Evidence map›Paper›PMID 36261409›Full record

ArticleNature communications2022

Sublinear scaling of the cellular proteome with ploidy.

G Yahya, P Menges, P S Amponsah, D A Ngandiri, D Schulz, A Wallek, N Kulak, M Mann, P Cramer, V Savage and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 38 citations in OpenAlex.

  1. Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026
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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

12 authors at 5 institutions in 4 countries.

G YahyaDepartment of Molecular Genetics, TU Kaiserslautern, Paul-Ehrlich Str. 24, 67663, Kaiserslautern, Germany.
P MengesDepartment of Molecular Genetics, TU Kaiserslautern, Paul-Ehrlich Str. 24, 67663, Kaiserslautern, Germany.
P S AmponsahDepartment of Molecular Genetics, TU Kaiserslautern, Paul-Ehrlich Str. 24, 67663, Kaiserslautern, Germany.ORCID 0000-0002-5891-5823
D A NgandiriDepartment of Molecular Genetics, TU Kaiserslautern, Paul-Ehrlich Str. 24, 67663, Kaiserslautern, Germany.ORCID 0000-0002-9325-5066
D SchulzInstitute of Molecular Biology, University of Zurich, Zurich, Switzerland.
A WallekMax Planck Institute of Biochemistry, 82152, Martinsried, Germany.
N KulakMax Planck Institute of Biochemistry, 82152, Martinsried, Germany.
M MannMax Planck Institute of Biochemistry, 82152, Martinsried, Germany.ORCID 0000-0003-1292-4799
P CramerMax Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0001-5454-7755
V SavageDepartment of Biomathematics, University of California at Los Angeles, Los Angeles, CA, 90095, USA.
M RäschleDepartment of Molecular Genetics, TU Kaiserslautern, Paul-Ehrlich Str. 24, 67663, Kaiserslautern, Germany.ORCID 0000-0002-6737-7203
Z StorchovaDepartment of Molecular Genetics, TU Kaiserslautern, Paul-Ehrlich Str. 24, 67663, Kaiserslautern, Germany. storchova@bio.uni-kl.de.ORCID 0000-0003-2376-7047
University of Kaiserslautern · DEMax Planck Institute of Biochemistry · DEMax Planck Institute for Multidisciplinary SciencesUniversity of California, Los Angeles · USUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ploidy changes are frequent in nature and contribute to evolution, functional specialization and tumorigenesis. Analysis of model organisms of different ploidies revealed that increased ploidy leads to an increase in cell and nuclear volume, reduced proliferation, metabolic changes, lower fitness, and increased genomic instability, but the underlying mechanisms remain poorly understood. To investigate how gene expression changes with cellular ploidy, we analyzed isogenic series of budding yeasts from 1N to 4N. We show that mRNA and protein abundance scales allometrically with ploidy, with tetraploid cells showing only threefold increase in protein abundance compared to haploids. This ploidy-dependent sublinear scaling occurs via decreased rRNA and ribosomal protein abundance and reduced translation. We demonstrate that the activity of Tor1 is reduced with increasing ploidy, which leads to diminished rRNA gene repression via a Tor1-Sch9-Tup1 signaling pathway. mTORC1 and S6K activity are also reduced in human tetraploid cells and the concomitant increase of the Tup1 homolog Tle1 downregulates the rDNA transcription. Our results suggest that the mTORC1-Sch9/S6K-Tup1/TLE1 pathway ensures proteome remodeling in response to increased ploidy.

Indexed as

ProteomeTetraploidyDNA, RibosomalHaploidyHumansMechanistic Target of Rapamycin Complex 1Ribosomal ProteinsRNA, MessengerRNA, RibosomalTranscription FactorsDNA, RibosomalMechanistic Target of Rapamycin Complex 1ProteomeRibosomal ProteinsRNA, MessengerRNA, RibosomalTranscription Factors

Identifiers

PMID36261409
PMCPMC9581932
OpenAlexW4306784287

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.