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Modulation of α2C‐adrenergic receptor export trafficking by multiple Rab GTPases

At 37°C, α2C‐adrenergic receptor (AR) is poorly transported to the plasma membrane. Cold exposure enhances α2C‐AR translocation to the cell surface and this effect is exaggerated in some individuals leading to Raynaud Phenomenon. To identify the factors limiting α2C‐AR transport, the receptor was co‐transfected with well defined Rab GTPase dominant negative mutants in HEK293T cells. Subsequently, the α2C‐AR plasma membrane levels were determined at 37°C and 30°C by [3H]RX‐821002 binding. Inhibition of the endoplasmic reticulum (ER) to Golgi traffic with Rab1N124I equally attenuated α2C‐AR cell surface targeting at both temperatures. Blockade of the retrograde traffic from the Golgi to the ER using Rab2N119I had no effect on α2C‐AR cell surface expression. In contrast, inhibition of the retrograde traffic by Rab6N126I augmented α2C‐AR plasma membrane levels at 30°C, but not at 37°C. Reduction of Golgi to plasma membrane traffic by Rab11N124I did not influenced receptor translocation to the cell surface. However, Rab8T22N decreased α2C‐AR plasma membrane levels with similar extent at 37°C and 30°C. Our data indicate that Rab6‐dependent retrograde traffic is required to prevent exaggerated transport of α2C‐AR to the plasma membrane at low temperature. (R01GM076167, 5P20RR018766)