Evidence map›Paper›PMID 8138159›Full record

ArticleGenetics1994

Fine structure mapping and deletion analysis of the murine piebald locus.

D L Metallinos, A J Oppenheimer, E M Rinchik, L B Russell, W Dietrich, S M Tilghman

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 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
2.1field-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, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. A new inbred strain JF1 established from Japanese fancy mouse carrying the classic piebald allele.Mammalian genome : official journal of the International Mammalian Genome Society · 1998
    Article
  6. Molecular characterization of four induced alleles at the Ednrb locus.Proceedings of the National Academy of Sciences of the United States of America · 1997
    Article
  7. Physical mapping of the endothelin receptor type B to bovine chromosome 12.Mammalian genome : official journal of the International Mammalian Genome Society · 1997
    Article
  8. Article
  9. Article
  10. Piebald lethal (sl) acts early to disrupt the development of neural crest-derived melanocytes.Proceedings of the National Academy of Sciences of the United States of America · 1994
    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 1 institution in 1 country.

D L MetallinosHoward Hughes Medical Institute, Department of Molecular Biology, Princeton University, New Jersey 08544.
A J Oppenheimer
E M Rinchik
L B Russell
W Dietrich
S M Tilghman
Howard Hughes Medical Institute · US

Funding

CELL REGULATION--BIOCHEMICALLY ISOLATED DNA SEGMENTSR01HG000198 · NHGRI · STANFORD UNIVERSITY · PI DAVIS, RONALD WAYNE · 1998 to 2001
$2.1M
GORDON CONFERENCE ON GENETIC TOXICOLOGY--1999R13ES010067 · NIEHS · GORDON RESEARCH CONFERENCES · PI SAMSON, LEONA D · 1999 to 1999
–
TECH DEVELOPMENT IN SUPPORT OF MAP AND SEQR37HG000198 · NHGRI · STANFORD UNIVERSITY · PI DAVIS, RONALD WAYNE · 1990 to 1997
–
NHGRI NIH HHS HG 00198NIEHS NIH HHS 222Y01-ES-10067
6 · The paper itself

Abstract

piebald (s) is a recessive mutation that affects the development of two cell types of neural crest origin: the melanocytes, responsible for pigment synthesis in the skin, and enteric ganglia, which innervate the lower bowel. As a result, mice carrying piebald mutations exhibit white spotting in the coat and aganglionic megacolon. Previously the gene had been localized to the distal half of mouse chromosome 14. To determine its precise location relative to molecular markers, an intersubspecific backcross was generated. Two anchor loci of chromosome 14, slaty and hypogonadal, in addition to simple sequence length repeat markers, were used to localize s to a 2-cM interval defined by the markers D14Mit38 and D14Mit42. The molecular markers were also used to characterize nine induced s alleles. Three of these mutations exhibited no deletions or rearrangements of the flanking markers, whereas the other six had two or more of these markers deleted. The extent of the deletions was found to be consistent with the severity of the homozygous phenotype. The location of deletion breakpoints in the induced alleles, coupled with the recombination breakpoints in the backcross progeny, provide useful molecular landmarks to define the location of the piebald gene.

Indexed as

Chromosome MappingGenes, RecessiveMutationAnimalsBase SequenceCrosses, GeneticDNADNA PrimersFemaleGenetic LinkageGenetic MarkersHair ColorHomozygoteLiverMaleMegacolonDNADNA PrimersGenetic Markers

Identifiers

PMID8138159
PMCPMC1205773
OpenAlexW1892782335

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.