Evidence map›Paper›PMID 34330317›Full record

ArticleEpigenetics & chromatin2021

Histone H2A.X phosphorylation and Caspase-Initiated Chromatin Condensation in late-stage erythropoiesis.

Nazish N Jeffery, Christina Davidson, Scott A Peslak, Paul D Kingsley, Yukio Nakamura, James Palis, Michael Bulger

Open access · goldAbstract read
In one paragraph

Article in Epigenetics & chromatin, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. MOF promotes cisplatin resistance in lung cancer cells by enhancing WSTF acetylation.In vitro cellular & developmental biology. Animal · 2025
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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 4 institutions in 2 countries.

Nazish N JefferyCenter for Pediatric Biomedical Research, Department of Pediatrics, University of Rochester, Rochester, NY, USA.
Christina DavidsonWilmot Cancer Institute, Department of Biomedical Genetics, University of Rochester, Rochester, NY, USA.
Scott A PeslakDepartment of Medicine, Division of Hematology/Oncology, Hospital of the University of Pennsylvania, Philadelphia, PA, USA.
Paul D KingsleyCenter for Pediatric Biomedical Research, Department of Pediatrics, University of Rochester, Rochester, NY, USA.
Yukio NakamuraCell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan.
James PalisCenter for Pediatric Biomedical Research, Department of Pediatrics, University of Rochester, Rochester, NY, USA.
Michael BulgerCenter for Pediatric Biomedical Research, Department of Pediatrics, University of Rochester, Rochester, NY, USA. Michael_Bulger@urmc.rochester.edu.ORCID 0000-0002-2010-9420
University of Rochester · USChildren's Hospital of Philadelphia · USRIKEN BioResource Research Center · JPUniversity of Rochester Medical Center · US

Funding

Histone H2A.X signaling and chromatin remodeling in late erythropoiesisR01HL158848 · NHLBI · UNIVERSITY OF ROCHESTER · PI BULGER, MICHAEL D · 2021 to 2023
$902k
NHLBI NIH HHS R01 HL158848
6 · The paper itself

Abstract

backgroundCondensation of chromatin prior to enucleation is an essential component of terminal erythroid maturation, and defects in this process are associated with inefficient erythropoiesis and anemia. However, the mechanisms involved in this phenomenon are not well understood. Here, we describe a potential role for the histone variant H2A.X in erythropoiesis.

resultsWe find in multiple model systems that this histone is essential for normal maturation, and that the loss of H2A.X in erythroid cells results in dysregulation in expression of erythroid-specific genes as well as a nuclear condensation defect. In addition, we demonstrate that erythroid maturation is characterized by phosphorylation at both S139 and Y142 on the C-terminal tail of H2A.X during late-stage erythropoiesis. Knockout of the kinase BAZ1B/WSTF results in loss of Y142 phosphorylation and a defect in nuclear condensation, but does not replicate extensive transcriptional changes to erythroid-specific genes observed in the absence of H2A.X.

conclusionsWe relate these findings to Caspase-Initiated Chromatin Condensation (CICC) in terminal erythroid maturation, where aspects of the apoptotic pathway are invoked while apoptosis is specifically suppressed.

Indexed as

ChromatinErythropoiesisCaspasesHistonesPhosphorylationCaspasesChromatinHistonesApoptosisBAZ1BCaspaseChromatin condensationErythropoiesisg-H2A.XH2A.XPhosphorylationTerminal erythroid maturationWSTF

Identifiers

PMID34330317
PMCPMC8325214
OpenAlexW3183327225

What OpenQuestion holds

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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.