Back

Human ribosome interactions reframe neomycin toxicity

Wu, M.; Zhu, L.; Zhang, X.; Jia, C.; Wu, K.; Yi, C.; Sun, S.; Zhang, Z.; Guo, L.; Hou, X.; Amunts, A.; Li, W.

2025-08-14 biochemistry
10.1101/2025.07.22.666027 bioRxiv
Show abstract

Aminoglycosides like neomycin are widely used but clinically limited due to toxicity, traditionally attributed to mitoribosome inhibition. Here, we demonstrate that this assumption requires re-evaluation by comparing neomycins interactions with human ribosomes in vitro and in cells. While cryo-EM and biochemical assays reveal strong in vitro binding to both mitoribosomes and cytosolic ribosomes, especially at conserved regions such as the helix 44 (h44) decoding center despite sequence divergence, and H69. Cellular analyses show minimal impact on global translation, reduced occupancy on cytosolic ribosomes, and a complete absence of neomycin on mitoribosomes. These discrepancies suggest limited mitochondrial permeability rather than direct mitoribosome inhibition underlies neomycins toxicity. Our findings redefine the mechanistic basis of aminoglycosides side effects and call for a reassessment of their cellular targets.

Matching journals

The top 1 journal accounts for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.