ArticlePLoS genetics2017
Post-Translational Dosage Compensation Buffers Genetic Perturbations to Stoichiometry of Protein Complexes.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 82 citations in OpenAlex.
- A systems perspective on monoallelic inborn errors of immunity.Nature genetics · 2026Review
- Protein-Ratio Rheostats: Integrating Stoichiometry, Abundance, and Binding Affinity in Cellular Function.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- The ER anchoring and abundance of the EEF1B complex is affected by tissue-specific alternative EEF1D splicing.Life science alliance · 2026Article
- Multi-omics analysis identifies a role forMicrobiology spectrum · 2026Article
- Evolutionary causes and consequences of gene duplication.Nature reviews. Genetics · 2026Review
- Protein buffering of aneuploidy is driven by coordinated factors identified through machine learning.Molecular systems biology · 2026Article
- Article
- Multilevel Gene Expression Changes in Lineages Containing Adaptive Copy Number Variants.Molecular biology and evolution · 2025Article
- Post-transcriptional regulation supports the homeostatic expression of mature RNA.Briefings in bioinformatics · 2024Article
- Multilevel gene expression changes in lineages containing adaptive copy number variants.bioRxiv : the preprint server for biology · 2024Article
- Forward programming of hiPSCs towards beta-like cells using Ngn3, Pdx1, and MafA.Scientific reports · 2024Article
- Repression of YEATS2 induces cellular senescence in hepatocellular carcinoma and inhibits tumor growth.Cell cycle (Georgetown, Tex.) · 2024Article
- Gene dosage compensation: Origins, criteria to identify compensated genes, and mechanisms including sensor loops as an emerging systems-level property in cancer.Cancer medicine · 2023Review
- Mendelian inheritance revisited: dominance and recessiveness in medical genetics.Nature reviews. Genetics · 2023Review
- YEATS2 regulates the activation of TAK1/NF-κB pathway and is critical for pancreatic ductal adenocarcinoma cell survival.Cell biology and toxicology · 2023Article
- Overexpression profiling reveals cellular requirements in the context of genetic backgrounds and environments.PLoS genetics · 2023Article
- Imaginal disk growth factors are Drosophila chitinase-like proteins with roles in morphogenesis and CO2 response.Genetics · 2023Article
- Paralog-based synthetic lethality: rationales and applications.Frontiers in oncology · 2023Review
- Maternal selection of human embryos in early gestation: Insights from recurrent miscarriage.Seminars in cell & developmental biology · 2022Review
- Proteotoxicity caused by perturbed protein complexes underlies hybrid incompatibility in yeast.Nature communications · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Understanding buffering mechanisms for various perturbations is essential for understanding robustness in cellular systems. Protein-level dosage compensation, which arises when changes in gene copy number do not translate linearly into protein level, is one mechanism for buffering against genetic perturbations. Here, we present an approach to identify genes with dosage compensation by increasing the copy number of individual genes using the genetic tug-of-war technique. Our screen of chromosome I suggests that dosage-compensated genes constitute approximately 10% of the genome and consist predominantly of subunits of multi-protein complexes. Importantly, because subunit levels are regulated in a stoichiometry-dependent manner, dosage compensation plays a crucial role in maintaining subunit stoichiometries. Indeed, we observed changes in the levels of a complex when its subunit stoichiometries were perturbed. We further analyzed compensation mechanisms using a proteasome-defective mutant as well as ribosome profiling, which provided strong evidence for compensation by ubiquitin-dependent degradation but not reduced translational efficiency. Thus, our study provides a systematic understanding of dosage compensation and highlights that this post-translational regulation is a critical aspect of robustness in cellular systems.
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Registered trials
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