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Sox9 regulates alternative splicing and pancreatic beta cell function

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE245406 | GEO | 2023/10/18

REPOSITORIES: GEO

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Sox9 regulates alternative splicing and pancreatic beta cell function.

Project description:Despite significant research, mechanisms underlying the failure of islet beta cells that result in type 2 diabetes (T2D) are still under investigation. Here, we report that Sox9, a transcriptional regulator of pancreas development, also functions in mature beta cells. Our results show that Sox9-depleted rodent beta cells have defective insulin secretion, and aging animals develop glucose intolerance, mimicking the progressive degeneration observed in T2D. Using genome editing in human stem cells, we show that beta cells lacking SOX9 have stunted first-phase insulin secretion. In human and rodent cells, loss of Sox9 disrupts alternative splicing and triggers accumulation of non-functional isoforms of genes with key roles in beta cell function. Sox9 depletion reduces expression of protein-coding splice variants of the serine-rich splicing factor arginine SRSF5, a major splicing enhancer that regulates alternative splicing. Our data highlight the role of SOX9 as a regulator of alternative splicing in mature beta cell function.

| S-EPMC10796970 | biostudies-literature

Sox9 regulates alternative splicing and pancreatic beta cell function [mouse]

Project description:Type 2 Diabetes Mellitus (T2D), a multifactorial disease, can result from perturbations in numerous pancreatic genes. We describe a previously unanticipated role for Sox9, a transcriptional regulator of embryonic pancreas and endocrine cell development, in mature beta cells. Our data demonstrate that Sox9 has continued function in beta cells as they mature, and elimination of Sox9 compromises beta cell activities. Sox9-depleted rodent beta cells fail to appropriately secrete insulin and exhibit glucose intolerance in aging animals, mimicking the progressive degeneration observed in T2D. Human beta cells lacking SOX9 are functionally impaired with stunted first phase insulin secretion. In both rodent and human, Sox9 loss in beta cells disrupts alternative splicing patterns, with significant implications for maintenance of cellular function. Thus, our data uncover a novel, unprecedented role for a developmental transcription factor in mature beta cell function.

2023-10-18 | GSE245405 | GEO

Sox9 regulates alternative splicing and pancreatic beta cell function [human]

2023-10-18 | GSE245404 | GEO

Sox9 regulates alternative splicing and pancreatic beta cell function

Project description:Sox9 regulates alternative splicing and pancreatic beta cell function

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Sox9 regulates alternative splicing and pancreatic beta cell function [mouse]

Project description:Sox9 regulates alternative splicing and pancreatic beta cell function [mouse]

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Sox9 regulates alternative splicing and pancreatic beta cell function [human]

Project description:Sox9 regulates alternative splicing and pancreatic beta cell function [human]

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The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Project description:This SuperSeries is composed of the SubSeries listed below.

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