Sprouty2 regulates PI(4,5)P2/Ca2+ signaling and HIV-1 Gag release.

Abstract:

:We reported recently that activation of the inositol 1,4,5-triphosphate receptor (IP3R) is required for efficient HIV-1 Gag trafficking and viral particle release. IP3R activation requires phospholipase C (PLC)-catalyzed hydrolysis of PI(4,5)P(2) to IP3 and diacylglycerol. We show that Sprouty2 (Spry2), which binds PI(4,5)P(2) and PLCγ, interfered with PI(4,5)P(2) in a manner similar to that of U73122, an inhibitor of PI(4,5)P(2) hydrolysis, suggesting that Spry2 negatively regulates IP3R by preventing formation of its activating ligand, IP3. Mutation to Asp of R252, a crucial determinant of PI(4,5)P(2) binding in the C-terminal domain of Spry2, prevented the interference, indicating that binding to the phospholipid is required. By contrast, deletion of the PLCγ binding region or mutation of a critical Tyr residue in the region did not prevent the interference but Spry2-PI(4,5)P(2) colocalization was not detected, suggesting that PLC binding is required for their stable association. Like U73122, Spry2 over-expression inhibited wild type Gag release as virus-like particles. Disrupting either binding determinant relieved the inhibition. IP3R-mediated Ca(2+)signaling, in turn, was found to influence Spry2 subcellular distribution and ERK, a Spry2 regulator. Our findings suggest that Spry2 influences IP3R function through control of PI(4,5)P(2) and IP3R influences Spry2 function by controlling its distribution and ERK activation.

journal_name

J Mol Biol

authors

Ehrlich LS,Medina GN,Carter CA

doi

10.1016/j.jmb.2011.04.069

subject

Has Abstract

pub_date

2011-07-22 00:00:00

pages

716-25

issue

4

eissn

0022-2836

issn

1089-8638

pii

S0022-2836(11)00512-2

journal_volume

410

pub_type

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