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Transcriptional regulation of endocrine cell differentiation by Insm1

ABSTRACT: Transcriptional regulation of endocrine cell differentiation by Insm1

PROVIDER: PRJEB4758 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR355986.fastq.gz	Fastqsanger.gz
	ERR355987.fastq.gz	Fastqsanger.gz
	ERR355988.fastq.gz	Fastqsanger.gz
	ERR355989.fastq.gz	Fastqsanger.gz
	ERR355990.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Genome-wide analysis of E17.5 pituitary gland gene expression of control and Insm1 mutant mice

Project description:The Insm1 gene encodes a zinc finger factor expressed in many endocrine organs. We show here that Insm1 is required for differentiation of all endocrine cell types in the pituitary. Thus, in Insm1 mutant mice, hormones characteristic of the different pituitary cell types (thyroid, follicle and melanocyte stimulating hormone, adrenocorticotrope hormone, growth hormone and prolactin) are absent or produced at markedly reduced levels. The differentiation deficit is accompanied by an up-regulated expression of components of the Notch signaling pathway. Further, skeletal muscle-specific genes are ectopically expressed, indicating that Insm1 blocks a muscle-specific expression program. Since Insm1 is also essential for differentiation of endocrine cells in the pancreas, intestine and adrenal gland, it is emerging as a transcription factor that acts in a pan-endocrine manner. The Insm1 factor contains a SNAG domain at its N-terminus, and we show here that the SNAG domain recruits histone modifying factors (Kdm1a, Hdac1/2 and Rcor1-3) and other proteins implicated in transcriptional regulation (Hmg20a/b and Gse1). Deletion of the SNAG domain in mice disrupted differentiation of pituitary endocrine cells, and resulted in an upregulated expression of components of the Notch signaling pathway and ectopic expression of skeletal muscle-specific genes. Our work demonstrates that Insm1 acts in the transcriptional network that controls differentiation of endocrine cells in the anterior pituitary gland, and requires the SNAG domain to exert this function in vivo. Analysis of genes regulated by Insm1 in embryonic day 17.5 pituitary gland. Total RNA from pituitary glands of E17.5 control embryos was compared to E17.5 Insm1 mutant embryos.

2013-10-20 | E-GEOD-46139 | biostudies-arrayexpress

Genome-wide analysis of E17.5 pituitary gland gene expression of control and Insm1 mutant mice

2013-10-20 | GSE46139 | GEO

Thymic mimetic cells function beyond self-tolerance [Insm1]

Project description:To examine the Endocrine thymic epithelial cell transcriptome within the mTEC-III compartment we sorted this population from young Insm1 cKO mice and performed bulk RNAseq

2023-08-28 | GSE236073 | GEO

E-MTAB-1929

Project description:Transcriptional regulation of endocrine cell differentiation by Insm1

2019-05-14 | E-MTAB-1929 | ExpressionAtlas

Trans-differentiation of outer hair cells into inner hair cells in the absence of INSM1

Project description:The mammalian cochlea contains two types of mechanosensory hair cell that have different and critical functions in hearing. Inner hair cells (IHCs), which have an elaborate presynaptic apparatus, signal to cochlear neurons and communicate sound information to the brain. Outer hair cells (OHCs) mechanically amplify sound-induced vibrations, providing enhanced sensitivity to sound and sharp tuning. Cochlear hair cells are solely generated during development, and hair cell death—most often of OHCs—is the most common cause of deafness. OHCs and IHCs, together with supporting cells, originate in embryos from the prosensory region of the otocyst, but how hair cells differentiate into two different types is unknown. Here we show that Insm1, which encodes a zinc finger protein that is transiently expressed in nascent OHCs, consolidates their fate by preventing trans-differentiation into IHCs. In the absence of INSM1, many hair cells that are born as OHCs switch fates to become mature IHCs. To identify the genetic mechanisms by which Insm1 operates, we compared the transcriptomes of immature IHCs and OHCs, and of OHCs with and without INSM1. In OHCs that lack INSM1, a set of genes is upregulated, most of which are normally preferentially expressed by IHCs. The homeotic cell transformation of OHCs without INSM1 into IHCs reveals a mechanism by which these neighbouring mechanosensory cells begin to differ: INSM1 represses a core set of early IHC-enriched genes in embryonic OHCs and makes them unresponsive to an IHC-inducing gradient, so that they proceed to mature as OHCs. Without INSM1, some of the OHCs in which these few IHC-enriched transcripts are upregulated trans-differentiate into IHCs, identifying candidate genes for IHC-specific differentiation.

2025-04-16 | GSE294736 | GEO

RNA-Seq analysis of E15.5 mouse Insm1, Neurod1 and Pax6 knockouts vs Insm1GFP.Cre/+ controls

Project description:This experiment used RNA-Seq technology to explore gene expression in mouse Insm1GFP.Cre/+ controls and Insm1 (Insm1GFP.Cre/GFP.Cre), Neurod1 (Insm1GFP.Cre/+; Neurod1LacZ/LacZ), or Pax6 (Insm1GFP.Cre/+; Pax6fl/fl) knockout FACS sorted pancreatic endocrine cells at E15.5. Comparison of Insm1GFP.Cre+/- and knockout animals revealed sets of differentially expressed genes that are required for endocrine cell specification and development.

2021-08-23 | E-MTAB-10262 | biostudies-arrayexpress

Transcriptional profiling of Ngn3-dependent pancreatic endocrine differentiation at E15.5

Project description:Transcriptional profiling of Ngn3-dependent pancreatic endocrine differentiation at E15.5

| PRJEB8694 | ENA

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

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic ?-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 ? cells during development, Here we show that Insm1 is essential for the maintenance of functionally mature pancreatic ? cells in mice. We used microarrays to analyse the global gene expression after deletion of insm1 in adult pancreatic ? cells and identified functional important genes and immature islets releated genes deregulated in the mutatant islets. We used 8 mutant and 8 litter matched control mice for the islets preparation.

2015-03-31 | E-GEOD-54044 | biostudies-arrayexpress

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