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Mus musculus

ABSTRACT: RNAseq data from mouse beta-cells expressing mutant (GCK Y214C) versus wild-type Glucokinase

PROVIDER: PRJNA343108 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4244850.fastq.gz	Fastqsanger.gz
	SRR4244851.fastq.gz	Fastqsanger.gz
	SRR4244852.fastq.gz	Fastqsanger.gz
	SRR4244853.fastq.gz	Fastqsanger.gz
	SRR4244854.fastq.gz	Fastqsanger.gz

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RNAseq data from mouse beta-cells expressing mutant (GCK Y214C) versus wild-type Glucokinase

Project description:The goal of this study is to compare the transcriptome of mouse beta-cells expressing mutant constitutively active Glucokinase versus wild-type Glucokinase.

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Citrullination of glucokinase is linked to autoimmune diabetes

Project description:Inflammation, including reactive oxygen species and inflammatory cytokines in tissues amplify various post-translational modifications (PTMs) of self-proteins. A number of PTMs have been identified as autoimmune biomarkers in the initiation and progression of Type 1 diabetes (T1D). In this study, we have identified the citrullination of pancreatic glucokinase (GK) as a result of inflammation, triggering autoimmunity and affecting GK biological functions. Glucokinase is expressed in hepatocytes to regulate glycogen synthesis, and in pancreatic beta cells as a glucose sensor to initiate glycolysis and insulin signaling. We identify autoantibodies and autoreactive CD4+ T cells to glucokinase epitopes in the circulation of T1D patients and NOD mice. Finally, citrullination alters GK biologic activity (Km) and suppresses glucose-stimulated insulin secretion. Our studies define glucokinase as a T1D biomarker, providing new insights of how inflammation drives PTMs to create both neoautoantigens and affect beta cell metabolism.

2022-03-17 | PXD028825 | Pride

Abnormal exocrine-endocrine cell crosstalk promotes β-cell dysfunction and loss in MODY8

Project description:MODY8 (maturity-onset diabetes of the young, type 8) is a dominantly inherited monogenic form of diabetes associated with frameshift mutations in the carboxyl ester lipase (CEL) gene expressed by pancreatic acinar cells. Patients carrying the mutation develop childhood-onset exocrine pancreas dysfunction followed by the manifestation of diabetes during adulthood. However, it is unclear how CEL mutations cause diabetes. Here we report the transfer of proteins from acinar cells to β-cells as a form of crosstalk between exocrine and endocrine cells. Human β-cells showed a relatively higher propensity for internalizing the mutant versus the wild-type CEL protein. Following internalization, the mutant protein formed stable intracellular aggregates leading to β-cell secretory dysfunction. To investigate the effects in vivo, we transplanted stem cell-derived wild-type or mutant pancreatic progenitors into independent mice and generated insulin-secreting β-like cells and CEL-expressing acinar-like cells. While the β-like cells derived from wild-type stem cells responded to glucose, the β-like cells derived from mutant stem cells were dysfunctional secondary to the accumulation of intracellular mutant CEL protein. Analysis of pancreas sections from a MODY8 patient also revealed the presence of CEL protein in the few extant β-cells. This study provides compelling evidence for the mechanism by which a mutant gene expressed specifically in acinar cells promotes dysfunction and loss of β-cells to cause diabetes.

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