Evidence map›Paper›PMID 39763795›Full record

ArticlebioRxiv : the preprint server for biology2024

Coordinated repression of totipotency-associated gene loci by histone methyltransferase EHMT2 through binding to LINE-1 regulatory elements.

K Chatterjee, C M Uyehara, K Kasliwal, S Madhuranath, L Scourzic, A Polyzos, E Apostolou, M Stadtfeld

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

K ChatterjeeSanford I. Weill Department of Medicine, Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY 10065, USA.ORCID 0000-0003-1663-8810
C M UyeharaSanford I. Weill Department of Medicine, Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY 10065, USA.ORCID 0000-0002-3210-9428
K KasliwalSanford I. Weill Department of Medicine, Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY 10065, USA.ORCID 0000-0003-0004-1593
S MadhuranathSanford I. Weill Department of Medicine, Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY 10065, USA.
L ScourzicSanford I. Weill Department of Medicine, Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY 10065, USA.ORCID 0000-0003-2875-1642
A PolyzosSanford I. Weill Department of Medicine, Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY 10065, USA.
E ApostolouSanford I. Weill Department of Medicine, Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY 10065, USA.ORCID 0000-0002-8111-0863
M StadtfeldSanford I. Weill Department of Medicine, Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY 10065, USA.ORCID 0000-0002-5852-9906

Funding

Structure, Function, and Dynamics of Macro-molecular Complexes that Execute and Regulate Genome FunctionRM1GM139738 · NIGMS · CORNELL UNIVERSITY · PI Thomas George Wade Graham, Steven Zvi Josefowicz · 2021 to 2026
$14.4M
Multidisciplinary Research Training in Cardiovascular DiseaseT32HL160520 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI Geoffrey S Pitt, Jonathan W. Weinsaft · 2022 to 2026
$2.0M
Organizational principles and functional role of 3D enhancer hubs in cell fate decisionsR01GM138635 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI APOSTOLOU, EFFIE · 2020 to 2023
$1.9M
Dissecting genetic determinants of epigenetic instability in pluripotent stem cellsR01GM145864 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI STADTFELD, MATTHIAS · 2022 to 2025
$1.7M
NHLBI NIH HHS T32 HL160520NIGMS NIH HHS R01 GM138635NIGMS NIH HHS R01 GM145864NIGMS NIH HHS RM1 GM139738
6 · The paper itself

Abstract

Mouse embryonic stem cells (mESCs) and other naïve pluripotent stem cells can reverse typical developmental trajectories and, at low frequency, de-differentiate into 2-cell-like cells (2CLCs) that resemble the mammalian embryo during zygotic genome activation (ZGA). This affords the opportunity to reveal molecular principles that govern the pre-implantation stages of mammalian development. We leveraged a multipurpose allele for acute protein depletion and efficient immunoprecipitation to dissect the molecular functions of the chromatin repressor EHMT2, a candidate antagonist of the mESC-to-2CLC transition. This allowed us to define categories of EHMT2 target genes characterized by distinct modes of EHMT2 chromatin engagement and repression. Most notably, EHMT2 directly represses large clusters of co-regulated gene loci that comprise a significant fraction of the 2CLC-specific transcriptome by initiating H3K9me2 spreading from distal LINE-1 elements. EHMT2 counteracts the recruitment of the activator DPPA2/4 to promoter-proximal endogenous retroviral elements (ERVs) at 2CLC genes. EHMT2 depletion elevates the expression of ZGA-associated transcripts in 2CLCs and synergizes with spliceosome inhibition and retinoic acid signaling in facilitating the mESC-to-2CLC transition. In contrast to ZGA-associated genes, repression of germ layer-associated transcripts by EHMT2 occurs outside of gene clusters in collaboration with ZFP462 and entails binding to non-repeat enhancers. Our observations show that EHMT2 attenuates the bidirectional differentiation potential of mouse pluripotent stem cells and define molecular modes for locus-specific transcriptional repression by this essential histone methyltransferase.

Indexed as

2-cell stageEHMT2gene clustersH3K9 methylationpluripotencyrepressive domainsretrotransposonstotipotency

Identifiers

PMID39763795
PMCPMC11702699

What OpenQuestion holds

Textmetadata
LicenceCC BY-ND
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.