Evidence map›Paper›PMID 7635289›Full record

ArticleGenetics1995

Heterozygosity mapping of partially congenic lines: mapping of a semidominant neurological mutation, Wheels (Whl), on mouse chromosome 4.

P M Nolan, P J Sollars, B A Bohne, W J Ewens, G E Pickard, M Bućan

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 1995. 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
5.2field-weighted citation impact, top 4% 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, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. New insights and advances in CHARGE syndrome: Diagnosis, etiologies, treatments, and research discoveries.American journal of medical genetics. Part C, Seminars in medical genetics · 2017
    Review
  4. Article
  5. Article
  6. ENU mutagenesis reveals a highly mutable locus on mouse Chromosome 4 that affects ear morphogenesis.Mammalian genome : official journal of the International Mammalian Genome Society · 2002
    Article
  7. Article
  8. Localization of the mouse gene releasing sex-limited expression of Slp.Proceedings of the National Academy of Sciences of the United States of America · 1996
    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

6 authors at 2 institutions in 1 country.

P M NolanDepartment of Psychiatry, University of Pennsylvania, Philadelphia 19104, USA.
P J Sollars
B A Bohne
W J Ewens
G E Pickard
M Bućan
California University of Pennsylvania · USUniversity of Pennsylvania · US

Funding

STOCHASTIC PROCESSES IN POPULATION GENETICSR01GM021135 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI EWENS, WARREN J. · 1985 to 2005
$348k
NIDCD NIH HHS DC-00071NIGMS NIH HHS GM-21135NIMH NIH HHS MH-47501
6 · The paper itself

Abstract

We identified a semidominant, chemically induced, mouse mutation with a complex array of abnormal behaviors including bidirectional circling and hyperactivity, abnormal circadian rhythmicity and abnormal responses to light. In this report, we genetically and phenotypically characterized the circling/waltzing component of the abnormal behavior. We mapped the locus controlling this trait by heterozygosity mapping of partially congenic lines carrying the mutagenized chromosome outcrossed to different inbred strains for three generations. Analysis of 68 PCR-based markers in 13 affected individuals indicated that the mutant locus, named Wheels (Whl), resides in the subcentromeric portion of mouse chromosome 4. The statistical evaluation of data obtained by heterozygosity mapping validates this efficient mapping approach. Further characterization of the Whl mutation demonstrated that Whl/Whl homozygotes die during embryonic life and that the penetrance of circling behavior depends on genetic background. Morphological analysis of the inner ears of Whl/+ mice revealed a variable number of abnormalities in the sensory and nonsensory portions of their semicircular canals. Abnormalities ranged from slight atrophy of one or more cristae to complete absence of the lateral crista and canal. The molecular characterization of the gene disrupted in the Whl mutation will provide insight into developmental mechanisms involved in inner ear formation.

Indexed as

Chromosome MappingGenes, DominantAnimalsCircadian RhythmGenetic MarkersMiceMice, Inbred BALB CMice, Inbred C3HMice, Inbred C57BLMice, Neurologic MutantsMotor ActivityPolymerase Chain ReactionSemicircular CanalsGenetic Markers

Identifiers

PMID7635289
PMCPMC1206551
OpenAlexW2109834341

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.