Evidence map›Paper›PMID 8088529›Full record

ArticleGenetics1994

Molecular genetics of the brown (b)-locus region of mouse chromosome 4. II. Complementation analyses of lethal brown deletions.

E M Rinchik

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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 29 citations in OpenAlex.

  1. Creating a "hopeful monster": mouse forward genetic screens.Methods in molecular biology (Clifton, N.J.) · 2011
    Article
  2. Article
  3. Genomic anatomy of the Tyrp1 (brown) deletion complex.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  4. X-ray-induced deletion complexes in embryonic stem cells on mouse chromosome 15.Mammalian genome : official journal of the International Mammalian Genome Society · 2005
    Article
  5. Article
  6. A high-resolution map of the brown (b, Tyrp1) deletion complex of mouse chromosome 4.Mammalian genome : official journal of the International Mammalian Genome Society · 1995
    Article
  7. 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

1 author at 1 institution in 1 country.

E M RinchikBiology Division, Oak Ridge National Laboratory, Tennessee 37831-8077.
Oak Ridge National Laboratory · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous new mutations at the brown (b) locus in mouse chromosome 4 have been recovered over the years in germ-cell mutagenesis experiments performed at the Oak Ridge National Laboratory. A large series of radiation- and chemical-induced b mutations known to be chromosomal deletions, and also known to be prenatally lethal when homozygous, were analyzed by pairwise complementation crosses as well as by pseudodominance tests involving flanking loci defined by externally visible phenotypes. These crosses were designed to determine the extent of each deletion on the genetic and phenotype map of the chromosomal region surrounding the b locus; the crosses also provided basic data that assigned deletions to complementation groups and defined four new loci associated with aberrancies in normal development. Specifically, the pseudodominance tests identified deletions that include the proximally mapping whirler (wi) and the distally mapping depilated (dep) genes, thereby bracketing these loci defined by visible developmental abnormalities with landmarks (deletion breakpoints) that are easily identified on the physical map. Furthermore, the complementation crosses, which were supplemented with additional crosses that allowed determination of the gross time of lethality of selected deletions, defined four new loci required for normal development. Homozygous deletion of one of these loci (b-associated fitness, baf) results in a runting syndrome evident during postnatal development; deletion of one locus [l(4)2Rn] causes death in the late gestation/neonatal period; and deletion of either of two loci [l(4)1Rn or l(4)3Rn] results in embryonic death, most likely in pre-, peri- or postimplantation stages. The placement of these new functionally defined loci on the evolving molecular map of the b region should be useful for continuing the analysis of the roles played in development by genes in this segment of chromosome 4.

Indexed as

Gene DeletionGenetic Complementation TestGerm-Line MutationMembrane GlycoproteinsOxidoreductasesAnimalsChromosome MappingCrosses, GeneticDNA Mutational AnalysisFemaleFetal DeathGenes, LethalGenetic LinkageHairHair ColorMaleeumelaninMelaninsMembrane GlycoproteinsOxidoreductasesProteinstyrosinase-related protein-1Tyrp1 protein, mouse

Identifiers

PMID8088529
PMCPMC1206045
OpenAlexW1915185013

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.