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AP-3 (adaptor complex 3) mediates traffic from the late Golgi or early endosomes to late endosomal compartments. In mammals, mutations in AP-3 cause Hermansky-Pudlak syndrome type 2, cyclic neutropenias, and a form of epileptic encephalopathy. In budding yeast, AP-3 carries cargo directly from the trans-Golgi to the lysosomal vacuole. Despite the pathway's importance and its discovery two decades ago, rapid screens and selections for AP-3 mutants have not been available. We now report GNSI, a synthetic, genetically encoded reporter that allows rapid plate-based assessment of AP-3 functional deficiency, using either chromogenic or growth phenotype readouts. This system identifies defects in both the formation and consumption of AP-3 carrier vesicles and is adaptable to high-throughput screening or selection in both plate array and liquid batch culture formats. Episomal and integrating plasmids encoding GNSI have been submitted to the Addgene repository. © 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Citation

Rachael L Plemel, Greg Odorizzi, Alexey J Merz. Genetically encoded multimode reporter of adaptor complex 3 traffic in budding yeast. Traffic (Copenhagen, Denmark). 2021 Jan;22(1-2):38-44

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PMID: 33225520

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