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G protein-regulated endocytic trafficking of adenylyl cyclase type 9

By André M Lazar, Roshanak Irannejad, Tanya A. Baldwin, Aparna A. Sundaram, J Silvio Gutkind, Asuka lnoue, Carmen W Dessauer, Mark von Zastrow

Posted 25 Apr 2020
bioRxiv DOI: 10.1101/2020.04.23.057026 (published DOI: 10.7554/eLife.58039)

GPCRs are increasingly recognized to initiate signaling via heterotrimeric G proteins as they move through the endocytic network, but little is known about how relevant G protein effectors are localized. Here we report dynamic trafficking of adenylyl cyclase type 9 (AC9) from the plasma membrane to endosomes, while adenylyl cyclase type 1 (AC1) remains in the plasma membrane, and stimulation of AC9 trafficking by ligand-induced activation of Gs-coupled GPCRs or Gs. AC9 transits a similar dynamin-dependent early endocytic pathway as activated GPCRs but, in contrast to GPCR trafficking which is regulated by β-arrestin but not Gs, AC9 trafficking is regulated by Gs but not β-arrestin. We also show that AC9, but not AC1, contributes to cAMP production from endosomes. These results reveal dynamic and isoform-specific trafficking of adenylyl cyclase in the endocytic network, and a discrete role of a heterotrimeric G protein in controlling subcellular location of a relevant effector.

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