Evidence map›Paper›PMID 31415586›Full record

ArticlePloS one2019

Clinical, histopathological and genetic characterisation of oculoskeletal dysplasia in the Northern Inuit Dog.

Renata Stavinohova, Claudia Hartley, Louise M Burmeister, Sally L Ricketts, Louise Pettitt, Roser Tetas Pont, Rebekkah J Hitti, Ellen Schofield, James A C Oliver, Cathryn S Mellersh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Genes · 2022
    Article
  4. Genes · 2021
    Article
  5. 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

10 authors at 1 institution in 1 country.

Renata StavinohovaUnit of Comparative Ophthalmology, Centre for Small Animal Studies, Animal Health Trust, Kentford, Newmarket, Suffolk, United Kingdom.ORCID 0000-0002-8628-9102
Claudia HartleyUnit of Comparative Ophthalmology, Centre for Small Animal Studies, Animal Health Trust, Kentford, Newmarket, Suffolk, United Kingdom.
Louise M BurmeisterKennel Club Genetics Centre, Animal Health Trust, Kentford, Newmarket, Suffolk, United Kingdom.
Sally L RickettsKennel Club Genetics Centre, Animal Health Trust, Kentford, Newmarket, Suffolk, United Kingdom.
Louise PettittKennel Club Genetics Centre, Animal Health Trust, Kentford, Newmarket, Suffolk, United Kingdom.
Roser Tetas PontUnit of Comparative Ophthalmology, Centre for Small Animal Studies, Animal Health Trust, Kentford, Newmarket, Suffolk, United Kingdom.
Rebekkah J HittiKennel Club Genetics Centre, Animal Health Trust, Kentford, Newmarket, Suffolk, United Kingdom.
Ellen SchofieldKennel Club Genetics Centre, Animal Health Trust, Kentford, Newmarket, Suffolk, United Kingdom.ORCID 0000-0003-0648-1418
James A C OliverUnit of Comparative Ophthalmology, Centre for Small Animal Studies, Animal Health Trust, Kentford, Newmarket, Suffolk, United Kingdom.
Cathryn S MellershKennel Club Genetics Centre, Animal Health Trust, Kentford, Newmarket, Suffolk, United Kingdom.
Animal Health Trust · GB

Funding

Wellcome TrustWellcome Trust 090532/Z/09/Z
6 · The paper itself

Abstract

Seven Northern Inuit Dogs (NID) were diagnosed by pedigree analysis with an autosomal recessive inherited oculoskeletal dysplasia (OSD). Short-limbed dwarfism, angular limb deformities and a variable combination of macroglobus, cataracts, lens coloboma, microphakia and vitreopathy were present in all seven dogs, while retinal detachment was diagnosed in five dogs. Autosomal recessive OSD caused by COL9A3 and COL9A2 mutations have previously been identified in the Labrador Retriever (dwarfism with retinal dysplasia 1-drd1) and Samoyed dog (dwarfism with retinal dysplasia 2-drd2) respectively; both of those mutations were excluded in all affected NID. Nine candidate genes were screened in whole genome sequence data; only one variant was identified that was homozygous in two affected NID but absent in controls. This variant was a nonsense single nucleotide polymorphism in COL9A3 predicted to result in a premature termination codon and a truncated protein product. This variant was genotyped in a total of 1,232 dogs. All seven affected NID were homozygous for the variant allele (T/T), while 31/116 OSD-unaffected NID were heterozygous for the variant (C/T) and 85/116 were homozygous for the wildtype allele (C/C); indicating a significant association with OSD (p = 1.41x10-11). A subset of 56 NID unrelated at the parent level were analysed to determine an allele frequency of 0.08, estimating carrier and affected rates to be 15% and 0.6% respectively in NID. All 1,109 non-NID were C/C, suggesting the variant is rare or absent in other breeds. Expression of retinal mRNA was similar between an OSD-affected NID and OSD-unaffected non-NID. In conclusion, a nonsense variant in COL9A3 is strongly associated with OSD in NID, and appears to be widespread in this breed.

Indexed as

MutationAnimalsCollagen Type IXDog DiseasesDogsDwarfismGenotypePedigreePolymorphism, Single NucleotideRetinal DetachmentCollagen Type IX

Identifiers

PMID31415586
PMCPMC6695176
OpenAlexW2967842534

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.