Evidence map›Paper›PMID 24469810›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

C-terminal region of activation-induced cytidine deaminase (AID) is required for efficient class switch recombination and gene conversion.

Somayeh Sabouri, Maki Kobayashi, Nasim A Begum, Jianliang Xu, Kouji Hirota, Tasuku Honjo

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Functional requirements of AID's higher order structures and their interaction with RNA-binding proteins.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  7. Article
  8. Identification of DNA cleavage- and recombination-specific hnRNP cofactors for activation-induced cytidine deaminase.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  9. Article
  10. Article
  11. IgH chain class switch recombination: mechanism and regulation.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Review
  12. Article
  13. Activation induced deaminase C-terminal domain links DNA breaks to end protection and repair during class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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.

Somayeh SabouriDepartments of Immunology and Genomic Medicine and Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshida Sakyo-ku, Kyoto 606-8501, Japan.
Maki Kobayashi
Nasim A Begum
Jianliang Xu
Kouji Hirota
Tasuku Honjo
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation-induced cytidine deaminase (AID) introduces single-strand breaks (SSBs) to initiate class switch recombination (CSR), gene conversion (GC), and somatic hypermutation (SHM). CSR is mediated by double-strand breaks (DSBs) at donor and acceptor switch (S) regions, followed by pairing of DSB ends in two S regions and their joining. Because AID mutations at its C-terminal region drastically impair CSR but retain its DNA cleavage and SHM activity, the C-terminal region of AID likely is required for the recombination step after the DNA cleavage. To test this hypothesis, we analyzed the recombination junctions generated by AID C-terminal mutants and found that 0- to 3-bp microhomology junctions are relatively less abundant, possibly reflecting the defects of the classical nonhomologous end joining (C-NHEJ). Consistently, the accumulation of C-NHEJ factors such as Ku80 and XRCC4 was decreased at the cleaved S region. In contrast, an SSB-binding protein, poly (ADP)-ribose polymerase1, was recruited more abundantly, suggesting a defect in conversion from SSB to DSB. In addition, recruitment of critical DNA synapse factors such as 53BP1, DNA PKcs, and UNG at the S region was reduced during CSR. Furthermore, the chromosome conformation capture assay revealed that DNA synapse formation is impaired drastically in the AID C-terminal mutants. Interestingly, these mutants showed relative reduction in GC compared with SHM in chicken DT40 cells. Collectively, our data indicate that the C-terminal region of AID is required for efficient generation of DSB in CSR and GC and thus for the subsequent pairing of cleaved DNA ends during recombination in CSR.

Indexed as

Gene ConversionRecombination, GeneticAICDA (Activation-Induced Cytidine Deaminase)AnimalsCells, CulturedChromatin ImmunoprecipitationCytidine DeaminaseDNA End-Joining RepairFlow CytometryImmunoglobulin Switch RegionMiceMice, Inbred C57BLMice, KnockoutAICDA (Activation-Induced Cytidine Deaminase)Cytidine DeaminaseCSR synapseDNA repair

Identifiers

PMID24469810
PMCPMC3926049
OpenAlexW1969106618

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.