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ASH2L controls ureteric bud morphogenesis via regulation of RET/GFRA1 signaling activity

ABSTRACT: ASH2L controls ureteric bud morphogenesis via regulation of RET/GFRA1 signaling activity

PROVIDER: PRJNA859007 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20218814_1.fastq.gz	Fastqsanger.gz
	SRR20218814_2.fastq.gz	Fastqsanger.gz
	SRR20218815_1.fastq.gz	Fastqsanger.gz
	SRR20218815_2.fastq.gz	Fastqsanger.gz
	SRR20218822_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

ASH2L controls ureteric bud morphogenesis via regulation of RET/GFRA1 signaling activity [RNA-seq]

Project description:ASH2L controls ureteric bud morphogenesis via regulation of RET/GFRA1 signaling activity [RNA-seq]

| PRJNA859015 | ENA

ASH2L controls ureteric bud morphogenesis via regulation of RET/GFRA1 signaling activity [CUT&Tag]

Project description:ASH2L controls ureteric bud morphogenesis via regulation of RET/GFRA1 signaling activity [CUT&Tag]

| PRJNA859014 | ENA

ASH2L controls ureteric bud morphogenesis via regulation of RET/GFRA1 signaling activity [CUT&Tag]

Project description:To elucidate the role of H3K4 methylation in metanephros development, we selectively inactivated ASH2L, core subunit of the COMPASS complex in mice UB lineage. We then performed histone H3K4me3 modification landscape profiling of the control (Hoxb7Cre-GFP+,Ash2l F/+) and mutant (Hoxb7Cre-GFP+,Ash2l F/F) FACS-sorted UB lineage cells at E16.5 by CUT&Tag-seq.

2023-01-18 | GSE208273 | GEO

ASH2L controls ureteric bud morphogenesis via regulation of RET/GFRA1 signaling activity [RNA-seq]

Project description:To elucidate the role of H3K4 methylation in metanephros development, we selectively inactivated ASH2L, core subunit of the COMPASS complex in mice UB lineage. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different FACS-sorted UB lineage cells at E16.5 of the control and cKO mouse embryos.

2023-01-18 | GSE208274 | GEO

ASH2L controls ureteric bud morphogenesis via regulation of RET/GFRA1 signaling activity

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

2023-01-18 | GSE208275 | GEO

HNF1B controls epithelial organization and cell polarity during ureteric bud branching and collecting duct morphogenesis

Project description:Kidney development depends critically on proper ureteric bud branching giving rise to the entire collecting duct system. The transcription factor HNF1B is required for the early steps of ureteric bud branching. Yet, the molecular and cellular events regulated by HNF1B are poorly understood. We report that specific removal of Hnf1b from the ureteric bud leads to defective cell-cell contacts and apico-basal polarity during the early branching events. High resolution ex vivo imaging combined with a membranous fluorescent reporter strategy show decreased mutant cell-rearrangements during mitosis-associated cell dispersal and severe epithelial disorganisation. Molecular analysis reveals downregulation of Gdnf-Ret pathway components and suggests that HNF1B acts both upstream and downstream of Ret-signaling by directly regulating Gfrα1 and Etv5. Subsequently, Hnf1b-deletion leads to massively mispatterned ureteric tree network, defective collecting duct differentiation and disrupted tissue architecture leading to cystogenesis. Consistently, mRNA-seq analysis performed from E15.5 control and mutant kidneys shows that the most impacted genes encode intrinsic cell-membrane components with transporter activity. Our study uncovers a fundamental and recurrring role of HNF1B in epithelial organization during early ureteric bud branching and further patterning and differentiation of the collecting duct system. Article submitted to Development. Authors: Audrey Desgrange, Claire Heliot,Ilya Skovorodkin, Saad U. Akram, Janne Heikkilä, Veli-Pekka Ronkainen, Ilkka Miinalainen I., Seppo J. Vainio and Silvia Cereghini

2017-12-15 | GSE106085 | GEO

Ret-dependent cell rearrangements in the Wolffian duct epithelium initiate ureteric bud morphogenesis.

