Evidence map›Paper›PMID 31950239›Full record

ArticleChromosoma2020

Heterochromatin formation in Drosophila requires genome-wide histone deacetylation in cleavage chromatin before mid-blastula transition in early embryogenesis.

Matthias Walther, Sandy Schrahn, Veiko Krauss, Sandro Lein, Jeannette Kessler, Thomas Jenuwein, Gunter Reuter

Open access · hybridAbstract read
In one paragraph

Article in Chromosoma, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Heterochromatin-based silencing of a foreign tandem repeat inbioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Adaptation ofInternational journal of molecular sciences · 2022
    Article
  6. Article
  7. 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

7 authors at 3 institutions in 1 country.

Matthias WaltherDevelopmental Genetics, Institute of Biology, Martin Luther University Halle, Weinbergweg 10, 06120, Halle/S., Germany.
Sandy SchrahnDevelopmental Genetics, Institute of Biology, Martin Luther University Halle, Weinbergweg 10, 06120, Halle/S., Germany.
Veiko KraussCluster of Excellence in Plant Science (CEPLAS), University of Cologne, Biocenter, 50674, Cologne, Germany.
Sandro LeinDevelopmental Genetics, Institute of Biology, Martin Luther University Halle, Weinbergweg 10, 06120, Halle/S., Germany.
Jeannette KesslerDevelopmental Genetics, Institute of Biology, Martin Luther University Halle, Weinbergweg 10, 06120, Halle/S., Germany.
Thomas JenuweinMax Planck Institute of Immunobiology and Epigenetics, Stübeweg 51, 79108, Freiburg, Germany.
Gunter ReuterDevelopmental Genetics, Institute of Biology, Martin Luther University Halle, Weinbergweg 10, 06120, Halle/S., Germany. reuter@genetik.uni-halle.de.
Martin Luther University Halle-Wittenberg · DEMax Planck Institute of Immunobiology and Epigenetics · DEUniversity of Cologne · DE

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
NIH HHS P40 OD018537
6 · The paper itself

Abstract

Su(var) mutations define epigenetic factors controlling heterochromatin formation and gene silencing in Drosophila. Here, we identify SU(VAR)2-1 as a novel chromatin regulator that directs global histone deacetylation during the transition of cleavage chromatin into somatic blastoderm chromatin in early embryogenesis. SU(VAR)2-1 is heterochromatin-associated in blastoderm nuclei but not in later stages of development. In larval polytene chromosomes, SU(VAR)2-1 is a band-specific protein. SU(VAR)2-1 directs global histone deacetylation by recruiting the histone deacetylase RPD3. In Su(var)2-1 mutants H3K9, H3K27, H4K8 and H4K16 acetylation shows elevated levels genome-wide and heterochromatin displays aberrant histone hyper-acetylation. Whereas H3K9me2- and HP1a-binding appears unaltered, the heterochromatin-specific H3K9me2S10ph composite mark is impaired in heterochromatic chromocenters of larval salivary polytene chromosomes. SU(VAR)2-1 contains an NRF1/EWG domain and a C2HC zinc-finger motif. Our study identifies SU(VAR)2-1 as a dosage-dependent, heterochromatin-initiating SU(VAR) factor, where the SU(VAR)2-1-mediated control of genome-wide histone deacetylation after cleavage and before mid-blastula transition (pre-MBT) is required to enable heterochromatin formation.

Indexed as

AnimalsBlastulaCentrosomeChromatin Assembly and DisassemblyCloning, MolecularCRISPR-Cas SystemsDrosophilaDrosophila ProteinsEmbryonic DevelopmentFemaleGene Expression Regulation, DevelopmentalGenome-Wide Association StudyHeterochromatinHistonesImmunohistochemistryIn Situ Hybridization, FluorescenceDrosophila ProteinsHeterochromatinHistonesDrosophila melanogasterHeterochromatinHistone deacetylationMid-blastula transition

Identifiers

PMID31950239
PMCPMC7021753
OpenAlexW3000097924

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.