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Neuron-enriched RNA-binding Proteins Regulate Pancreatic Beta Cell Function and Survival.

Jonàs Juan-Mateu1, Tatiana H Rech1, Olatz Villate1

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The Journal of Biological Chemistry
|January 13, 2017
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Pancreatic beta cells share neuron-like splicing regulators with the brain. These regulators impact insulin secretion and beta cell survival, suggesting their dysfunction contributes to diabetes.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Neuroscience

Background:

  • Pancreatic beta cell failure is central to diabetes development.
  • Beta cells exhibit neuronal traits, relying on neuron-like transcription programs for function.
  • Alternative splicing significantly impacts neuronal development and function, but its role in beta cells is less understood.

Purpose of the Study:

  • To investigate the role of alternative splicing regulators in pancreatic beta cells.
  • To identify splicing regulators common to both beta cells and neurons.
  • To explore the functional impact of specific splicing regulators on beta cell survival and insulin secretion.

Main Methods:

  • RNA sequencing was used to compare splicing-regulatory RNA-binding protein expression in human islets, brain, and other tissues.
  • Four key splicing regulators (Elavl4, Nova2, Rbfox1, Rbfox2) were selected for functional studies.
  • Gene silencing experiments were performed in rat INS-1E cells, human EndoC-βH1 cells, and primary rat beta cells.

Main Results:

  • A cluster of splicing regulators was identified as common to both beta cells and brain.
  • Silencing Elavl4 and Nova2 led to increased beta cell apoptosis.
  • Silencing Rbfox1 and Rbfox2 enhanced insulin content and secretion, with Rbfox1 modulating gelsolin splicing.

Conclusions:

  • Beta cells and neurons share common splicing regulators and gene expression programs.
  • These shared regulators are crucial for insulin release and beta cell survival.
  • Dysregulation of these splicing factors may contribute to the loss of beta cell mass in diabetes.