InsP3R channel gating altered by clustering?

Horia Vais, J. Kevin Foskett and Don-On Daniel Mak ()
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Horia Vais: University of Pennsylvania Perleman School of Medicine
J. Kevin Foskett: University of Pennsylvania Perleman School of Medicine
Don-On Daniel Mak: University of Pennsylvania Perleman School of Medicine

Nature, 2011, vol. 478, issue 7368, E1-E2

Abstract: Abstract Arising from T. Rahman, A. Skupin, M. Falcke & C. W. Taylor Nature 458, 655–659 (2009)10.1038/nature07763 The inositol trisphosphate receptor (InsP3R) forms a calcium channel that resides in the membrane of the endoplasmic reticulum and is activated by inositol trisphosphate (InsP3). InsP3 is a phosphorylated monosaccharide that is generated via hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2), a phospholipid that is located in the plasma membrane, and activation of the InsP3R is involved in a broad range of biological processes, including cell division, apoptosis and development. Rahman et al.1,2 reported that exposure to low concentrations of InsP3 induces rapid clustering of InsP3R Ca2+ release channels normally randomly distributed in endoplasmic reticulum/outer nuclear membranes. Importantly, clustered channels gate differently from lone channels. Using similar protocols, we observed InsP3R channel clustering without exposure to InsP3 (Fig. 1a), as we found in other systems3,4,5 with protocols designed to avoid InsP3 pre-exposure. More significantly, we find that clustering has no effect on InsP3R channel gating. For this reason, we believe that InsP3-induced channel clustering and modification of channel gating by clustering may not be universal phenomena.

Date: 2011
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DOI: 10.1038/nature10493

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