Evidence map›Paper›PMID 8045933›Full record

ArticleThe Journal of cell biology1994

Transformation of Drosophila melanogaster with the wild-type myosin heavy-chain gene: rescue of mutant phenotypes and analysis of defects caused by overexpression.

R M Cripps, K D Becker, M Mardahl, W A Kronert, D Hodges, S I Bernstein

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-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

27 citing papers in PubMed, 49 citations in OpenAlex.

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  6. An undergraduate laboratory class using CRISPR/Cas9 technology to mutate drosophila genes.Biochemistry and molecular biology education : a bimonthly publication of the International Union of Biochemistry and Molecular Biology · 2016
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  16. mef2 activity levels differentially affect gene expression during Drosophila muscle development.Proceedings of the National Academy of Sciences of the United States of America · 2008
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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 at 1 institution in 1 country.

R M CrippsDepartment of Biology, San Diego State University, California 92182-0057.
K D Becker
M Mardahl
W A Kronert
D Hodges
S I Bernstein
San Diego State University · US

Funding

Genetics and Molecular Biology of Striated Muscle MyosinR01GM032443 · NIGMS · SAN DIEGO STATE UNIVERSITY · PI BERNSTEIN, SANFORD I · 1985 to 2016
$6.4M
Genetics and Molecular Biology of Striated Muscle MyosinR37GM032443 · NIGMS · SAN DIEGO STATE UNIVERSITY · PI Sanford I Bernstein · 2017 to 2026
$5.5M
T-TUBULE MEMBRANE STRUCTURE AND FUNCTIONS06GM045765 · NIGMS · SAN DIEGO STATE UNIVERSITY · PI HARRIS, GREG L · 1991 to 1998
–
NIGMS NIH HHS GM32443NIGMS NIH HHS GM45765
6 · The paper itself

Abstract

We have transformed Drosophila melanogaster with a genomic construct containing the entire wild-type myosin heavy-chain gene, Mhc, together with approximately 9 kb of flanking DNA on each side. Three independent lines stably express myosin heavy-chain protein (MHC) at approximately wild-type levels. The MHC produced is functional since it rescues the mutant phenotypes of a number of different Mhc alleles: the amorphic allele Mhc1, the indirect flight muscle and jump muscle-specific amorphic allele Mhc10, and the hypomorphic allele Mhc2. We show that the Mhc2 mutation is due to the insertion of a transposable element in an intron of Mhc. Since a reduction in MHC in the indirect flight muscles alters the myosin/actin protein ratio and results in myofibrillar defects, we determined the effects of an increase in the effective copy number of Mhc. The presence of four copies of Mhc results in overabundance of the protein and a flightless phenotype. Electron microscopy reveals concomitant defects in the indirect flight muscles, with excess thick filaments at the periphery of the myofibrils. Further increases in copy number are lethal. These results demonstrate the usefulness and potential of the transgenic system to study myosin function in Drosophila. They also show that overexpression of wild-type protein in muscle may disrupt the function of not only the indirect flight but also other muscles of the organism.

Indexed as

Transformation, GeneticAllelesAnimalsBase SequenceCloning, MolecularDNADNA Transposable ElementsDrosophila melanogasterFemaleGene Expression RegulationMaleMolecular Sequence DataMutationMyosinsPhenotypeDNADNA Transposable ElementsMyosins

Identifiers

PMID8045933
PMCPMC2120147
OpenAlexW1999697181

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.