceptive axons, we performed FACS of dorsal root ganglion of E14.5 Ret-Tdtomato+ RA mechanoreceptors. Our analyses revealed a high enrichment of radial glial-specific markers in the LCM replicates compared to Ret-Tdt samples. In contrast, neuronal-specific markers were more highly enriched in the Ret-Tdt samples, as expected. These data suggest the midline RGLCs are of radial glial identity. Others may find these data helpful in determining potential RGLC-mechanoreceptor molecular interactions in subsequent studies.

2018-05-30 | GSE114193 | GEO

RNA-SEQ analysis of E14.5 ALL Ret-positive (EGFP-labeled) FACSd dorsal root ganglia neurons.

Project description:The goal of this set is to build expression data using FACS isolated Ret-positive cells harvested from a Ret-EGFP reporter mouse (embryonic day E14.5). These can be used as a time point in comparative analysis of ontogeny of genes expressed at various developmental time points.

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Transcriptome profile of wildtype and Ret homozygote null mouse guts at E10.5 ,E12.5 and E14.5

Project description:Total mRNA seq was perfomed on widtype and Ret null mouse embryonic gut at 3 stages of devlopment- E10.5, E12.5 and E14.5

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Gene expression profiling of laser-captured microdissected avascular neocortex in E14.5 neocortical cells were compared by microarray transcription profiling

Project description:Gene expression profiles among avascular region (around ventricular zone), highly vascularized region with honeycomb-patterned vascular plexus (around subventricular zone and intermediate zone), and cortical plate with vertically oriented vessels from laser-captured microdissected E14.5 neocortex were compared by microarray

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laser-captured chondrocyte transcriptomes from cranial base

Project description:laser-captured chondrocyte transcriptomes from cranial base

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Expression data of mouse ENCCs and mouse embryonic Gut E14.5

Project description:Signaling of the RET receptor is crucial for the migration, proliferation, differentiation and survival of enteric neural crest cells (ENCCs) that form the enteric nervous system (ENS). Disturbances in RET signaling are associated with ENS defects, as is seen in patients with Hirschsprung disease. However, the downstream effectors of RET signalling in ENCCs is largely unknown. This study aims to gain new insight into the pathways involved in or triggered by RET in ENCCs. We used microarrays to detect the gene expression of mouse embryonic ENCCs when we stimulated with GDNF compare to control without GDNF and also compare to the gene expression of mouse embryonic gut (all are isolated from mouse embryonic day 14.5). Our aim is to gain insight of RET-GDNF downstream effectors and also all signalling pathways that regulate by RET-GDNF in ENCCs during development. We performed gene expression profiling with RNA isolated from GDNF- (the RET ligand) stimulated and non-stimulated mouse ENCCs and also from mouse embryonic gut E14.5. We compare these three set of microarray data to each other and analyzed single-gene analysis methods. by this analysis we could detect genes that regulate by RET-GDNF signalling in ENCCs and by comparing data of ENCCs with and without GDNF to the expression data of mouse embryonic gut in the same stage of development, we could also detect gene that specifically express in ENCCs dependent and independently of RET-GDNF signalling. We analyzed the gene expression data of ENCCs with and without GDNF by gene set enrichment analysis (GSEA) to detect which pathways are down- and up-regulated by RET-GDNF signalling.

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RNA-seq of RET-aberrant cancer cell lines treated with RET-TKI selpercatinib

Project description:RET-aberrant cancer discovered as a relevant targetable oncogene in several types of tumors, whose inhibitors have marked efficacy. However, some of patients with RET-aberrant cancer are insensitive to RET- tyrosine kinase inhibitors (TKIs) and are clinically non-responders. Recently, drug-tolerant mechanisms have been gaining attention as targets for initial therapies aimed at overcoming drug resistance. However, the underlying mechanisms of drug-tolerant cells emergence treated with RET-TKIs derived from RET-aberrant cancer cells remains unknown. In this study, HER3 signal activity through YAP1 was led to maintaining cell survival and inducing the emergence of cells tolerant to RET-TKIs selpercatinib and pralsetinib in high YAP1 expressed RET- rearranged cancer cells. These results suggested that YAP1-HER3 axis plays pivotal roles for cell survival under an exposure with RET-TKIs in the intrinsic resistance to RET-TKIs and the emergence of tolerant cells by RET-TKIs in YAP1 expressed RET-aberrant cancer, suggesting that YAP1/HER3 inhibition and RET-TKIs is a highly potent combination for initial treatment.

2024-09-30 | GSE261830 | GEO

Ret loss-of-function decreases neural crest progenitor proliferation and restricts developmental fate potential during enteric nervous system development

Project description:The receptor tyrosine kinase gene RET plays a critical role in the fate specification of enteric neural crest cells (ENCCs) during enteric nervous system (ENS) development. Pathogenic RET loss of function (LoF) alleles are associated with Hirschsprung disease (HSCR), which is marked by aganglionosis of the gastrointestinal (GI) tract. ENCCs invade the developing GI tract, proliferate, migrate caudally, and differentiate into all of the major ENS cell types. Although the major phenotypic consequences, and the underlying transcriptional changes from Ret LoF in the developing ENS have been described, its cell type and state-specific effects are unknown. Consequently, we performed single-cell RNA sequencing (scRNA-seq) on an enriched population of ENCCs isolated from the developing GI tract of Ret null heterozygous and homozygous mouse embryos at embryonic day (E)12.5 and E14.5. We demonstrate four significant findings: (1) Ret-expressing ENCCs are a heterogeneous population composed of ENS progenitors as well as glial and neuronal committed cells; (2) neurons committed to a predominantly inhibitory motor neuron developmental trajectory are not produced under Ret LoF, leaving behind a mostly excitatory motor neuron developmental program; (3) HSCR-associated and Ret gene regulatory network genes exhibit distinct expression patterns across Ret-expressing ENCC cells with their expression impacted by Ret LoF; and (4) Ret deficiency leads to precocious differentiation and reduction in the number of proliferating ENS precursors. Our results support a model in which Ret contributes to multiple distinct cellular phenotypes and that Ret LoF contributes to GI aganglionosis in multiple independent ways.

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RET fusion genes, BCR-RET and FGFR1OP-RET, are associated with chronic myelomonocytic leukemia, display sensitivity to Sorafenib, an inhibitor of tyrosine-kinase activity and enhance monocytic differentiation

Project description:Myeloproliferative neoplasms are frequently associated with aberrant constitutive tyrosine kinase (TK) activity resulting from point mutations or chimaeric fusion genes, such as BCR ABL1 or JAK2 V617F. We report here for the first time in hematological malignancies, two novel fusion genes involving the TK RET, BCR-RET and FGFR1OP-RET, in chronic myelo monocytic leukemia (CMML) cases. The two RET fusion genes lead to the aberrant activation of RET, are able to transform hematopoietic cells and skew the hematopoietic differentiation program towards the monocytic/macrophage lineage. We also report that the BCR-RET fusion protein is insensitive to Imatinib but sensitive to Sorafenib in vivo. CMML is an hematopoietic malignancy associated with the frequent activation of the RAS pathway. The RET fusion genes seems to constitutively mimic the same signaling pathway than RAS mutations. Overall, the RET fusion genes behaviors in the monocytic lineage underlie the role of the normal RET TK activity during the physiological monocytic differentiation. We analysed BAF/3 cells infected by BCR-RET, FGFR1OP-RET or BCR-ABL1P210 fusion genes retroviruses and sorted out using EGFP fluorescence, with Affymetrix GeneChip MouseGene 1.0 ST platform.

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