Evidence map›Paper›PMID 34875212›Full record

ArticleMolecular cell2022

SUMOylation of linker histone H1 drives chromatin condensation and restriction of embryonic cell fate identity.

Daoud Sheban, Tom Shani, Roey Maor, Alejandro Aguilera-Castrejon, Nofar Mor, Bernardo Oldak, Merav D Shmueli, Avital Eisenberg-Lerner, Jonathan Bayerl, Jakob Hebert and 17 more

Open access · greenAbstract read
In one paragraph

Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

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  16. Protein sumoylation in normal and cancer stem cells.Frontiers in molecular biosciences · 2022
    Review
  17. The regulation of totipotency transcription: Perspective fromFrontiers in cell and developmental biology · 2022
    Review
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

27 authors at 2 institutions in 2 countries.

Daoud ShebanDepartment of Immunology, Weizmann Institute of Science, Rehovot 7610001, Israel; Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Tom ShaniDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Roey MaorDepartment of Immunology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Alejandro Aguilera-CastrejonDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Nofar MorDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Bernardo OldakDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Merav D ShmueliDepartment of Immunology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Avital Eisenberg-LernerDepartment of Immunology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Jonathan BayerlDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Jakob HebertChemical Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Tri-Institutional PhD Program in Chemical Biology, New York, NY, USA.
Sergey ViukovDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Guoyun ChenDepartment of Immunology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Assaf KacenDepartment of Immunology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Vladislav KrupalnikDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Valeriya ChugaevaDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Shadi TaraziDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Alejandra Rodríguez-delaRosaDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Mirie ZerbibDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Adi UlmanDepartment of Immunology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Solaiman MasarwiDepartment of Immunology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Meital KupervaserDe Botton Institute for Protein Profiling, INCPM, Weizmann Institute of Science, Rehovot 7610001, Israel.
Yishai LevinDe Botton Institute for Protein Profiling, INCPM, Weizmann Institute of Science, Rehovot 7610001, Israel.
Efrat ShemaDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 7610001, Israel.
Yael DavidChemical Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Tri-Institutional PhD Program in Chemical Biology, New York, NY, USA.
Noa NovershternDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.
Jacob H HannaDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel. Electronic address: jacob.hanna@weizmann.ac.il.
Yifat MerblDepartment of Immunology, Weizmann Institute of Science, Rehovot 7610001, Israel. Electronic address: yifat.merbl@weizmann.ac.il.
Weizmann Institute of Science · ILMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Investigating histone glycation as a new dynamic epigenetic markR35GM138386 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI DAVID-SHTERNBERG, YAEL E · 2020 to 2024
$2.2M
NCI NIH HHS P30 CA008748NIGMS NIH HHS R35 GM138386
6 · The paper itself

Abstract

The fidelity of the early embryonic program is underlined by tight regulation of the chromatin. Yet, how the chromatin is organized to prohibit the reversal of the developmental program remains unclear. Specifically, the totipotency-to-pluripotency transition marks one of the most dramatic events to the chromatin, and yet, the nature of histone alterations underlying this process is incompletely characterized. Here, we show that linker histone H1 is post-translationally modulated by SUMO2/3, which facilitates its fixation onto ultra-condensed heterochromatin in embryonic stem cells (ESCs). Upon SUMOylation depletion, the chromatin becomes de-compacted and H1 is evicted, leading to totipotency reactivation. Furthermore, we show that H1 and SUMO2/3 jointly mediate the repression of totipotent elements. Lastly, we demonstrate that preventing SUMOylation on H1 abrogates its ability to repress the totipotency program in ESCs. Collectively, our findings unravel a critical role for SUMOylation of H1 in facilitating chromatin repression and desolation of the totipotent identity.

Indexed as

Cell LineageChromatin Assembly and DisassemblyAnimalsBlastocystChromatinEmbryo Culture TechniquesEmbryonic DevelopmentGene Expression Regulation, DevelopmentalHEK293 CellsHistonesHumansMiceMouse Embryonic Stem CellsPhenotypeSmall Ubiquitin-Related Modifier ProteinsSumoylationChromatinHistonesSmall Ubiquitin-Related Modifier ProteinsSUMO2 protein, mouseSumo3 protein, mouseUbiquitins

Identifiers

PMID34875212
PMCPMC11822872
OpenAlexW4200139583

What OpenQuestion holds

Textmetadata
LicenceTDM
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.