Extended Data Fig. 6: Accumulation of p62 and P-eIF2α in RPS26KO/+.
From: Ribosomopathy-associated mutations cause proteotoxic stress that is alleviated by TOR inhibition
(a, b) RPS26cKO was inactivated (and tubulin-mCherry deleted) by crossing to hedgehog-GAL4, UAS-FLP. In the resulting RPS26KO/+ posterior compartment, immunoreactivity against p62 and P-eIF2α was higher than in the control anterior compartment. Scale bars represent 50 µm. Genotypes for each figure panel are available in Supplementary Table 1. Experiments were repeated independently three times with similar results.
