Cellular and Molecular Life Sciences

, Volume 75, Issue 7, pp 1303–1305 | Cite as

Author Correction: Beta cell connectivity in pancreatic islets: a type 2 diabetes target?

  • Guy A. Rutter
  • David J. Hodson
Author Correction

Author Correction to: Cell. Mol. Life Sci. (2015) 72:453–467

The original version of this article unfortunately contained a mistake. Legends of Figs. 1 and 2 were interchanged. The correct versions are given below.
Fig. 1

Imaging and mapping beta cell network topology. (Above) Functional multicellular Ca2+ imaging is used to monitor the large-scale organization of glucose-induced population dynamics (above, left). By subjecting the resulting traces (from ~ 50–100 individual cells per islet) to correlation analyses, cells with coordinated activity can be identified and a functional connectivity map plotted based upon position within the imaged field (x–y) (above, right). Scale-free connection distributions are typified by a minority of cells that host the majority of connections (nodes), while maintaining streamlined information flow due to a short pathlength. Although robust in the face of random attack, they are prone to collapse following a targeted attack (below, left). By contrast, nonscale-free networks (e.g., random or lattice) may not efficiently propagate signals due to a long pathlength, and random attacks significantly reduce capacity (below, right)

Fig. 2

Schematic showing single cell and population-level beta cell signaling. At the molecular level, glucose is transported into the beta cell before undergoing glycolysis to increase the ratio of free cytosolic ATP:ADP. This closes KATP channels, leading to opening of VDCC, Ca2+ influx, and Ca2+-dependent exocytosis. At the population-level, beta cell dynamics are further dictated by signaling circuits involving paracrine, juxtacrine, autocrine, electrotonic (GJ), neural and ciliary communications

Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Section of Cell Biology, Department of Medicine, Imperial College LondonImperial Centre for Translational and Experimental Medicine, Hammersmith HospitalLondonUK

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