Evidence map›Paper›PMID 20520827›Full record

ArticlePloS one2010

CF2 represses Actin 88F gene expression and maintains filament balance during indirect flight muscle development in Drosophila.

Kathleen M Gajewski, Robert A Schulz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

24 citing papers in PubMed, 45 citations in OpenAlex.

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  10. Tumors overcome the action of the wasting factor ImpL2 by locally elevating Wnt/Wingless.Proceedings of the National Academy of Sciences of the United States of America · 2021
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  16. TheeLife · 2016
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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

2 authors at 2 institutions in 1 country.

Kathleen M GajewskiDepartment of Systems Biology, University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA. kmgajews@mdanderson.org
Robert A Schulz
The University of Texas MD Anderson Cancer Center · USUniversity of Notre Dame · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TRANSCRIPTIONAL REGULATORS OF CARDIAC GENE EXPRESSIONR01HL059151 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SCHULZ, ROBERT A. · 1998 to 2017
$3.7M
NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NHLBI NIH HHS HL059151NHLBI NIH HHS R01 HL059151
6 · The paper itself

Abstract

The zinc finger protein CF2 is a characterized activator of muscle structural genes in the body wall muscles of the Drosophila larva. To investigate the function of CF2 in the indirect flight muscle (IFM), we examined the phenotypes of flies bearing five homozygous viable mutations. The gross structure of the IFM was not affected, but the stronger hypomorphic alleles caused an increase of up to 1.5X in the diameter of the myofibrils. This size increase did not cause any disruption of the hexameric arrangement of thick and thin filaments. RT-PCR analysis revealed an increase in the transcription of several structural genes. Ectopic overexpression of CF2 in the developing IFM disrupts muscle formation. While our results indicate a role for CF2 as a direct negative regulator of the thin filament protein gene Actin 88F (Act88F), effects on levels of transcripts of myosin heavy chain (mhc) appear to be indirect. This role is in direct contrast to that described in the larval muscles, where CF2 activates structural gene expression. The variation in myofibril phenotypes of CF2 mutants suggest the CF2 may have separate functions in fine-tuning expression of structural genes to insure proper filament stoichiometry, and monitoring and/or controlling the final myofibril size.

Indexed as

Flight, AnimalGene Expression Regulation, DevelopmentalActin CytoskeletonActinsAnimalsCell NucleusDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsEnhancer Elements, GeneticMuscle DevelopmentMuscle ProteinsMusclesMutationMyofibrilsMyosin Heavy ChainsActinsCf2 protein, DrosophilaDNA-Binding ProteinsDrosophila Proteinsflight muscle protein, Act88FMuscle ProteinsMyosin Heavy ChainsProtein IsoformsRepressor ProteinsRNA, MessengerTranscription Factors

Identifiers

PMID20520827
PMCPMC2876027
OpenAlexW2035154738

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.