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The role of Itgb1 in islet development

ABSTRACT: The role of Itgb1 in islet development

PROVIDER: PRJNA641689 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12083466.fastq.gz	Fastqsanger.gz
	SRR12083467.fastq.gz	Fastqsanger.gz
	SRR12083468.fastq.gz	Fastqsanger.gz
	SRR12083469.fastq.gz	Fastqsanger.gz
	SRR12083470.fastq.gz	Fastqsanger.gz

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The role of Itgb1 in islet development

Project description:Pancreatic development requires appropriate environmental cues, in which ECM-Integrin signaling plays a central role in the process. Specifically, we investigated how ECM-Integrin signaling in Ngn3+ cell (endocrine progenitors) regulates islet architecture and functions. Here we showed disruption of ECM-Integrin signaling affects beta cell functional maturation and potential non-autonomous regulation around islets.

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Investigating the role of cell adhesion molecule alpha-catenin during islet development

Project description:Purpose: Alpha catenin mediates cell-cell adhesion through the cadherin-catenin complex. It is important to maintain cell-cell adhesion and tissue organization. In this study we explore how cell-cell adhesion mediated by alpha catenin regulates islet aggregation and analyze the gene expression profiling related with islet adhesion, structure and function. Methods: We selective ablate alpha catenin (Ctnna1) in endocrine cells of murine pancreas. Total RNA was extracted from pancreatic islets isolated from 8 weeks old mice of Ngn3-Cre; Ctnna1flox/flox and Wild-type controls. There were four animals for each group. Results: We mapped about 60 million sequence reads per mouse sample. Our results showed that 245 genes were upregulated and 74 were downregulated by alpha catenin ablation. Conclusions: Our results indicate that alpha catenin is required for normal islet aggregation and cellular composition.

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Project description:Cystic fibrosis (CF)-related diabetes (CFRD) is an increasingly common and devastating comorbidity of CF, affecting ~35% of adults with CF. However, the underlying causes of CFRD are unclear. Here, we examined cystic fibrosis transmembrane conductance regulator (CFTR) islet expression and whether the CFTR participates in islet endocrine cell function using murine models of b cell CFTR deletion, and normal and CF human pancreas and islets. Specific deletion of CFTR from murine b cells did not affect b cell function. In human islets, CFTR mRNA was minimally expressed, and CFTR protein/electrical activity was not detected. Isolated CF/CFRD islets demonstrated appropriate insulin and glucagon secretion with few changes in key islet-regulatory transcripts. Furthermore, ~65% of b cell area was lost in CF donors, compounded by pancreatic remodeling and immune infiltration of the islet. These results indicate that CFRD is not caused by intrinsic islet dysfunction from CFTR mutation, but rather, by b cell loss and intra-islet inflammation in the setting of a complex pleiotropic disease

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Identification and analysis of pancreatic islet specific enhancers

Project description:We anticipated that the identification of cis-regulatory regions active in pancreatic islets would help increase our understanding of islet biology and the pathology of diabetes. Towards this end we used histone H3 lysine 4 monomethylation-based nucleosome predictions genome-wide, in conjunction with binding data for PDX1, FOXA2, MAFA, and NEUROD1, to identify 3,654 putative enhancers that are H3K4me1-enriched uniquely in islets as compared to 14 other tissue or cell-types. We show that these islet-specific enhancers are associated with genes with significantly higher islet specificity than genes associated with non-specific enhancers. Further, islet-specific enhancers were not enriched for typical active or repressive histone methylations in embryonic stem cells and liver, suggesting they are formed by de novo histone methylation during pancreas development. We also identify a subset of enhancers bivalently marked by both H3K4me1 and H3K27me3 in adult pancreatic islets. Further, we show that islet-specific enhancers triple- or quadruple- bound by PDX1, MAFA, NEUROD1 and/or FOXA2 are associated with genes with particularly high islet-specificity, and that these loci are enriched in regions with functional activity in islet cell types. Finally, we demonstrate that cytokines reduce H3K4me1 enrichment levels at selected triple- or quadruple-bound islet-specific enhancers, suggesting that epigenetic changes may contribute to cytokine-induced b-cell dysfunction. In conjunction with data from Hoffman et al Genome Research 2010, an analysis of histone modifications and transcription factor binding sites to identify enhancer regions

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