Evidence map›Paper›PMID 35502750›Full record

ArticleDevelopment (Cambridge, England)2022

Inversion of a topological domain leads to restricted changes in its gene expression and affects interdomain communication.

Rafael Galupa, Christel Picard, Nicolas Servant, Elphège P Nora, Yinxiu Zhan, Joke G van Bemmel, Fatima El Marjou, Colin Johanneau, Maud Borensztein, Katia Ancelin and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Two bHLH Transcription Factor GenesPlants (Basel, Switzerland) · 2026
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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

12 authors at 5 institutions in 2 countries.

Rafael GalupaMammalian Developmental Epigenetics Group, Genetics and Developmental Biology Unit, Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934, Paris 75005, France.ORCID 0000-0001-7319-043X
Christel PicardMammalian Developmental Epigenetics Group, Genetics and Developmental Biology Unit, Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934, Paris 75005, France.
Nicolas ServantBioinformatics, Biostatistics, Epidemiology and Computational Systems Unit, Institut Curie, PSL Research University, INSERM U900, Paris 75005, France.
Elphège P NoraMammalian Developmental Epigenetics Group, Genetics and Developmental Biology Unit, Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934, Paris 75005, France.
Yinxiu ZhanFriedrich Miescher Institute for Biomedical Research, Basel 4058, Switzerland.
Joke G van BemmelMammalian Developmental Epigenetics Group, Genetics and Developmental Biology Unit, Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934, Paris 75005, France.ORCID 0000-0001-7034-3664
Fatima El MarjouTransgenesis Facility, Institut Curie, Paris 75005, France.
Colin JohanneauTransgenesis Facility, Institut Curie, Paris 75005, France.
Maud BorenszteinMammalian Developmental Epigenetics Group, Genetics and Developmental Biology Unit, Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934, Paris 75005, France.ORCID 0000-0002-4378-5018
Katia AncelinMammalian Developmental Epigenetics Group, Genetics and Developmental Biology Unit, Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934, Paris 75005, France.ORCID 0000-0002-2117-9754
Luca GiorgettiFriedrich Miescher Institute for Biomedical Research, Basel 4058, Switzerland.
Edith HeardMammalian Developmental Epigenetics Group, Genetics and Developmental Biology Unit, Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934, Paris 75005, France.ORCID 0000-0001-8052-7117
Centre National de la Recherche Scientifique · FRTransgene (France) · FRFriedrich Miescher Institute · CHInserm · FRUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interplay between the topological organization of the genome and the regulation of gene expression remains unclear. Depletion of molecular factors (e.g. CTCF) underlying topologically associating domains (TADs) leads to modest alterations in gene expression, whereas genomic rearrangements involving TAD boundaries disrupt normal gene expression and can lead to pathological phenotypes. Here, we targeted the TAD neighboring that of the noncoding transcript Xist, which controls X-chromosome inactivation. Inverting 245 kb within the TAD led to expected rearrangement of CTCF-based contacts but revealed heterogeneity in the 'contact' potential of different CTCF sites. Expression of most genes therein remained unaffected in mouse embryonic stem cells and during differentiation. Interestingly, expression of Xist was ectopically upregulated. The same inversion in mouse embryos led to biased Xist expression. Smaller inversions and deletions of CTCF clusters led to similar results: rearrangement of contacts and limited changes in local gene expression, but significant changes in Xist expression in embryos. Our study suggests that the wiring of regulatory interactions within a TAD can influence the expression of genes in neighboring TADs, highlighting the existence of mechanisms of inter-TAD communication.

Indexed as

RNA, Long NoncodingX Chromosome InactivationAnimalsCCCTC-Binding FactorChromatinCommunicationGene ExpressionGenomeMiceCCCTC-Binding FactorChromatinRNA, Long NoncodingGene expressionGenomic engineeringTADsX-inactivationXist

Identifiers

PMID35502750
PMCPMC9148567
OpenAlexW4225386909

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.