CTCF is a barrier for 2C-like reprogramming.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
11 08 2021
Historique:
received: 05 01 2021
accepted: 17 07 2021
entrez: 12 8 2021
pubmed: 13 8 2021
medline: 24 8 2021
Statut: epublish

Résumé

Totipotent cells have the ability to generate embryonic and extra-embryonic tissues. Interestingly, a rare population of cells with totipotent-like potential, known as 2 cell (2C)-like cells, has been identified within ESC cultures. They arise from ESC and display similar features to those found in the 2C embryo. However, the molecular determinants of 2C-like conversion have not been completely elucidated. Here, we show that the CCCTC-binding factor (CTCF) is a barrier for 2C-like reprogramming. Indeed, forced conversion to a 2C-like state by the transcription factor DUX is associated with DNA damage at a subset of CTCF binding sites. Depletion of CTCF in ESC efficiently promotes spontaneous and asynchronous conversion to a 2C-like state and is reversible upon restoration of CTCF levels. This phenotypic reprogramming is specific to pluripotent cells as neural progenitor cells do not show 2C-like conversion upon CTCF-depletion. Furthermore, we show that transcriptional activation of the ZSCAN4 cluster is necessary for successful 2C-like reprogramming. In summary, we reveal an unexpected relationship between CTCF and 2C-like reprogramming.

Identifiants

pubmed: 34381034
doi: 10.1038/s41467-021-25072-x
pii: 10.1038/s41467-021-25072-x
pmc: PMC8358036
doi:

Substances chimiques

CCCTC-Binding Factor 0
Ctcf protein, mouse 0
Homeodomain Proteins 0
Transcription Factors 0
Zscan4c protein, mouse 0

Types de publication

Journal Article Research Support, N.I.H., Intramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4856

Subventions

Organisme : NIGMS NIH HHS
ID : R35 GM142792
Pays : United States

Informations de copyright

© 2021. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.

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Auteurs

Teresa Olbrich (T)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA.

Maria Vega-Sendino (M)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA.

Desiree Tillo (D)

Genetics Branch, CCR, NCI, NIH, Bethesda, MD, USA.

Wei Wu (W)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA.

Nicholas Zolnerowich (N)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA.

Raphael Pavani (R)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA.

Andy D Tran (AD)

Laboratory of Cancer Biology and Genetics, CCR, NCI, NIH, Bethesda, MD, USA.

Catherine N Domingo (CN)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA.

Mariajose Franco (M)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA.

Marta Markiewicz-Potoczny (M)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA.

Gianluca Pegoraro (G)

Laboratory of Receptor Biology and Gene Expression, CCR, NCI, NIH, Bethesda, MD, USA.

Peter C FitzGerald (PC)

Genome Analysis Unit, CCR, NCI, NIH, Bethesda, MD, USA.

Michael J Kruhlak (MJ)

Laboratory of Cancer Biology and Genetics, CCR, NCI, NIH, Bethesda, MD, USA.

Eros Lazzerini-Denchi (E)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA.

Elphege P Nora (EP)

Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA.
Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, CA, USA.

André Nussenzweig (A)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA.

Sergio Ruiz (S)

Laboratory of Genome Integrity, CCR, NCI, NIH, Bethesda, MD, USA. sergio.ruizmacias@nih.gov.

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Classifications MeSH