Evidence map›Paper›PMID 24613310›Full record

ArticleCurrent biology : CB2014

Identification of transcriptional and metabolic programs related to mammalian cell size.

Teemu P Miettinen, Heli K J Pessa, Matias J Caldez, Tobias Fuhrer, M Kasim Diril, Uwe Sauer, Philipp Kaldis, Mikael Björklund

Open access · hybridAbstract read
In one paragraph

Article in Current biology : CB, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

86 citing papers in PubMed, 141 citations in OpenAlex.

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26 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 3 countries.

Teemu P MiettinenDivision of Cell and Developmental Biology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
Heli K J PessaDivision of Cell and Developmental Biology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
Matias J CaldezInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, 61 Biopolis Drive, Proteos #03-09, Singapore 138673, Singapore; Department of Biochemistry, National University of Singapore, Singapore 117597, Singapore.
Tobias FuhrerInstitute of Molecular Systems Biology, Eidgenössische Technische Hochschule Zürich, Wolfgang-Pauli Strasse 16, 8093 Zürich, Switzerland.
M Kasim DirilInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, 61 Biopolis Drive, Proteos #03-09, Singapore 138673, Singapore.
Uwe SauerInstitute of Molecular Systems Biology, Eidgenössische Technische Hochschule Zürich, Wolfgang-Pauli Strasse 16, 8093 Zürich, Switzerland.
Philipp KaldisInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, 61 Biopolis Drive, Proteos #03-09, Singapore 138673, Singapore; Department of Biochemistry, National University of Singapore, Singapore 117597, Singapore.
Mikael BjörklundDivision of Cell and Developmental Biology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, UK. Electronic address: m.bjorklund@dundee.ac.uk.
ETH Zurich · CHNational University of Singapore · SGUniversity of Dundee · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRegulation of cell size requires coordination of growth and proliferation. Conditional loss of cyclin-dependent kinase 1 in mice permits hepatocyte growth without cell division, allowing us to study cell size in vivo using transcriptomics and metabolomics.

resultsLarger cells displayed increased expression of cytoskeletal genes but unexpectedly repressed expression of many genes involved in mitochondrial functions. This effect appears to be cell autonomous because cultured Drosophila cells induced to increase cell size displayed a similar gene-expression pattern. Larger hepatocytes also displayed a reduction in the expression of lipogenic transcription factors, especially sterol-regulatory element binding proteins. Inhibition of mitochondrial functions and lipid biosynthesis, which is dependent on mitochondrial metabolism, increased the cell size with reciprocal effects on cell proliferation in several cell lines.

conclusionsWe uncover that large cell-size increase is accompanied by downregulation of mitochondrial gene expression, similar to that observed in diabetic individuals. Mitochondrial metabolism and lipid synthesis are used to couple cell size and cell proliferation. This regulatory mechanism may provide a possible mechanism for sensing metazoan cell size.

Indexed as

Cell SizeAerobiosisAnimalsCell ProliferationCytoskeletonFemaleGene Expression RegulationGlycolysisLipid MetabolismLiverMetabolomeMiceMitochondria, LiverTranscription, Genetic

Identifiers

PMID24613310
PMCPMC3991852
OpenAlexW2004954151

What OpenQuestion holds

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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.