Quantitative profiling of basal and stress-induced ribosome collisions
- 1Vanderbilt University
Abstract
Background: Ribosomes stall when they encounter problematic codons or cellular stress that perturbs translation. Stalled ribosomes can lead to the formation of ribosome collisions, also known as disomes, that engage cellular surveillance and stress signaling pathways. How many disomes form during basal conditions and how disome levels change under stress remain poorly understood. Results: We used spike-in normalized Ribo-seq and Disome-seq to quantify transcriptome-wide disome levels. Applying this approach in yeast and human cells, we found that disomes generate approximately 2-10% of all footprints under basal conditions. A high-resolution Disome-seq experiment in human cells identified reproducible disome-forming sites that contribute to the basal level of disome formation in the cell. Exposure of yeast cells to methyl methanesulfonate and human cells to anisomycin increased disome abundance up to four-fold and redistributed collisions in a stress-specific and context-dependent manner. Conclusions: These data provide a quantitative, transcriptome-wide framework for measuring disome levels and reveal how translational stress reshapes the landscape of ribosome collisions in cells.
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BibTeX
@misc{marks2026quantitative,
title = {{Quantitative profiling of basal and stress-induced ribosome collisions}},
author = {J. Marks and P. H. Ayres-Galhardo and B. Tamilselvam and A. B. Roberson and R. Pitts and N. R. Guydosh and S. Meydan},
howpublished = {bioRxiv},
year = {2026},
month = jul,
doi = {10.64898/2026.07.21.739814},
url = {https://www.biorxiv.org/content/10.64898/2026.07.21.739814v2},
note = {CC0},
}
RIS
TY - UNPB
TI - Quantitative profiling of basal and stress-induced ribosome collisions
AU - J. Marks
AU - P. H. Ayres-Galhardo
AU - B. Tamilselvam
AU - A. B. Roberson
AU - R. Pitts
AU - N. R. Guydosh
AU - S. Meydan
PY - 2026
DA - 2026/07/21
PB - bioRxiv
DO - 10.64898/2026.07.21.739814
UR - https://www.biorxiv.org/content/10.64898/2026.07.21.739814v2
AB - Background: Ribosomes stall when they encounter problematic codons or cellular stress that perturbs translation. Stalled ribosomes can lead to the formation of ribosome collisions, also known as disomes, that engage cellular surveillance and stress signaling pathways. How many disomes form during basal conditions and how disome levels change under stress remain poorly understood. Results: We used spike-in normalized Ribo-seq and Disome-seq to quantify transcriptome-wide disome levels. Applying this approach in yeast and human cells, we found that disomes generate approximately 2-10% of all footprints under basal conditions. A high-resolution Disome-seq experiment in human cells identified reproducible disome-forming sites that contribute to the basal level of disome formation in the cell. Exposure of yeast cells to methyl methanesulfonate and human cells to anisomycin increased disome abundance up to four-fold and redistributed collisions in a stress-specific and context-dependent manner. Conclusions: These data provide a quantitative, transcriptome-wide framework for measuring disome levels and reveal how translational stress reshapes the landscape of ribosome collisions in cells.
ER -