Evidence map›Paper›PMID 30604745›Full record

ArticleNature communications2019

The non-canonical SMC protein SmcHD1 antagonises TAD formation and compartmentalisation on the inactive X chromosome.

Michal R Gdula, Tatyana B Nesterova, Greta Pintacuda, Jonathan Godwin, Ye Zhan, Hakan Ozadam, Michael McClellan, Daniella Moralli, Felix Krueger, Catherine M Green and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
13.0field-weighted citation impact, top 1% 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

72 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

12 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

15 authors at 6 institutions in 3 countries.

Michal R GdulaDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK.ORCID http://orcid.org/0000-0002-8667-7359
Tatyana B NesterovaDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK.ORCID http://orcid.org/0000-0001-7740-4386
Greta PintacudaDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK.ORCID http://orcid.org/0000-0001-5126-2279
Jonathan GodwinDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK.
Ye ZhanProgram in Systems Biology, Department of Medicine, Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Howard Hughes Medical Institute, Worcester, MA, 01605, USA.ORCID http://orcid.org/0000-0001-9280-1718
Hakan OzadamProgram in Systems Biology, Department of Medicine, Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Howard Hughes Medical Institute, Worcester, MA, 01605, USA.
Michael McClellanLudwig Cancer Research, Nuffield Department of Medicine, University of Oxford, Oxford, OX3 7DQ, UK.
Daniella MoralliThe Wellcome Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.ORCID http://orcid.org/0000-0001-7977-8496
Felix KruegerBioinformatics Group, The Babraham Institute, Cambridge, CB22 AT, UK.ORCID http://orcid.org/0000-0002-5513-3324
Catherine M GreenThe Wellcome Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Wolf ReikEpigenetics Program, The Babraham Institute, Cambridge, CB22 AT, UK.
Skirmantas KriaucionisLudwig Cancer Research, Nuffield Department of Medicine, University of Oxford, Oxford, OX3 7DQ, UK.
Edith HeardInstitut Curie, PSL Research University, CNRS UMR3215, INSERM U934, UPMC Paris-Sorbonne, 26 Rue d'Ulm, 75005, Paris, France.ORCID http://orcid.org/0000-0001-8052-7117
Job DekkerProgram in Systems Biology, Department of Medicine, Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Howard Hughes Medical Institute, Worcester, MA, 01605, USA.ORCID http://orcid.org/0000-0001-5631-0698
Neil BrockdorffDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK. neil.brockdorff@bioch.ox.ac.uk.
University of Oxford · GBHoward Hughes Medical Institute · USBabraham Institute · GBCentre for Human Genetics · GBOpen Data Institute · GBCentre National de la Recherche Scientifique · FR

Funding

Structural Annotation of the Human GenomeR01HG003143 · NHGRI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Job Dekker · 2003 to 2026
$15.4M
Biotechnology and Biological Sciences Research Council BB/M001873/1European Research Council 340081NHGRI NIH HHS R01 HG003143Wellcome Trust
6 · The paper itself

Abstract

The inactive X chromosome (Xi) in female mammals adopts an atypical higher-order chromatin structure, manifested as a global loss of local topologically associated domains (TADs), A/B compartments and formation of two mega-domains. Here we demonstrate that the non-canonical SMC family protein, SmcHD1, which is important for gene silencing on Xi, contributes to this unique chromosome architecture. Specifically, allelic mapping of the transcriptome and epigenome in SmcHD1 mutant cells reveals the appearance of sub-megabase domains defined by gene activation, CpG hypermethylation and depletion of Polycomb-mediated H3K27me3. These domains, which correlate with sites of SmcHD1 enrichment on Xi in wild-type cells, additionally adopt features of active X chromosome higher-order chromosome architecture, including A/B compartments and partial restoration of TAD boundaries. Xi chromosome architecture changes also occurred following SmcHD1 knockout in a somatic cell model, but in this case, independent of Xi gene derepression. We conclude that SmcHD1 is a key factor in defining the unique chromosome architecture of Xi.

Indexed as

X Chromosome InactivationAllelesAnimalsCell LineChromosomal Proteins, Non-HistoneCpG IslandsCRISPR-Cas SystemsDNA MethylationExonsFemaleFibroblastsGene Knockout TechniquesHistonesMaleMicePoint MutationChromosomal Proteins, Non-HistoneHistonesPolycomb-Group ProteinsSmcHD1 protein, mouse

Identifiers

PMID30604745
PMCPMC6318279
OpenAlexW2908027894

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.