Evidence map›Paper›PMID 11560901›Full record

ArticleGenetics2001

Technical knockout, a Drosophila model of mitochondrial deafness.

J M Toivonen, K M O'Dell, N Petit, S C Irvine, G K Knight, M Lehtonen, M Longmuir, K Luoto, S Touraille, Z Wang and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

50 citing papers in PubMed, 99 citations in OpenAlex.

  1. The First Report of a Bang-Sensitive Strain inInternational journal of molecular sciences · 2026
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  11. Frontiers in immunology · 2020
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  13. Groove structure of porous hydroxyapatite scaffolds (HAS) modulates immune environment via regulating macrophages and subsequently enhances osteogenesis.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2019
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  14. Minimal effects ofBiology open · 2019
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  16. Cleave and Rescue, a novel selfish genetic element and general strategy for gene drive.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
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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

13 authors at 6 institutions in 3 countries.

J M ToivonenInstitute of Medical Technology & Tampere University Hospital, FIN-33014 University of Tampere, Finland.
K M O'Dell
N Petit
S C Irvine
G K Knight
M Lehtonen
M Longmuir
K Luoto
S Touraille
Z Wang
S Alziari
Z H Shah
H T Jacobs
Tampere University · FIUniversity of Glasgow · GBCentre National de la Recherche Scientifique · FRTampere University · FITampere University Hospital · FIUniversité Clermont Auvergne · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in mtDNA-encoded components of the mitochondrial translational apparatus are associated with diverse pathological states in humans, notably sensorineural deafness. To develop animal models of such disorders, we have manipulated the nuclear gene for mitochondrial ribosomal protein S12 in Drosophila (technical knockout, tko). The prototypic mutant tko(25t) exhibits developmental delay, bang sensitivity, impaired male courtship, and defective response to sound. On the basis of a transgenic reversion test, these phenotypes are attributable to a single substitution (L85H) at a conserved residue of the tko protein. The mutant is hypersensitive to doxycyclin, an antibiotic that selectively inhibits mitochondrial protein synthesis, and mutant larvae have greatly diminished activities of mitochondrial redox enzymes and decreased levels of mitochondrial small-subunit rRNA. A second mutation in the tko gene, Q116K, which is predicted to impair the accuracy of mitochondrial translation, results in the completely different phenotype of recessive female sterility, based on three independent transgenic insertions. We infer that the tko(25t) mutant provides a model of mitochondrial hearing impairment resulting from a quantitative deficiency of mitochondrial translational capacity.

Indexed as

MutationAnimalsAnimals, Genetically ModifiedAnti-Bacterial AgentsBlotting, NorthernBlotting, SouthernCell NucleusCloning, MolecularCrosses, GeneticDeafnessDisease Models, AnimalDNA, MitochondrialDose-Response Relationship, DrugDoxycyclineDrosophilaFemaleAnti-Bacterial AgentsDNA, MitochondrialDoxycyclineOligonucleotidesRibosomal Proteinsribosomal protein S12RNA, Ribosomal

Identifiers

PMID11560901
PMCPMC1461776
OpenAlexW1840694617

What OpenQuestion holds

Textmetadata
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.