KRAP tethers IP3 receptors to actin and licenses them to evoke cytosolic Ca2+ signals

Nagendra Babu Thillaiappan (), Holly A. Smith, Peace Atakpa-Adaji and Colin W. Taylor ()
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Nagendra Babu Thillaiappan: Tennis Court Road
Holly A. Smith: Tennis Court Road
Peace Atakpa-Adaji: Tennis Court Road
Colin W. Taylor: Tennis Court Road

Nature Communications, 2021, vol. 12, issue 1, 1-13

Abstract: Abstract Regulation of IP3 receptors (IP3Rs) by IP3 and Ca2+ allows regenerative Ca2+ signals, the smallest being Ca2+ puffs, which arise from coordinated openings of a few clustered IP3Rs. Cells express thousands of mostly mobile IP3Rs, yet Ca2+ puffs occur at a few immobile IP3R clusters. By imaging cells with endogenous IP3Rs tagged with EGFP, we show that KRas-induced actin-interacting protein (KRAP) tethers IP3Rs to actin beneath the plasma membrane. Loss of KRAP abolishes Ca2+ puffs and the global increases in cytosolic Ca2+ concentration evoked by more intense stimulation. Over-expressing KRAP immobilizes additional IP3R clusters and results in more Ca2+ puffs and larger global Ca2+ signals. Endogenous KRAP determines which IP3Rs will respond: it tethers IP3R clusters to actin alongside sites where store-operated Ca2+ entry occurs, licenses IP3Rs to evoke Ca2+ puffs and global cytosolic Ca2+ signals, implicates the actin cytoskeleton in IP3R regulation and may allow local activation of Ca2+ entry.

Date: 2021
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DOI: 10.1038/s41467-021-24739-9

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