한빛사논문
Washington University School of Medicine
Jung Hoon Cho 1, Zipeng A Li 1, Lifei Zhu 1, Brian D Muegge 1 2, Henry F Roseman 1, Eun Young Lee 1 3, Toby Utterback 4, Louis G Woodhams 4, Philip V Bayly 4, Jing W Hughes 1
1Department of Medicine, Washington University School of Medicine, 660 South Euclid Ave, St. Louis, MO, USA.
2Department of Medicine, VA Medical Center, 915 North Grand Blvd, St. Louis, MO, USA.
3Division of Endocrinology and Metabolism, Department of Internal Medicine, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, South Korea.
4Department of Mechanical Engineering and Materials Science, Washington University McKelvey School of Engineering, 1 Brookings Drive, St. Louis, MO, USA.
Corresponding author: Jing W Hughes
Abstract
Primary cilia are specialized cell-surface organelles that mediate sensory perception and, in contrast to motile cilia and flagella, are thought to lack motility function. Here, we show that primary cilia in human and mouse pancreatic islets exhibit movement that is required for glucose-dependent insulin secretion. Islet primary cilia contain motor proteins conserved from those found in classic motile cilia, and their three-dimensional motion is dynein-driven and dependent on adenosine 5′-triphosphate and glucose metabolism. Inhibition of cilia motion blocks beta cell calcium influx and insulin secretion. Human beta cells have enriched ciliary gene expression, and motile cilia genes are altered in type 2 diabetes. Our findings redefine primary cilia as dynamic structures having both sensory and motile function and establish that pancreatic islet cilia movement plays a regulatory role in insulin secretion.
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