Project description:While the genetic control of renal branching morphogenesis has been extensively described, the cellular basis of this process remains obscure. GDNF/RET signaling is required for ureter and kidney development, and cells lacking Ret are excluded from the tips of the branching ureteric bud in chimeric kidneys. Here, we find that this exclusion results from earlier Ret-dependent cell rearrangements in the caudal Wolffian duct, which generate a specialized epithelial domain that later emerges as the tip of the primary ureteric bud. By juxtaposing cells with elevated or reduced RET activity, we find that Wolffian duct cells compete, based on RET signaling levels, to contribute to this domain. At the same time, the caudal Wolffian duct transiently converts from a simple to a pseudostratified epithelium, a process that does not require Ret. Thus, both Ret-dependent cell movements and Ret-independent changes in the Wolffian duct epithelium contribute to ureteric bud formation.

| S-EPMC2762206 | biostudies-literature

Semaphorin3a inhibits ureteric bud branching morphogenesis.

Project description:Class 3 semaphorins are guidance proteins involved in axon pathfinding, vascular patterning and lung branching morphogenesis in the developing mouse embryo. Semaphorin3a (Sema3a) is expressed in renal epithelia throughout kidney development, including podocytes and ureteric bud cells. However, the role of Sema3a in ureteric bud branching is unknown. Here we demonstrate that Sema3a plays a role in patterning the ureteric bud tree in both metanephric organ cultures and Sema3a mutant mice. In vitro ureteric bud injection with Sema3a antisense morpholino resulted in increased branching, whereas recombinant SEMA3A inhibited ureteric bud branching and decreased the number of developing glomeruli. Additional studies revealed that SEMA3A effects on ureteric bud branching involve downregulation of glial cell-line derived neurotrophic factor (GDNF) signaling, competition with vascular endothelial growth factor A (VEGF-A) and decreased activity of Akt survival pathways. Deletion of Sema3a in mice is associated with increased ureteric bud branching, confirming its inhibitory role in vivo. Collectively, these data suggest that Sema3a is an endogenous antagonist of ureteric bud branching and hence, plays a role in patterning the renal collecting system as a negative regulator.

| S-EPMC3992265 | biostudies-literature

Generation of kidney ureteric bud and collecting duct organoid

Project description:A platform for generating expandable, branching and gene-editable ureteric bud organoid from primary mouse and human ureteric bud progenitor cells and human pluripotent stem cells, and its maturation into collecting duct organoid.

2021-05-11 | GSE149109 | GEO

Gdnf-treated murine intestinal organoids and sorted Ret+ and Ret- single cells

Project description:Adjacent stroma, including subepithelial fibroblasts, are believed to coordinate the differentiation process of epithelial cells, but the mechanisms are not well understood. Glial cell line-derived neurotrophic factor (GDNF) is expressed in the intestinal Pdgfra high subepithelial myofibroblasts (SEMFs), while the GDNF receptor RET is expressed in a subset of enteroendocrine cells (EECs), indicating regulatory crosstalk. In this experiment, single RET+ intestinal cells were sorted the gene expression profile was compared to non-RET cells. This provided knowledge about RET+ cell types. RET+ cells were upregulated with most of the EEC markers, indicating that RET+ cells are expressed in EECs. We also observed the differences in the gene expression profile of stromal-derived GDNF ligand on intestinal organoids. Organoids were derived from intestinal crypts of WT mice C57BL/6J and treated with 500ng/ml of Gdnf and Gfra1. GDNF-treated organoids induced the expression of EEC genes such as Pyy, Tac1, Tph1, and Cck, indicating enhanced differentiation of EC cell and L-I-N cell lineages. This highlights a stroma-epithelium crosstalk pathway regulating the differentiation of intestinal EEC subtypes.

2024-10-17 | GSE259326 | GEO

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