Evidence map›Paper›PMID 26158850›Full record

ArticlePLoS genetics2015

Blimp1/Prdm1 Functions in Opposition to Irf1 to Maintain Neonatal Tolerance during Postnatal Intestinal Maturation.

Arne W Mould, Marc A J Morgan, Andrew C Nelson, Elizabeth K Bikoff, Elizabeth J Robertson

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. An autoimmune transcriptional circuit drives FOXP3Science translational medicine · 2024
    Article
  5. Article
  6. Article
  7. Blimp-1 and c-Maf regulateWellcome open research · 2023
    Article
  8. Review
  9. Observational
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

5 authors at 1 institution in 1 country.

Arne W MouldSir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
Marc A J MorganSir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
Andrew C NelsonSir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
Elizabeth K BikoffSir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
Elizabeth J RobertsonSir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
University of Oxford · GB

Funding

Medical Research Council G0700089Medical Research Council G0900747Medical Research Council MC_PC_15004Wellcome Trust 102811
6 · The paper itself

Abstract

The neonatal intestine is a very complex and dynamic organ that must rapidly adapt and remodel in response to a barrage of environmental stimuli during the first few postnatal weeks. Recent studies demonstrate that the zinc finger transcriptional repressor Blimp1/Prdm1 plays an essential role governing postnatal reprogramming of intestinal enterocytes during this period. Functional loss results in global changes in gene expression patterns, particularly in genes associated with metabolic function. Here we engineered a knock-in allele expressing an eGFP-tagged fusion protein under control of the endogenous regulatory elements and performed genome wide ChIP-seq analysis to identify direct Blimp1 targets and further elucidate the function of Blimp1 in intestinal development. Comparison with published human and mouse datasets revealed a highly conserved core set of genes including interferon-inducible promoters. Here we show that the interferon-inducible transcriptional activator Irf1 is constitutively expressed throughout fetal and postnatal intestinal epithelium development. ChIP-seq demonstrates closely overlapping Blimp1 and Irf1 peaks at key components of the MHC class I pathway in fetal enterocytes. The onset of MHC class I expression coincides with down-regulated Blimp1 expression during the suckling to weaning transition. Collectively, these experiments strongly suggest that in addition to regulating the enterocyte metabolic switch, Blimp1 functions as a gatekeeper in opposition to Irf1 to prevent premature activation of the MHC class I pathway in villus epithelium to maintain tolerance in the neonatal intestine.

Indexed as

AnimalsCell DifferentiationCell Line, TumorEnterocytesFemaleGene Expression Regulation, DevelopmentalGene Knock-In TechniquesGreen Fluorescent ProteinsHistocompatibility Antigens Class IHumansInterferon Regulatory Factor-1Intestinal MucosaMicePlacentaPositive Regulatory Domain I-Binding Factor 1Pregnancyenhanced green fluorescent proteinGreen Fluorescent ProteinsHistocompatibility Antigens Class IInterferon Regulatory Factor-1Irf1 protein, mousePositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseTranscription Factors

Identifiers

PMID26158850
PMCPMC4497732
OpenAlexW773545097

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.