Evidence map›Paper›PMID 34244507›Full record

ArticleNature communications2021

Transcription coordinates histone amounts and genome content.

Kora-Lee Claude, Daniela Bureik, Dimitra Chatzitheodoridou, Petia Adarska, Abhyudai Singh, Kurt M Schmoller

Abstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–field-weighted citation impact
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

35 citing papers in PubMed.

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  9. A Fkh1/2 binding site array in thebioRxiv : the preprint server for biology · 2025
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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

6 authors.

Kora-Lee ClaudeInstitute of Functional Epigenetics, Helmholtz Zentrum München, Neuherberg, Germany.
Daniela BureikInstitute of Functional Epigenetics, Helmholtz Zentrum München, Neuherberg, Germany.
Dimitra ChatzitheodoridouInstitute of Functional Epigenetics, Helmholtz Zentrum München, Neuherberg, Germany.
Petia AdarskaInstitute of Functional Epigenetics, Helmholtz Zentrum München, Neuherberg, Germany.
Abhyudai SinghDepartment of Electrical & Computer Engineering, University of Delaware, Newark, DE, USA.ORCID http://orcid.org/0000-0002-1451-2838
Kurt M SchmollerInstitute of Functional Epigenetics, Helmholtz Zentrum München, Neuherberg, Germany. kurt.schmoller@helmholtz-muenchen.de.ORCID http://orcid.org/0000-0001-5790-5204

Funding

Consequences and Control of Randomness in Timing of Intracellular EventsR01GM124446 · NIGMS · UNIVERSITY OF DELAWARE · PI SINGH, ABHYUDAI · 2017 to 2020
$914k
Stochastic hybrid systems approach to uncovering cell-size control mechanisms R01GM126557 · NIGMS · UNIVERSITY OF DELAWARE · PI SINGH, ABHYUDAI · 2017 to 2019
$675k
NIGMS NIH HHS R01 GM124446NIGMS NIH HHS R01 GM126557
6 · The paper itself

Abstract

Biochemical reactions typically depend on the concentrations of the molecules involved, and cell survival therefore critically depends on the concentration of proteins. To maintain constant protein concentrations during cell growth, global mRNA and protein synthesis rates are tightly linked to cell volume. While such regulation is appropriate for most proteins, certain cellular structures do not scale with cell volume. The most striking example of this is the genomic DNA, which doubles during the cell cycle and increases with ploidy, but is independent of cell volume. Here, we show that the amount of histone proteins is coupled to the DNA content, even though mRNA and protein synthesis globally increase with cell volume. As a consequence, and in contrast to the global trend, histone concentrations decrease with cell volume but increase with ploidy. We find that this distinct coordination of histone homeostasis and genome content is already achieved at the transcript level, and is an intrinsic property of histone promoters that does not require direct feedback mechanisms. Mathematical modeling and histone promoter truncations reveal a simple and generalizable mechanism to control the cell volume- and ploidy-dependence of a given gene through the balance of the initiation and elongation rates.

Indexed as

Models, GeneticTranscription, GeneticDNA, FungalGenome, FungalHistonesPloidiesPromoter Regions, GeneticProtein BiosynthesisRNA, FungalRNA, MessengerSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA, FungalHistonesRNA, FungalRNA, MessengerSaccharomyces cerevisiae Proteins

Identifiers

PMID34244507
PMCPMC8270936

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Registered trials

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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.