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Insm1 induces neural progenitor delamination in developing neocortex via down-regulation of the adherens junction belt-specific protein Plekha7

ABSTRACT: Insm1 induces neural progenitor delamination in developing neocortex via down-regulation of the adherens junction belt-specific protein Plekha7

PROVIDER: PRJNA431778 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6514750.fastq.gz	Fastqsanger.gz
	SRR6514751.fastq.gz	Fastqsanger.gz
	SRR6514746.fastq.gz	Fastqsanger.gz
	SRR6514747.fastq.gz	Fastqsanger.gz
	SRR6514748.fastq.gz	Fastqsanger.gz

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Insm1 induces neural progenitor delamination in developing neocortex via down-regulation of the adherens junction belt-specific protein Plekha7

Project description:Delamination of neural progenitor cells (NPCs) from the ventricular surface is a crucial prerequisite to form the subventricular zone, the germinal layer linked to the expansion of the mammalian neocortex in development and evolution. Here, we dissect the molecular mechanism by which the transcription factor Insm1 promotes the generation of basal progenitors (BPs). Insm1 protein is most highly expressed in newborn BPs in mouse and human developing neocortex. Forced Insm1 expression in embryonic mouse neocortex causes NPC delamination, converting apical to basal radial glia. Insm1 represses the expression of the apical adherens junction belt-specific protein Plekha7. CRISPR/Cas9-mediated disruption of Plekha7 expression suffices to cause NPC delamination. Plekha7 overexpression impedes the intrinsic, and counteracts the Insm1-induced, NPC delamination. Our findings uncover a novel molecular mechanism underlying NPC delamination in which a BP-genic transcription factor specifically targets the integrity of the apical adherens junction belt, rather than adherens junction components as such.

2018-02-15 | GSE109709 | GEO

RNA regulation by the cell-cell adhesion component PLEKHA7

Project description:We have identified PLEKHA7 as a cell-cell adhesion protein that interacts with and regulates RNAi compelxes, miRNAs and mRNAs at adherens junctions of well-differentiated epithelial cells. This study was conducted to identify global effects of PLEKHA7 depletion on total RNA expression in colon epithelial cells

2024-06-03 | GSE156860 | GEO

Effects of PLEKHA7 depletion on miRNA expression

Project description:Global miRNAs expression profilling of Caco2 cells after shRNA-mediated knockdown of PLEKHA7 Caco2 cells were infected and selected either with a non-target (NT) or with a PLEKHA7-targeting shRNA (shPLEKHA7). Total RNA was isolated from three independent sets of infections and was used to assess total miRNA expression using NanoString's nCounter Human v2 miRNA Expression Assay Kit

2015-08-03 | E-GEOD-61593 | biostudies-arrayexpress

Effects of PLEKHA7 depletion on miRNA expression

Project description:Global miRNAs expression profilling of Caco2 cells after shRNA-mediated knockdown of PLEKHA7

2015-08-03 | GSE61593 | GEO

Transcriptional regulation of endocrine cell differentiation by Insm1

Project description:This experiment used RNA-Seq technology to explore gene expression in mouse Insm1^GFP/Pdx1^CFP HIGH [het/het] FACS sorted pancreatic cells (pre-beta cells) and Insm1^GFP/Pdx1^CFP LOW [het/het] cells (other endocrine progenitors) at E15.5 and E18.5. Comparison of Insm1 +/Pdx HIGH and Insm1 +/Pdx LOW cells revealed a set of differentially expressed genes that are required for beta cell specification.

2014-07-01 | E-MTAB-1929 | biostudies-arrayexpress

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Insm1, Neurod1 and Foxa2 ChipSeq data from pancreatic beta cell)

Project description:Genome-wide Insm1 binding sites analysis revealed an overrepresentation of sequences predicted to bind bHLH and/or forkhead factors, and further analyses demonstrated that most Insm1 sites in the genome are co-occupied by Neurod1 and Foxa2. Binding regions co-occupied by all three factors but not single Insm1 sites explained a significant fraction of gene expression changes in Insm1 mutant β-cells. Together, our data provide evidence that an Insm1, Neurod1 and Foxa2 network maintains a mature gene expression program in β-cells.

2015-03-31 | GSE54046 | GEO

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Insm1, Neurod1 and Foxa2 ChipSeq data from pancreatic beta cell)

2015-03-31 | E-GEOD-54046 | biostudies-arrayexpress

Insm1 regulates the expression of thymic tissue-restricted antigens and the immune tolerance [RNA-seq]

Project description:Insm1, encoding a zinc finger protein, is expressed specifically in neuroendocrine cells. Recent study showed the first evidence of Insm1 expression in medullary thymic epithelial cells (mTEC). Here we investigated the expression and function of Insm1 in mTEC. Mutation of Insm1 resulted in decreased proportion of mTEChi although normal development of other types of thymic cells. We detected altered expression of a subset of tissue-restricted antigens (TRAs) and mild decreased expression of Aire and Fezf2 in Insm1 mutant mTEC. We further showed that Insm1 recognizes a DNA sequence which is similar to the CCCTC-Binding factor (CTCF) binding motif. Mutation of Insm1 altered CTCF binding genome widely and thus the expression of genes. In nude mice transplanted with Insm1 mutant thymus, autoimmune responses were observed in multiple peripheral tissues. In thymus specific Insm1 mutant mice, we detected decreased induction of regulatory T (Treg) cells in the thymus, obvious lymphocytes infiltration and autoimmune antibody reaction in several peripheral tissues. In thymic epithelial cells specific Insm1 overexpression mice, we detected enlarged mTEC proportion and increased expression of mTEC specific genes. Thus, we suggest that Insm1 is a novel regulator of mTEC function and autoimmunity.

2024-01-01 | GSE193927 | GEO

Insm1 regulates the expression of thymic tissue-restricted antigens and the immune tolerance [CUT&Tag]

2024-01-01 | GSE193926 | GEO

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Expression data from islets of control and Insm1 conditional deleted adult pancreatic islets)

Project description:The zinc finger factor Insm1 is known to regulate differentiation of pancreatic β cells during development, Here we show that Insm1 is essential for the maintenance of functionally mature pancreatic β cells in mice. We used microarrays to analyse the global gene expression after deletion of insm1 in adult pancreatic β cells and identified functional important genes and immature islets releated genes deregulated in the mutatant islets.

2015-03-31 | GSE54044 | GEO

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