Fig. 8.

Model for modes of surface protein regulation in response to glucose. Schematic diagram shows the regulation of cell surface membrane protein cargoes in response to glucose starvation. When cells have access to glucose for maximal growth, internalisation occurs at a basal level through Mig1 (and Mig2) repression of endocytic adaptor genes YAP1801/YAP1802. Whilst resident at the surface, nutrient transporters diffuse in and out of eisosomes. The expression of many eisosome genes are repressed in glucose conditions (left). Following glucose starvation, Mig1 translocates from the nucleus, resulting in increased expression of YAP1801/YAP1802, which triggers increased cargo endocytosis and ubiquitin-mediated trafficking through the multivesicular body (MVB) pathway to the lysosome for degradation (right). Although most nutrient transporters are degraded following glucose starvation, a small reserve pool is sequestered in eisosomes, which are transcriptionally activated during starvation. Efficient cargo retention relies on Ygr130c, and eisosomes that specifically retain cargo during glucose starvation exhibit biochemical and biophysical changes in Pil1. This reserve pool of eisosomally retained nutrient transporters can be deployed upon a return to glucose-replete conditions for efficient recovery following the period of glucose starvation.