|Start Date / Time||December 7, 2016 at 9:00 AM|
|End Date / Time||December 7, 2016 at 9:55 AM|
|Location||512 Light Hall|
|Presenter Name||Nicholas C. Vierra (Jacobson lab)|
|Presentation Title||TALK-1 K+ flux controls the unique oscillatory signature of beta-cell ER calcium handling|
|Status||This meeting has already occurred|
The type 2-diabetes associated K+ channel TALK-1 is the most highly expressed K+ channel in the islet, where it limits beta-cell cytosolic Ca2+ (Ca2+c) oscillations and insulin secretion. However, the mechanisms by which it modulates Ca2+ oscillations are unclear. Furthermore, its role in other islet cell types has not been determined. Using a variety of transgenic mice, Ca2+ sensors, and heterologous expression systems, we have discovered that TALK-1 channels serve a critical role in controlling beta-cell endoplasmic reticulum (ER) Ca2+ handling. Additionally, we have found that TALK-1 regulates delta-cell Ca2+c and somatostatin secretion, providing a paracrine signalling mechanism to control alpha-cell function. Importantly, altered TALK-1 function may perturb islet-cell ER Ca2+ homeostasis and paracrine signalling mechanisms, which can affect hormone release and contribute to disease pathogenesis.