Evidence map›Paper›PMID 27240603›Full record

ArticleTransgenic research2016

Analysis of compound heterozygotes reveals that the mouse floxed Pax6 (tm1Ued) allele produces abnormal eye phenotypes.

Natalie J Dorà, Aaron J F Crookshanks, Karen K Y Leung, T Ian Simpson, John O Mason, David J Price, John D West

Abstract read
In one paragraph

Article in Transgenic research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

7 authors.

Natalie J DoràGenes and Development Group, Centre for Integrative Physiology, Biomedical Sciences, University of Edinburgh Medical School, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK.
Aaron J F CrookshanksGenes and Development Group, Centre for Integrative Physiology, Biomedical Sciences, University of Edinburgh Medical School, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK.
Karen K Y LeungGenes and Development Group, Centre for Integrative Physiology, Biomedical Sciences, University of Edinburgh Medical School, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK.
T Ian SimpsonGenes and Development Group, Centre for Integrative Physiology, Biomedical Sciences, University of Edinburgh Medical School, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK.
John O MasonGenes and Development Group, Centre for Integrative Physiology, Biomedical Sciences, University of Edinburgh Medical School, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK.
David J PriceGenes and Development Group, Centre for Integrative Physiology, Biomedical Sciences, University of Edinburgh Medical School, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK.
John D WestGenes and Development Group, Centre for Integrative Physiology, Clinical Sciences, University of Edinburgh Medical School, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK. John.West@ed.ac.uk.

Funding

Medical Research Council G0800429Medical Research Council MR/J003662/1Wellcome Trust
6 · The paper itself

Abstract

Analysis of abnormal phenotypes produced by different types of mutations has been crucial for our understanding of gene function. Some floxed alleles that retain a neomycin-resistance selection cassette (neo cassette) are not equivalent to wild-type alleles and provide useful experimental resources. Pax6 is an important developmental gene and the aim of this study was to determine whether the floxed Pax6 (tm1Ued) (Pax6 (fl) ) allele, which has a retained neo cassette, produced any abnormal eye phenotypes that would imply that it differs from the wild-type allele. Homozygous Pax6 (fl/fl) and heterozygous Pax6 (fl/+) mice had no overt qualitative eye abnormalities but morphometric analysis showed that Pax6 (fl/fl) corneas tended be thicker and smaller in diameter. To aid identification of weak effects, we produced compound heterozygotes with the Pax6 (Sey-Neu) (Pax6 (-)) null allele. Pax6 (fl/-) compound heterozygotes had more severe eye abnormalities than Pax6 (+/-) heterozygotes, implying that Pax6 (fl) differs from the wild-type Pax6 (+) allele. Immunohistochemistry showed that the Pax6 (fl/-) corneal epithelium was positive for keratin 19 and negative for keratin 12, indicating that it was abnormally differentiated. This Pax6 (fl) allele provides a useful addition to the existing Pax6 allelic series and this study demonstrates the utility of using compound heterozygotes with null alleles to unmask cryptic effects of floxed alleles.

Indexed as

AllelesAnimalsEpithelium, CornealEyeEye AbnormalitiesGenotypeHeterozygoteHomozygoteMiceMice, KnockoutPAX6 Transcription FactorPhenotypePax6 protein, mousePAX6 Transcription FactorCorneal epitheliumEyeFloxed alleleKeratin 12Pax6

Identifiers

PMID27240603
PMCPMC5023747

What Socratic holds

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LicenceCC BY
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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 Socratic graph.