Evidence map›Paper›PMID 8041773›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1994

Structural analysis of chromosomal rearrangements associated with the developmental mutations Ph, W19H, and Rw on mouse chromosome 5.

D L Nagle, P Martin-DeLeon, R B Hough, M Bućan

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Notochordal and foregut abnormalities correlate with elevated neural crest apoptosis in Patch embryos.Birth defects research. Part A, Clinical and molecular teratology · 2011
    Article
  3. Article
  4. Article
  5. Article
  6. Rump white inversion in the mouse disrupts dipeptidyl aminopeptidase-like protein 6 and causes dysregulation of Kit expression.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
  7. Article
  8. Embryonic mesoderm cells spread in response to platelet-derived growth factor and signaling by phosphatidylinositol 3-kinase.Proceedings of the National Academy of Sciences of the United States of America · 1996
    Article
  9. D5Ucl1 and Els1 are closely linked to W on mouse chromosome 5 but lie distal to the W19H deletion.Mammalian genome : official journal of the International Mammalian Genome Society · 1996
    Article
  10. 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

4 authors at 2 institutions in 1 country.

D L NagleDepartment of Psychiatry, University of Pennsylvania, Philadelphia 19104.
P Martin-DeLeon
R B Hough
M Bućan
University of Pennsylvania · USUniversity of Delaware · US

Funding

TRAINING PROGRAM IN CELL AND MOLECULAR BIOLOGYT32GM007229 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BARTOLOMEI, MARISA S. · 1985 to 2023
$14.0M
PHYSICAL MAP OF THE PH, W, AND RW REGIONR01HD028410 · NICHD · UNIVERSITY OF PENNSYLVANIA · PI BUCAN, MAJA · 1991 to 2006
$2.5M
FELLOWSHIP IN IV TREATMENT RESEARCHT32DA007241 · NIDA · UNIVERSITY OF PENNSYLVANIA · PI O'BRIEN, CHARLES P · 1990 to 2006
$1.5M
NICHD NIH HHS HD 28410NIDA NIH HHS T32-DA07241NIGMS NIH HHS GM07229-19
6 · The paper itself

Abstract

We are studying the chromosomal structure of three developmental mutations, dominant spotting (W), patch (Ph), and rump white (Rw) on mouse chromosome 5. These mutations are clustered in a region containing three genes encoding tyrosine kinase receptors (Kit, Pdgfra, and Flk1). Using probes for these genes and for a closely linked locus, D5Mn125, we established a high-resolution physical map covering approximately 2.8 Mb. The entire chromosomal segment mapped in this study is deleted in the W19H mutation. The map indicates the position of the Ph deletion, which encompasses not more than 400 kb around and including the Pdgfra gene. The map also places the distal breakpoint of the Rw inversion to a limited chromosomal segment between Kit and Pdgfra. In light of the structure of the Ph-W-Rw region, we interpret the previously published complementation analyses as indicating that the pigmentation defect in Rw/+ heterozygotes could be due to the disruption of Kit and/or Pdgfra regulatory sequences, whereas the gene(s) responsible for the recessive lethality of Rw/Rw embryos is not closely linked to the Ph and W loci and maps proximally to the W19H deletion. The structural analysis of chromosomal rearrangements associated with W19H, Ph, and Rw combined with the high-resolution physical mapping points the way toward the definition of these mutations in molecular terms and isolation of homologous genes on human chromosome 4.

Indexed as

Chromosome AberrationsGene DeletionGene RearrangementMutationAnimalsElectrophoresis, Gel, Pulsed-FieldGenes, LethalGenetic Complementation TestGenetic LinkageHumansMiceMice, Inbred C3HMice, Inbred C57BLReceptor Protein-Tyrosine KinasesRestriction MappingReceptor Protein-Tyrosine Kinases

Identifiers

PMID8041773
PMCPMC44374
OpenAlexW2024448250

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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 OpenQuestion graph.