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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

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

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

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

Comparison of E14.5 embryonic kidney transcriptomes (Grb2 ureteric-specific knockout vs wild-type)

Project description:Grb2 is a small SH2-SH3 adaptor molecule that interacts with activated tyrosine kinase receptors (RTKs), providing a crucial link towards downstream activation of pro-proliferative and pro-survival ERK and Akt signaling pathways. Ret and FGFR2, two RTKs that interact with Grb2, play important roles in ureteric branching and the proper establishment of the renal collecting duct system, but it is unclear whether Grb2 is required in this process. In this study, we selectively ablated a conditional floxed allele of the Grb2 gene within the ureteric epithelial lineage in mice and demonstrate that Grb2 signaling is essentially required for proper collecting duct development. Ureteric Grb2 deficiency results in perinatal lethality and severe renal hypodysplasia closely reminiscent of the rudimentary kidney phenotypes observed in Ret-null mutant mice. Grb2 loss attenuates ERK and Akt activation in the ureteric epithelia resulting in pronounced impairment of ureteric branching. Gene expression analysis reveals that Grb2 deficiency results in defective induction of genes implicated in both ureteric branching and reciprocal mesenchymal metanephric induction. Our findings therefore strongly indicate that Grb2 is a physiologically-relevant major RTK signaling relay partner that promotes renal branching morphogenesis and the proper development of the collecting duct system and the urogenital tract. Microarray was used to profile and compare the transcriptomes of developing kidneys of E14.5 Grb2 conditional knockout (ureteric-bud specific) and wild-type embryos

2023-12-01 | GSE163040 | GEO

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

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