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Review
. 2011 Dec;14(6):715-20.
doi: 10.1016/j.pbi.2011.08.001. Epub 2011 Aug 22.

The ins and outs of cellular Ca(2+) transport

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Review

The ins and outs of cellular Ca(2+) transport

Edgar P Spalding et al. Curr Opin Plant Biol. 2011 Dec.

Abstract

The cytoplasmic Ca(2+) signals that participate in nearly all aspects of plant growth and development encode information as binary switches or information-rich signatures. They are the result of influx (thermodynamically passive) and efflux (thermodynamically active) activities mediated by membrane transport proteins. On the influx side, confirming the molecular identities of Ca(2+)-permeable channels is still a major research topic. Cyclic nucleotide-gated channels and glutamate receptor-like channels are candidates well supported by evidence. On the efflux side, CAX antiporters and P-type ATPase pumps are the principal molecular entities. Both of these active transporters load Ca(2+) into specific compartments and have the potential to reduce the magnitude and duration of a Ca(2+) transient. Recent studies indicate calmodulin-activated Ca(2+) pumps in endomembrane systems can dampen the magnitude and duration of a Ca(2+) transient that could otherwise grow into a Ca(2+) cell death signature. An important challenge following molecular characterization of the influx and efflux pathways is to understand how they are coordinately regulated to produce a Ca(2+) switch or encode specific information into a Ca(2+) signature.

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Figures

Figure 1
Figure 1
Ca2+ circuits are created with different membrane systems by the coordinated regulation of influx and efflux pathways (top). Evidence indicates that a loss of specific endomembrane efflux pathways can result in a greater magnitude and prolonged duration of a Ca2+ signature that correlates with triggering cell death (bottom). Not indicated in the figure is the role of Ca2+ buffering, which can affect flux rates and magnitudes [57].

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