Genetically encoded multimode reporter of adaptor complex 3 traffic in budding yeast

Traffic. 2021 Jan;22(1-2):38-44. doi: 10.1111/tra.12772. Epub 2020 Dec 7.

Abstract

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.

Keywords: invertase; lysosome; organelle; saccharomyces; vesicle coat.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adaptor Protein Complex 3
  • Animals
  • Endosomes
  • Hermanski-Pudlak Syndrome*
  • Saccharomycetales*
  • Transport Vesicles
  • Vacuoles

Substances

  • Adaptor Protein Complex 3