Evidence map›Paper›PMID 24886829›Full record

ArticleDevelopmental biology2014

Daughterless homodimer synergizes with Eyeless to induce Atonal expression and retinal neuron differentiation.

Miho Tanaka-Matakatsu, John Miller, Daniel Borger, Wei-Jen Tang, Wei Du

Abstract read
In one paragraph

Article in Developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Daughterless, theDisease models & mechanisms · 2020
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
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  12. Article
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

5 authors.

Miho Tanaka-MatakatsuBen May Department for Cancer Research, The University of Chicago, 929 E. 57th Street, Chicago, IL 60637, USA.
John MillerBen May Department for Cancer Research, The University of Chicago, 929 E. 57th Street, Chicago, IL 60637, USA.
Daniel BorgerBen May Department for Cancer Research, The University of Chicago, 929 E. 57th Street, Chicago, IL 60637, USA.
Wei-Jen TangBen May Department for Cancer Research, The University of Chicago, 929 E. 57th Street, Chicago, IL 60637, USA.
Wei DuBen May Department for Cancer Research, The University of Chicago, 929 E. 57th Street, Chicago, IL 60637, USA. Electronic address: wei@uchicago.edu.

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Control of Cell Proliferation and Differentiation in the Developing RetinaR01GM074197 · NIGMS · UNIVERSITY OF CHICAGO · PI DU, WEI · 2006 to 2013
$2.4M
A novel approach to target Rb mutant cancersR01CA149275 · NCI · UNIVERSITY OF CHICAGO · PI DU, WEI · 2011 to 2015
$1.6M
NCATS NIH HHS UL1 TR000430NCI NIH HHS CA149275NCI NIH HHS R01 CA149275NIGMS NIH HHS GM074197NIGMS NIH HHS R01 GM074197
6 · The paper itself

Abstract

Class I Basic Helix-Loop-Helix (bHLH) transcription factors form homodimers or heterodimers with class II bHLH proteins. While bHLH heterodimers are known to have diverse roles, little is known about the role of class I homodimers. In this manuscript, we show that a linked dimer of Daughterless (Da), the only Drosophila class I bHLH protein, activates Atonal (Ato) expression and retinal neuron differentiation synergistically with the retinal determination factor Eyeless (Ey). The HLH protein Extramacrocheate (Emc), which forms heterodimer with Da, antagonizes the synergistic activation from Da but not the Da-Da linked dimer with Ey. We show that Da directly interacts with Ey and promotes Ey binding to the Ey binding site in the Ato 3׳ enhancer. Interestingly, the Ey binding site in the Ato 3׳ enhancer contains an embedded E-box that is also required for the synergistic activation by Ey and Da. Finally we show that mammalian homologs of Ey and Da can functionally replace their Drosophila counterparts to synergistically activate the Ato enhancer, suggesting that the observed function is evolutionary conserved.

Indexed as

Models, MolecularAnimalsAnimals, Genetically ModifiedBasic Helix-Loop-Helix ProteinsCell DifferentiationChromatin ImmunoprecipitationDimerizationDNA-Binding ProteinsDNA PrimersDrosophilaDrosophila ProteinsGene Expression Regulation, DevelopmentalImaginal DiscsImmunohistochemistryMicroscopy, FluorescenceNerve Tissue Proteinsato protein, DrosophilaBasic Helix-Loop-Helix ProteinsDa protein, DrosophilaDNA-Binding ProteinsDNA PrimersDrosophila Proteinsey protein, DrosophilaNerve Tissue ProteinsAtonalbHLH proteinsDaughterlessDrosophila eye developmentEyelessPax6

Identifiers

PMID24886829
PMCPMC4106475

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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.