Evidence map›Paper›PMID 37679564›Full record

ArticleNature structural & molecular biology2023

Regulation with cell size ensures mitochondrial DNA homeostasis during cell growth.

Anika Seel, Francesco Padovani, Moritz Mayer, Alissa Finster, Daniela Bureik, Felix Thoma, Christof Osman, Till Klecker, Kurt M Schmoller

Open access · hybridAbstract read
In one paragraph

Article in Nature structural & molecular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Anika SeelInstitute of Functional Epigenetics, Molecular Targets and Therapeutics Center, Helmholtz Zentrum München, Neuherberg, Germany.
Francesco PadovaniInstitute of Functional Epigenetics, Molecular Targets and Therapeutics Center, Helmholtz Zentrum München, Neuherberg, Germany.ORCID http://orcid.org/0000-0003-2540-8240
Moritz MayerInstitute of Cell Biology, University of Bayreuth, Bayreuth, Germany.
Alissa FinsterInstitute of Functional Epigenetics, Molecular Targets and Therapeutics Center, Helmholtz Zentrum München, Neuherberg, Germany.
Daniela BureikInstitute of Functional Epigenetics, Molecular Targets and Therapeutics Center, Helmholtz Zentrum München, Neuherberg, Germany.
Felix ThomaFaculty of Biology, Ludwig-Maximilians-Universität München, Planegg-Martinsried, Germany.ORCID http://orcid.org/0000-0002-0227-8079
Christof OsmanFaculty of Biology, Ludwig-Maximilians-Universität München, Planegg-Martinsried, Germany.
Till KleckerInstitute of Cell Biology, University of Bayreuth, Bayreuth, Germany.ORCID http://orcid.org/0000-0003-0149-042X
Kurt M SchmollerInstitute of Functional Epigenetics, Molecular Targets and Therapeutics Center, Helmholtz Zentrum München, Neuherberg, Germany. kurt.schmoller@helmholtz-munich.de.ORCID http://orcid.org/0000-0001-5790-5204
Helmholtz Zentrum München · DELudwig-Maximilians-Universität München · DEUniversity of Bayreuth · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To maintain stable DNA concentrations, proliferating cells need to coordinate DNA replication with cell growth. For nuclear DNA, eukaryotic cells achieve this by coupling DNA replication to cell-cycle progression, ensuring that DNA is doubled exactly once per cell cycle. By contrast, mitochondrial DNA replication is typically not strictly coupled to the cell cycle, leaving the open question of how cells maintain the correct amount of mitochondrial DNA during cell growth. Here, we show that in budding yeast, mitochondrial DNA copy number increases with cell volume, both in asynchronously cycling populations and during G1 arrest. Our findings suggest that cell-volume-dependent mitochondrial DNA maintenance is achieved through nuclear-encoded limiting factors, including the mitochondrial DNA polymerase Mip1 and the packaging factor Abf2, whose amount increases in proportion to cell volume. By directly linking mitochondrial DNA maintenance to nuclear protein synthesis and thus cell growth, constant mitochondrial DNA concentrations can be robustly maintained without a need for cell-cycle-dependent regulation.

Indexed as

DNA, MitochondrialDNA ReplicationCell CycleCell SizeHomeostasisDNA, Mitochondrial

Identifiers

PMID37679564
PMCPMC10584693
OpenAlexW4386495862

What OpenQuestion holds

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LicenceCC BY
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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.