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Plos One : Altered Pancreatic Islet Function and Morphology in Mice Lacking the Beta-cell Surface Protein Neuroligin-2, Volume 8

By Maedler, Kathrin

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Book Id: WPLBN0003943603
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Reproduction Date: 2015

Title: Plos One : Altered Pancreatic Islet Function and Morphology in Mice Lacking the Beta-cell Surface Protein Neuroligin-2, Volume 8  
Author: Maedler, Kathrin
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection
Historic
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Publisher: Plos

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Maedler, K. (n.d.). Plos One : Altered Pancreatic Islet Function and Morphology in Mice Lacking the Beta-cell Surface Protein Neuroligin-2, Volume 8. Retrieved from http://netlibrary.net/


Description
Description : Neuroligin-2 is a transmembrane, cell-surface protein originally identified as an inhibitory synapse-associated protein in the central nervous system. Neuroligin-2 is also present on the pancreatic beta-cell surface, and there it engages in transcellular interactions that drive functional maturation of the insulin secretory machinery: these are necessary for normal insulin secretion. The effects of neuroligin-2 deficiency on brain and neuronal function and morphology and on behavior and coordination have been extensively characterized using neuroligin-2 knockout mice. The effects of absent neuroligin-2 expression on islet development and function, however, are unknown. Here, to help test whether neuroligin-2 is necessary for normal islet development, we characterized islet morphology in mice lacking neuroligin-2. To test whether–as predicted by our earlier co-culture studies–absence of neuroligin-2 impairs beta cell function, we compared glucose-stimulated insulin secretion by islets from mutant and wild-type mice. Our results show that while islets from neuroligin-2-deficient mice do not to appear to differ architecturally from wild-type islets, they are smaller, fewer in number, and contain beta cells with lower insulin content. Evaluation of transcript levels suggests that upregulation of neuroligin-1 helps compensate for loss of neuroligin-2. Surprisingly, under both basal and stimulating glucose levels, isolated islets from the knockout mice secreted more of their intracellular insulin content. Rat islets with shRNA-mediated neuroligin-2 knockdown also exhibited increased insulin secretion. Neurexin transcript levels were lower in the knockout mice and, consistent with our prior finding that neurexin is a key constituent of the insulin granule docking machinery, insulin granule docking was reduced. These results indicate that neuroligin-2 is not necessary for the formation of pancreatic islets but that neuroligin-2 influences islet size and number. Neuroligin-2–perhaps through its effects on the expression and/or activity of its binding partner neurexin– promotes insulin granule docking, a known constraint on insulin secretion.

 

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