Evidence map›Paper›PMID 10082543›Full record

ArticleMolecular and cellular biology1999

Regulation of V(D)J recombination by transcriptional promoters.

M L Sikes, C C Suarez, E M Oltz

Abstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
  2. The center of accessibility: Dβ control of V(D)J recombination.Archivum immunologiae et therapiae experimentalis · 2010
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Elucidation of IgH intronic enhancer functions via germ-line deletion.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  12. Article
  13. Article
  14. 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
  15. Article
  16. 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
  17. Article
  18. Article
  19. V(D)J recombination becomes accessible.The Journal of experimental medicine · 2001
    Article
  20. Review
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

3 authors.

M L SikesDepartment of Microbiology and Immunology, Vanderbilt University, Nashville, Tennessee 37232, USA.
C C Suarez
E M Oltz

Funding

MOLECULAR CONTROL OF ANTIGEN RECEPTOR GENE ASSEMBLYR01AI036944 · NIAID · VANDERBILT UNIVERSITY · PI OLTZ, EUGENE M. · 1995 to 2002
$807k
MOLECULAR CONTROL OF ANTIGEN RECEPTOR GENE ASSEMBLYR21AI036944 · NIAID · VANDERBILT UNIVERSITY · PI OLTZ, EUGENE M. · 2000 to 2000
$172k
MOLECULAR DETERMINANTS OF RECOMBINATIONAL ACCESSIBILITYF32GM019597 · NIGMS · VANDERBILT UNIVERSITY · PI SIKES, MICHAEL LYNN · 1998 to 1998
–
NIAID NIH HHS AI01412NIAID NIH HHS AI36944NIGMS NIH HHS F32 GM019597NIGMS NIH HHS GM19597
6 · The paper itself

Abstract

Enhancer elements potentiate the rearrangement of antigen receptor loci via changes in the accessibility of gene segment clusters to V(D)J recombinase. Here, we show that enhancer activity per se is insufficient to target T-cell receptor beta miniloci for DbetaJbeta recombination. Instead, a promoter situated 5' to Dbeta1 (PDbeta) was required for efficient rearrangement of chromosomal substrates. A critical function for promoters in regulating gene segment accessibility was further supported by the ability of heterologous promoters to direct rearrangement of enhancer-containing substrates. Importantly, activation of a synthetic tetracycline-inducible promoter (Ptet) positioned upstream from the Dbeta gene segment was sufficient to target recombination of miniloci lacking a distal enhancer element. The latter result suggests that DNA loops, generated by interactions between flanking promoter and enhancer elements, are not required for efficient recognition of chromosomal gene segments by V(D)J recombinase. Unexpectedly, the Ptet substrate exhibited normal levels of rearrangement despite its retention of a hypermethylated DNA status within the DbetaJbeta cluster. Together, our findings support a model in which promoter activation, rather than intrinsic properties of enhancers, is the primary determinant for regulating recombinational accessibility within antigen receptor loci.

Indexed as

Gene Rearrangement, beta-Chain T-Cell Antigen ReceptorRecombination, GeneticRegulatory Sequences, Nucleic AcidDNA MethylationDNA NucleotidyltransferasesEnhancer Elements, GeneticGerm CellsPromoter Regions, GeneticReceptors, Antigen, T-Cell, alpha-betaTranscription, GeneticVDJ RecombinasesDNA NucleotidyltransferasesReceptors, Antigen, T-Cell, alpha-betaVDJ Recombinases

Identifiers

PMID10082543
PMCPMC84070

What OpenQuestion holds

Texttitle and abstract
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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.