213V Poster - 01. Cell Stress and cell death
Wednesday April 06, 4:00 PM - 7:00 PM

Ribosome protein mutant cells rely on the GR64 cluster of gustatory receptors for survival and proteostasis in Drosophila


Authors:
Michael Baumgartner 1,3; Alex Mastrogiannopoulos 1; Iwo Kucinski 2,4; Eugenia Piddini 1

Affiliations:
1) School of Cellular and Molecular Medicine, University of Bristol, Biomedical Sciences Building, University Walk, Bristol BS8 1TD, UK.; 2) The Wellcome Trust/Cancer Research UK Gurdon Institute and Zoology Department, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK; 3) Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Blvd, Philadelphia, PA, 19104; 4) Wellcome & MRC Cambridge Stem Cell Institute and Department 17 of Haematology, University of Cambridge, UK

Keywords:
b. death mutants/genes; r. proteostasis

Mutations in ribosome protein (Rp) genes and ribosome biogenesis factors result in debilitating diseases known as ribosomopathies. Recent studies in Drosophila have shown that cells heterozygous mutant for Rp genes (Rp/+) exhibit proteotoxic stress and aggregates, which drive stress pathway activation and apoptosis. Understanding how Rp/+ cells fend off proteotoxic stress could suggest mechanisms to ameliorate these and other conditions caused by proteotoxic stress. Here we find that Rp/+ epithelial cells express all six Gustatory Receptor 64 (Gr64) genes, a cluster of sugar receptors involved in taste sensation. We show that Rp/+ cells depend on Gr64 for survival and that loss of Gr64 autonomously exacerbates stress pathway activation and proteotoxic stress by negatively effecting autophagy and proteasome function in Rp/+ cells. This work identifies a non-canonical role in proteostasis maintenance for a family of gustatory receptors known for their function in neuronal sensation.