ArticlePLoS genetics2020
Exploring the Complexity of Protein-Level Dosage Compensation that Fine-Tunes Stoichiometry of Multiprotein Complexes.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Protein-Ratio Rheostats: Integrating Stoichiometry, Abundance, and Binding Affinity in Cellular Function.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Genome-wide pQTL mapping in human skin identifies specific genetic regulators and mechanistic links to skin disorders.Nature communications · 2026Article
- Multilevel Gene Expression Changes in Lineages Containing Adaptive Copy Number Variants.Molecular biology and evolution · 2025Article
- Challenges and opportunities for the diverse substrates of SPOP E3 ubiquitin ligase in cancer.Theranostics · 2025Review
- Altered mRNA transport and local translation in iNeurons with RNA binding protein knockdown.bioRxiv : the preprint server for biology · 2024Article
- Multilevel gene expression changes in lineages containing adaptive copy number variants.bioRxiv : the preprint server for biology · 2024Article
- Chromatin accessibility, not 5mC methylation covaries with partial dosage compensation in crows.PLoS genetics · 2023Article
- Multilayered regulation of proteome stoichiometry.Current genetics · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proper control of gene expression levels upon various perturbations is a fundamental aspect of cellular robustness. Protein-level dosage compensation is one mechanism buffering perturbations to stoichiometry of multiprotein complexes through accelerated proteolysis of unassembled subunits. Although N-terminal acetylation- and ubiquitin-mediated proteasomal degradation by the Ac/N-end rule pathway enables selective compensation of excess subunits, it is unclear how widespread this pathway contributes to stoichiometry control. Here we report that dosage compensation depends only partially on the Ac/N-end rule pathway. Our analysis of genetic interactions between 18 subunits and 12 quality control factors in budding yeast demonstrated that multiple E3 ubiquitin ligases and N-acetyltransferases are involved in dosage compensation. We find that N-acetyltransferases-mediated compensation is not simply predictable from N-terminal sequence despite their sequence specificity for N-acetylation. We also find that the compensation of Pop3 and Bet4 is due in large part to a minor N-acetyltransferase NatD. Furthermore, canonical NatD substrates histone H2A/H4 were compensated even in its absence, suggesting N-acetylation-independent stoichiometry control. Our study reveals the complexity and robustness of the stoichiometry control system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.