Evidence map›Paper›PMID 9694796›Full record

ArticleGenes & development1998

Enhancer control of V(D)J recombination at the TCRbeta locus: differential effects on DNA cleavage and joining.

W M Hempel, P Stanhope-Baker, N Mathieu, F Huang, M S Schlissel, P Ferrier

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. V(D)J recombination: Born to be wild.Seminars in cancer biology · 2010
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The T cell receptor beta enhancer promotes access and pairing of Dbeta and Jbeta gene segments during V(D)J recombination.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  11. Article
  12. Regulation of V(D)J recombination: a dominant role for promoter positioning in gene segment accessibility.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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 4 institutions in 2 countries.

W M HempelCentre d'Immunologie Institut National de la Santé et de la Recherche Médicale-Centre National de la Recherche Scientifique de Marseille-Luminy, Marseille Cedex 9, France.
P Stanhope-Baker
N Mathieu
F Huang
M S Schlissel
P Ferrier
Centre d’Immunologie de Marseille-Luminy · FRInserm · FRJohns Hopkins Medicine · USJohns Hopkins University · US

Funding

BIOCHEMISTRY AND REGULATION OF V(D)J RECOMBINATIONR01AI040227 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI SCHLISSEL, MARK S. · 1996 to 2004
$1.5M
NIAID NIH HHS R01 AI040227
6 · The paper itself

Abstract

Deletion of the TCRbeta transcriptional enhancer (Ebeta) results in nearly complete inhibition of V(D)J recombination at the TCRbeta locus and a block in alpha beta T cell development. This result, along with previous work from many laboratories, has led to the hypothesis that transcriptional enhancers affect V(D)J recombination by regulating the accessibility of the locus to the recombinase. Here we test this hypothesis by performing a detailed analysis of the recombination defect in Ebeta-deleted (Ebeta-/-) mice using assays that detect various reaction intermediates and products. We found double-strand DNA breaks at recombination signal sequences flanking Dbeta and Jbeta gene segments in Ebeta-/- thymuses at about one-third to one-thirtieth the level found in thymuses with an unaltered TCRbeta locus. These sites are also subject to in vitro cleavage by the V(D)J recombinase in both Ebeta-/- and Ebeta+/+ thymocyte nuclei. However, the corresponding Dbeta-to-Jbeta coding joints are further reduced (by 100- to 300-fold) in Ebeta-/- thymuses. Formation of extrachromosomal Dbeta-to-Jbeta signal joints appears to be intermediately affected and nonstandard Dbeta-to-Dbeta joining occurs at the Ebeta-deleted alleles. These data indicate that, unexpectedly, loss of accessibility alone cannot explain the loss of TCRbeta recombination in the absence of the Ebeta element and suggest an additional function for Ebeta in the process of DNA repair at specific TCRbeta sites during the late phase of the recombination reaction.

Indexed as

Enhancer Elements, GeneticRecombination, GeneticAllelesAnimalsBase SequenceDNADNA NucleotidyltransferasesDNA PrimersGene Rearrangement, beta-Chain T-Cell Antigen ReceptorMiceMice, Inbred C57BLMice, KnockoutPolymerase Chain ReactionReceptors, Antigen, T-Cell, alpha-betaT-LymphocytesVDJ RecombinasesDNADNA NucleotidyltransferasesDNA PrimersReceptors, Antigen, T-Cell, alpha-betaVDJ Recombinases

Identifiers

PMID9694796
PMCPMC317053
OpenAlexW2132150197

What OpenQuestion holds

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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.