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Global profiling of Nkx2.2 SD-domain mutant pancreas during development and adulthood compared to transcriptional profiling of SD-domain mutant expressing neural progenitors.

ABSTRACT: Global profiling of Nkx2.2 SD-domain mutant pancreas during development and adulthood compared to transcriptional profiling of SD-domain mutant expressing neural progenitors.

PROVIDER: PRJNA939831 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23649130.fastq.gz	Fastqsanger.gz
	SRR23649131.fastq.gz	Fastqsanger.gz
	SRR23649132.fastq.gz	Fastqsanger.gz
	SRR23649133.fastq.gz	Fastqsanger.gz
	SRR23649134.fastq.gz	Fastqsanger.gz

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Global profiling of Nkx2.2 SD-domain mutant pancreas during development and adulthood compared to transcriptional profiling of SD-domain mutant expressing neural progenitors.

Project description:The consolidation of unambiguous cell fate commitment relies on the ability of transcription factors (TFs) to exert tissue-specific regulation of complex genetic networks. The mechanisms by which TFs establish such precise control over gene expression, however, have remained elusive—especially in instances where a single TF operates in two or more discrete cellular systems. In this study, we demonstrate that  cell specific functions of NKX2.2 are driven by the highly conserved NK2-Specific Domain (SD). Mutation of the endogenous NKX2.2 SD domain prevents the developmental progression of beta cell precursors into mature, insulin-expressing beta cells, resulting in overt neonatal diabetes. Within the adult beta cell, the SD domain stimulates beta cell performance through the activation and repression of a subset of NKX2.2-regulated transcripts critical for beta cell function. These irregularities in beta cell gene expression may be mediated via SD domain-contingent interactions with components of the nuclear pore complex. In stark contrast to these pancreatic phenotypes, however, the SD domain is entirely dispensable for the development of NKX2.2-dependent cell types within the CNS. Together, these results reveal a previously undetermined mechanism through which NKX2.2 directs disparate transcriptional programs in the pancreas vs. neuroepithelium.

2024-02-21 | GSE226345 | GEO

Functional analysis of the Nkx2.2 SD domain: gene expression profiling of E16.5 Nkx2.2 SD mutant pancreata versus wild-type littermate pancreata

Project description:The experiment consists of 7 one channel assays for analyzing embryonic pancreas at E16.5. There are three or four replicates per condition. At E16.5, we are looking at differential gene expression across two mouse lines, WT vs Nkx2.2 SD mutants.

2015-01-29 | E-MTAB-3349 | biostudies-arrayexpress

RNAseq analysis of the duodenum of intestine-specific adult SD mutant mice

Project description:Aim: Transcriptional analysis of the duodenum of adult Nkx2.2flox/SD;Villin-Cre (SDint) mice versus control Methods: 2 cm of the duodenum (as measured from the stomach) of 6 week old control and mutant mice were dissected and total RNA extracted. Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq. Results: 206 genes with a p-value <0.05 were significantly changed. Among these are some enteroendocrine hormones. Conclusion: The SD domain of Nkx2.2 regulates specification of some enteroendocrine cells

2016-07-28 | GSE72762 | GEO

RNA-Seq analysis of E15.5 pancreas of both whole body Nkx2.2 mutant embryos and endocrine progenitor specific Nkx2.2 mutant embryos

Project description:Aim: Transcriptional analysis of E15.5 whole pancreas of Nkx2.2-LacZ/LacZ embryos versus control and Ngn3-Cre; Nkx2.2-flox/flox embryos versus control Methods: Embryonic pancreata were isolated at E15.5 from Nkx2.2 mutant mice and controls. Total RNA was extracted. Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq. Results: There is significant overlap between the differentially expressed genes of whole body Nkx2.2 mutant embryos and endocrine progenitor specific Nkx2.2 mutant embryos; many of the downregulated genes (p-value < 0.05) are genes involved in beta cell function. Conclusion: Nkx2.2 functions within the endocrine progenitor lineage to activate beta cell genes

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RNAseq analysis of the duodenum of intestine-specific adult SD mutant mice

2016-07-28 | E-GEOD-72762 | biostudies-arrayexpress

NKX2.2

Project description:NKX2.2

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RNA-Seq analysis of the pancreatic islets of beta cell specific adult Nkx2.2 mutant mice

Project description:Aim:Transcriptional analysis of the pancreatic islets of adult Nkx2.2 flox/flox; RipCre mice versus control Methods:Pancreatic islets from 4week old Nkx2.2 mutant mice and controls were isolated and total RNA was extracted.Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq. Results: Among the downregulated genes with a p-value=0.05 are important genes for beta cell function and idenity.Among the upregulated genes with a p-value=0.05 are non beta endocrine hormones. Conclusion: Nkx2.2 activates important beta cell genes and actively represses non beta cell genes

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Transcription profiling of mouse wild type and Nkx2.2 mutant embryos at E12.5 and E13.5 to identify a transcripional program that Nkx2.2 regulation in the pancreas

Project description:The goal of this experiment was to analyze expression changes in the pancreas at embryonic days 12.5 and 13.5 between wild type and Nkx2.2 null mice. We know that Nkx2.2 is essential for pancreatic endocrine differentiation and development. At these early time points which are critical for endocrine cell specification, we would like to identify a transcriptional program that Nkx2.2 regulates. We would also like to identify direct and functional transcriptional targets of Nkx2.2.

2009-11-05 | E-CBIL-44 | biostudies-arrayexpress

Gene expression profiling of wild-type, Nkx2.2 null, NeuroD null and Nkx2.2/NeuroD double KO E13.5 pancreata

Project description:The experiment consist of 16 one channel assays for analyzing embryonic pancreas at E13. There are four replicates per condition. We are looking at differential gene expression across four mouse lines: WT, Nkx2.2, NeuroD and Nkx2.2/NeuroD double mutants at E13.5.

2015-02-03 | E-MTAB-3350 | biostudies-arrayexpress

Identification of dysregulated transcripts in nkx2.2(RNAi) planarians.

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2022-05-24 | GSE174228 | GEO

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