DMCA
pancreatic beta cells (2014)
BibTeX
@MISC{Villate14pancreaticbeta,
author = {Olatz Villate and Jean-valery Turatsinze and Loriana G. Mascali and Fabio A. Grieco and C. Nogueira and Daniel A. Cunha and Tarlliza R. Nardelli and Michael Sammeth and Vishal A. Salunkhe and Jonathan L. S. Esguerra and Lena Eliasson and Lorella Marselli and Piero Marchetti and Decio L. Eizirik},
title = {pancreatic beta cells},
year = {2014}
}
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Abstract
Alternative splicing (AS) is a fundamental mecha-nism for the regulation of gene expression. It affects more than 90 % of human genes but its role in the regulation of pancreatic beta cells, the producers of insulin, remains unknown. Our recently published data indicated that the ‘neuron-specific ’ Nova1 splic-ing factor is expressed in pancreatic beta cells. We have presently coupled specific knockdown (KD) of Nova1 with RNA-sequencing to determine all splice variants and downstream pathways regulated by this protein in beta cells. Nova1 KD altered the splicing of nearly 5000 transcripts. Pathway analysis indicated that these genes are involved in exocytosis, apop-tosis, insulin receptor signaling, splicing and tran-scription. In line with these findings, Nova1 silenc-ing inhibited insulin secretion and induced apoptosis basally and after cytokine treatment in rodent and hu-man beta cells. These observations identify a novel layer of regulation of beta cell function, namely AS controlled by key splicing regulators such as Nova1.
