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Published online
doi:10.1083/jcb.200611096
The Journal of Cell Biology, Vol. 178, No. 1, 141-153
The Rockefeller University Press, 0021-9525 $30.00
© Xu et al.
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Article

Locally controlled inhibitory mechanisms are involved in eukaryotic GPCR-mediated chemosensing



Xuehua Xu1, Martin Meier-Schellersheim2, Jianshe Yan1, and Tian Jin1

1 Chemotaxis Signal Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852
2 Program in Systems Immunology and Infectious Disease Modeling, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892

Correspondence to Tian Jin: tjin{at}niaid.nih.gov

Gprotein–coupled receptor (GPCR) signaling mediates a balance of excitatory and inhibitory activities that regulate Dictyostelium chemosensing to cAMP. The molecular nature and kinetics of these inhibitors are unknown. We report that transient cAMP stimulations induce PIP3 responses without a refractory period, suggesting that GPCR-mediated inhibition accumulates and decays slowly. Moreover, exposure to cAMP gradients leads to asymmetric distribution of the inhibitory components. The gradients induce a stable accumulation of the PIP3 reporter PHCrac-GFP in the front of cells near the cAMP source. Rapid withdrawal of the gradient led to the reassociation of G protein subunits, and the return of the PIP3 phosphatase PTEN and PHCrac-GFP to their pre-stimulus distribution. Reapplication of cAMP stimulation produces a clear PHCrac-GFP translocation to the back but not to the front, indicating that a stronger inhibition is maintained in the front of a polarized cell. Our study demonstrates a novel spatiotemporal feature of currently unknown inhibitory mechanisms acting locally on the PI3K activation pathway.

Abbreviations used in this paper: CRAC, cytosolic regulator of adenylyl cyclase; GPCR, G protein–coupled receptor; PH, pleckstrin homology; WT, wild type.


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