Evidence map›Paper›PMID 37126494›Full record

ArticlePLoS genetics2023

Substrate-specific effects of natural genetic variation on proteasome activity.

Mahlon A Collins, Randi Avery, Frank W Albert

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Mahlon A CollinsDepartment of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, Minnesota, United States of America.ORCID 0000-0001-6799-5645
Randi AveryDepartment of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, Minnesota, United States of America.
Frank W AlbertDepartment of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, Minnesota, United States of America.ORCID 0000-0002-1380-8063
University of Minnesota · US

Funding

Genomic approaches for dissecting regulatory variationR35GM124676 · NIGMS · UNIVERSITY OF MINNESOTA · PI Frank Wolfgang Albert · 2017 to 2026
$4.6M
Genetic Influences on Protein Degradation in Large Yeast PopulationsF32GM128302 · NIGMS · UNIVERSITY OF MINNESOTA · PI COLLINS, MAHLON · 2019 to 2019
$63k
NIGMS NIH HHS F32 GM128302NIGMS NIH HHS R35 GM124676
6 · The paper itself

Abstract

Protein degradation is an essential biological process that regulates protein abundance and removes misfolded and damaged proteins from cells. In eukaryotes, most protein degradation occurs through the stepwise actions of two functionally distinct entities, the ubiquitin system and the proteasome. Ubiquitin system enzymes attach ubiquitin to cellular proteins, targeting them for degradation. The proteasome then selectively binds and degrades ubiquitinated substrate proteins. Genetic variation in ubiquitin system genes creates heritable differences in the degradation of their substrates. However, the challenges of measuring the degradative activity of the proteasome independently of the ubiquitin system in large samples have limited our understanding of genetic influences on the proteasome. Here, using the yeast Saccharomyces cerevisiae, we built and characterized reporters that provide high-throughput, ubiquitin system-independent measurements of proteasome activity. Using single-cell measurements of proteasome activity from millions of genetically diverse yeast cells, we mapped 15 loci across the genome that influence proteasomal protein degradation. Twelve of these 15 loci exerted specific effects on the degradation of two distinct proteasome substrates, revealing a high degree of substrate-specificity in the genetics of proteasome activity. Using CRISPR-Cas9-based allelic engineering, we resolved a locus to a causal variant in the promoter of RPT6, a gene that encodes a subunit of the proteasome's 19S regulatory particle. The variant increases RPT6 expression, which we show results in increased proteasome activity. Our results reveal the complex genetic architecture of proteasome activity and suggest that genetic influences on the proteasome may be an important source of variation in the many cellular and organismal traits shaped by protein degradation.

Indexed as

Proteasome Endopeptidase ComplexSaccharomyces cerevisiae ProteinsGenetic VariationProteolysisSaccharomyces cerevisiaeUbiquitinProteasome Endopeptidase ComplexSaccharomyces cerevisiae ProteinsUbiquitin

Identifiers

PMID37126494
PMCPMC10174532
OpenAlexW4367597147

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.