Evidence map›Paper›PMID 10430925›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Mitotic recombination produces the majority of recessive fibroblast variants in heterozygous mice.

C Shao, L Deng, O Henegariu, L Liang, N Raikwar, A Sahota, P J Stambrook, J A Tischfield

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 130 citations in OpenAlex.

  1. An overlooked subset of Cx3cr1Journal of neuroinflammation · 2022
    Article
  2. Mitotic Antipairing of Homologous Chromosomes.Results and problems in cell differentiation · 2022
    Article
  3. Review
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  13. Chronic centrosome amplification without tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2015
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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

8 authors at 3 institutions in 1 country.

C ShaoDepartment of Medical and Molecular Genetics and The Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
L Deng
O Henegariu
L Liang
N Raikwar
A Sahota
P J Stambrook
J A Tischfield
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · USUniversity of Cincinnati Medical Center · US

Funding

INBORN ERRORS OF A PURINE SALVAGE PATHWAYR01DK038185 · NIDDK · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI TISCHFIELD, JAY ARNOLD · 1987 to 2000
$288k
NIDDK NIH HHS DK38185NIEHS NIH HHS ES05652
6 · The paper itself

Abstract

Mice heterozygous at Aprt (adenine phosphoribosyltransferase) were used as a model to study in vivo loss of heterozygosity (LOH) in normal fibroblasts. Somatic cell variants that exhibited functional loss of the wild-type Aprt in vivo were recovered as APRT-deficient cell colonies after culturing in selection medium containing 2, 6-diaminopurine (DAP), an adenine analog that is toxic only to cells with APRT enzyme activity. DAP-resistant (DAP(r)) fibroblast variants were recovered at a median frequency of 12 x 10(-5) from individual ears from progeny of crosses between mouse strains 129/Sv and C3H/HeJ. The frequency of DAP(r) variants varied greatly among individual ears, suggesting that they preexisted in vivo and arose at various times during development. Polymorphic molecular markers and a cytological marker on the centromere of chromosome 8 made it possible to discriminate between each of six possible mechanistic pathways of LOH. The majority (about 80%) of the DAP(r) variants were a consequence of mitotic recombination. The prevalence of mitotic recombination in regions proximal to Aprt did not correlate with meiotic map distances. In particular, there was a higher than expected frequency of crossovers within the interval 59 cM to 67 cM. The high spontaneous frequency of Aprt LOH, mediated primarily by mitotic recombination, is fully consistent with our previous results with human peripheral T cells from individuals known to be heterozygous at APRT. Thus, this Aprt heterozygote mouse is a valid model for studying somatic mutagenesis and mitotic recombination in vivo.

Indexed as

Chromosome MappingGenetic VariationHeterozygoteLoss of HeterozygosityRecombination, GeneticAdenine PhosphoribosyltransferaseAnimalsCrosses, GeneticEar, ExternalExonsFemaleFibroblastsGenes, RecessiveHumansMaleMiceAdenine Phosphoribosyltransferase

Identifiers

PMID10430925
PMCPMC17762
OpenAlexW1987050896

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.