Evidence map›Paper›PMID 26327126›Full record

ArticlePloS one2015

A COLQ Missense Mutation in Sphynx and Devon Rex Cats with Congenital Myasthenic Syndrome.

Marie Abitbol, Christophe Hitte, Philippe Bossé, Nicolas Blanchard-Gutton, Anne Thomas, Lionel Martignat, Stéphane Blot, Laurent Tiret

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Effects ofAnimals : an open access journal from MDPI · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Congenital Myasthenic Syndrome in a Mixed Breed Dog.Frontiers in veterinary science · 2017
    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

8 authors at 6 institutions in 1 country.

Marie AbitbolInserm, IMRB U955-E10, 94000, Créteil, France; Université Paris Est, Ecole nationale vétérinaire d'Alfort, 94700, Maisons-Alfort, & Faculté de médecine, 94000, Créteil, France; Etablissement Français du Sang, 94017, Créteil, France; APHP, Hôpitaux Universitaires Henri Mondor, DHU Pepsy & Centre de référence des maladies neuromusculaires GNMH, 94000 Créteil, France.
Christophe HitteInstitut de Génétique et Développement de Rennes IGDR, UMR6290 CNRS-Université de Rennes 1, Rennes, France.
Philippe BosséInserm, IMRB U955-E10, 94000, Créteil, France; Université Paris Est, Ecole nationale vétérinaire d'Alfort, 94700, Maisons-Alfort, & Faculté de médecine, 94000, Créteil, France; Etablissement Français du Sang, 94017, Créteil, France; APHP, Hôpitaux Universitaires Henri Mondor, DHU Pepsy & Centre de référence des maladies neuromusculaires GNMH, 94000 Créteil, France.
Nicolas Blanchard-GuttonInserm, IMRB U955-E10, 94000, Créteil, France; Université Paris Est, Ecole nationale vétérinaire d'Alfort, 94700, Maisons-Alfort, & Faculté de médecine, 94000, Créteil, France; Etablissement Français du Sang, 94017, Créteil, France; APHP, Hôpitaux Universitaires Henri Mondor, DHU Pepsy & Centre de référence des maladies neuromusculaires GNMH, 94000 Créteil, France.
Anne ThomasAntagene, Animal Genetics Laboratory, La Tour de Salvagny, France.
Lionel MartignatONIRIS, UP Sécurité Sanitaire en Biotechnologies de la Reproduction, Nantes, France.
Stéphane BlotInserm, IMRB U955-E10, 94000, Créteil, France; Université Paris Est, Ecole nationale vétérinaire d'Alfort, 94700, Maisons-Alfort, & Faculté de médecine, 94000, Créteil, France; Etablissement Français du Sang, 94017, Créteil, France; APHP, Hôpitaux Universitaires Henri Mondor, DHU Pepsy & Centre de référence des maladies neuromusculaires GNMH, 94000 Créteil, France.
Laurent TiretInserm, IMRB U955-E10, 94000, Créteil, France; Université Paris Est, Ecole nationale vétérinaire d'Alfort, 94700, Maisons-Alfort, & Faculté de médecine, 94000, Créteil, France; Etablissement Français du Sang, 94017, Créteil, France; APHP, Hôpitaux Universitaires Henri Mondor, DHU Pepsy & Centre de référence des maladies neuromusculaires GNMH, 94000 Créteil, France.
École Nationale Vétérinaire d'Alfort · FRÉtablissement Français du Sang · FRÉco-Anthropologie · FRInstitut de génétique et de développement de Rennes · FRInstitut Mondor de Recherche Biomédicale · FROniris · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An autosomal recessive neuromuscular disorder characterized by skeletal muscle weakness, fatigability and variable electromyographic or muscular histopathological features has been described in the two related Sphynx and Devon Rex cat breeds (Felis catus). Collection of data from two affected Sphynx cats and their relatives pointed out a single disease candidate region on feline chromosome C2, identified following a genome-wide SNP-based homozygosity mapping strategy. In that region, we further identified COLQ (collagen-like tail subunit of asymmetric acetylcholinesterase) as a good candidate gene, since COLQ mutations were identified in affected humans and dogs with endplate acetylcholinesterase deficiency leading to a synaptic form of congenital myasthenic syndrome (CMS). A homozygous c.1190G>A missense variant located in exon 15 of COLQ, leading to a C397Y substitution, was identified in the two affected cats. C397 is a highly-conserved residue from the C-terminal domain of the protein; its mutation was previously shown to produce CMS in humans, and here we confirmed in an affected Sphynx cat that it induces a loss of acetylcholinesterase clustering at the neuromuscular junction. Segregation of the c.1190G>A variant was 100% consistent with the autosomal recessive mode of inheritance of the disorder in our cat pedigree; in addition, an affected, unrelated Devon Rex cat recruited thereafter was also homozygous for the variant. Genotyping of a panel of 333 cats from 14 breeds failed to identify a single carrier in non-Sphynx and non-Devon Rex cats. Finally, the percentage of healthy carriers in a European subpanel of 81 genotyped Sphynx cats was estimated to be low (3.7%) and 14 control Devon Rex cats were genotyped as wild-type individuals. Altogether, these results strongly support that the neuromuscular disorder reported in Sphynx and Devon Rex breeds is a CMS caused by a unique c.1190G>A missense mutation, presumably transmitted through a founder effect, which strictly and slightly disseminated in these two breeds. The presently available DNA test will help owners avoid matings at risk.

Indexed as

Mutation, MissenseAcetylcholinesteraseAnimalsCatsMolecular Sequence DataMuscle ProteinsMyasthenic Syndromes, CongenitalSpecies SpecificityAcetylcholinesteraseMuscle Proteins

Identifiers

PMID26327126
PMCPMC4556666
OpenAlexW2134507987

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.