Evidence map›Paper›PMID 29494583›Full record

ArticlePLoS genetics2018

Atf3 links loss of epithelial polarity to defects in cell differentiation and cytoarchitecture.

Colin D Donohoe, Gábor Csordás, Andreia Correia, Marek Jindra, Corinna Klein, Bianca Habermann, Mirka Uhlirova

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 44 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

7 authors at 4 institutions in 2 countries.

Colin D DonohoeInstitute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Gábor CsordásInstitute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.ORCID 0000-0001-6871-6839
Andreia CorreiaInstitute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Marek JindraBiology Center, Czech Academy of Sciences, Institute of Entomology, Ceske Budejovice, Czech Republic.ORCID 0000-0002-2196-9924
Corinna KleinMax Planck Institute for Biology of Ageing, Cologne, Germany.
Bianca HabermannMax Planck Institute of Biochemistry, Martinsried, Germany.
Mirka UhlirovaInstitute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.ORCID 0000-0002-5735-8287
University of Cologne · DECzech Academy of Sciences · CZMax Planck Institute for Biology of Ageing · DEMax Planck Institute of Biochemistry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interplay between apicobasal cell polarity modules and the cytoskeleton is critical for differentiation and integrity of epithelia. However, this coordination is poorly understood at the level of gene regulation by transcription factors. Here, we establish the Drosophila activating transcription factor 3 (atf3) as a cell polarity response gene acting downstream of the membrane-associated Scribble polarity complex. Loss of the tumor suppressors Scribble or Dlg1 induces atf3 expression via aPKC but independent of Jun-N-terminal kinase (JNK) signaling. Strikingly, removal of Atf3 from Dlg1 deficient cells restores polarized cytoarchitecture, levels and distribution of endosomal trafficking machinery, and differentiation. Conversely, excess Atf3 alters microtubule network, vesicular trafficking and the partition of polarity proteins along the apicobasal axis. Genomic and genetic approaches implicate Atf3 as a regulator of cytoskeleton organization and function, and identify Lamin C as one of its bona fide target genes. By affecting structural features and cell morphology, Atf3 functions in a manner distinct from other transcription factors operating downstream of disrupted cell polarity.

Indexed as

Activating Transcription Factor 3AnimalsAnimals, Genetically ModifiedCell DifferentiationCell PolarityChromatin ImmunoprecipitationDrosophila melanogasterDrosophila ProteinsEndosomesEyeImaginal DiscsLamin Type ALarvaMAP Kinase Signaling SystemMembrane ProteinsNucleotide MotifsActivating Transcription Factor 3dlg1 protein, DrosophilaDrosophila Proteinslamin CLamin Type AMembrane ProteinsProtein Kinase CScrib protein, DrosophilaTumor Suppressor Proteins

Identifiers

PMID29494583
PMCPMC5849342
OpenAlexW2951918610

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.