Evidence map›Paper›PMID 29887375›Full record

ArticleCell2018

SMCHD1 Merges Chromosome Compartments and Assists Formation of Super-Structures on the Inactive X.

Chen-Yu Wang, Teddy Jégu, Hsueh-Ping Chu, Hyun Jung Oh, Jeannie T Lee

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing 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

114 citing papers in PubMed.

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  17. eLife · 2025
    Article
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54 more citing papers are in PubMed but not listed here.

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.

Chen-Yu WangHoward Hughes Medical Institute, Massachusetts General Hospital, Boston, MA, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA.
Teddy JéguHoward Hughes Medical Institute, Massachusetts General Hospital, Boston, MA, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA.
Hsueh-Ping ChuHoward Hughes Medical Institute, Massachusetts General Hospital, Boston, MA, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA.
Hyun Jung OhHoward Hughes Medical Institute, Massachusetts General Hospital, Boston, MA, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA.
Jeannie T LeeHoward Hughes Medical Institute, Massachusetts General Hospital, Boston, MA, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA. Electronic address: lee@molbio.mgh.harvard.edu.

Funding

Regulation of X-chromosome Inactivation and Imprinting by Non-coding ElementsR37GM058839 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI LEE, JEANNIE T · 2012 to 2021
$4.1M
Polycomb complexes targeted to specific loci by non-coding RNA co-factorsR01GM090278 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI LEE, JEANNIE T · 2010 to 2017
$3.7M
Howard Hughes Medical InstituteNIGMS NIH HHS R01 GM090278NIGMS NIH HHS R37 GM058839
6 · The paper itself

Abstract

Mammalian chromosomes are partitioned into A/B compartments and topologically associated domains (TADs). The inactive X (Xi) chromosome, however, adopts a distinct conformation without evident compartments or TADs. Here, through exploration of an architectural protein, structural-maintenance-of-chromosomes hinge domain containing 1 (SMCHD1), we probe how the Xi is reconfigured during X chromosome inactivation. A/B compartments are first fused into "S1" and "S2" compartments, coinciding with Xist spreading into gene-rich domains. SMCHD1 then binds S1/S2 compartments and merges them to create a compartment-less architecture. Contrary to current views, TADs remain on the Xi but in an attenuated state. Ablating SMCHD1 results in a persistent S1/S2 organization and strengthening of TADs. Furthermore, loss of SMCHD1 causes regional defects in Xist spreading and erosion of heterochromatic silencing. We present a stepwise model for Xi folding, where SMCHD1 attenuates a hidden layer of Xi architecture to facilitate Xist spreading.

Indexed as

X Chromosome InactivationAllelesAnimalsCell LineChromosomal Proteins, Non-HistoneChromosomes, MammalianDNA MethylationFemaleHeterochromatinHistonesMaleMiceMouse Embryonic Stem CellsPrincipal Component AnalysisRNA, Long NoncodingChromosomal Proteins, Non-HistoneHeterochromatinHistonesRNA, Long NoncodingSmcHD1 protein, mouseXIST non-coding RNAchromosome conformationcompartmentslong noncoding RNAsnuclear organizationPolycomb complexesSMCHD1TADstopologically associating domainsX chromosome inactivationXist RNA

Identifiers

PMID29887375
PMCPMC6475921

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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.