Evidence map›Paper›PMID 37266576›Full record

ArticleeLife2023

Polycomb repressive complex 1.1 coordinates homeostatic and emergency myelopoiesis.

Yaeko Nakajima-Takagi, Motohiko Oshima, Junichiro Takano, Shuhei Koide, Naoki Itokawa, Shun Uemura, Masayuki Yamashita, Shohei Andoh, Kazumasa Aoyama, Yusuke Isshiki and 8 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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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

18 authors at 5 institutions in 3 countries.

Yaeko Nakajima-TakagiDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID 0000-0002-2341-2409
Motohiko OshimaDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Junichiro TakanoLaboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Shuhei KoideDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Naoki ItokawaDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Shun UemuraDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID 0000-0002-1520-6808
Masayuki YamashitaDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID 0000-0001-9459-4329
Shohei AndohDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Kazumasa AoyamaDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Yusuke IsshikiDepartment of Cellular and Molecular Medicine, Chiba University, Chiba, Japan.
Daisuke ShinodaDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Atsunori SarayaDepartment of Cellular and Molecular Medicine, Chiba University, Chiba, Japan.
Fumio AraiDepartment of Stem Cell Biology and Medicine, Kyushu University, Fukuoka, Japan.
Kiyoshi YamaguchiDivision of Clinical Genome Research,Advanced Clinical Research Center, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Yoichi FurukawaDivision of Clinical Genome Research,Advanced Clinical Research Center, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID 0000-0003-0462-8631
Haruhiko KosekiLaboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.ORCID 0000-0001-8424-5854
Tomokatsu IkawaDivision of Immunobiology, Research Institute for Biomedical Sciences, Tokyo University of Science, Chiba, Japan.
Atsushi IwamaDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID 0000-0001-9410-8992
Institute for Stem Cell Biology and Regenerative Medicine · INTokyo University of Science · JPChiba University · JPRIKEN Center for Integrative Medical Sciences · JPKyushu University · JP

Funding

Japan Agency for Medical Research and Development 21zf0127003h0001Japan Agency for Medical Research and Development JP223fa627001Japan Society for the Promotion of Science 19H05653Japan Society for the Promotion of Science 19H05746Japan Society for the Promotion of Science 20K08728
6 · The paper itself

Abstract

Polycomb repressive complex (PRC) 1 regulates stem cell fate by mediating mono-ubiquitination of histone H2A at lysine 119. While canonical PRC1 is critical for hematopoietic stem and progenitor cell (HSPC) maintenance, the role of non-canonical PRC1 in hematopoiesis remains elusive. PRC1.1, a non-canonical PRC1, consists of PCGF1, RING1B, KDM2B, and BCOR. We recently showed that PRC1.1 insufficiency induced by the loss of PCGF1 or BCOR causes myeloid-biased hematopoiesis and promotes transformation of hematopoietic cells in mice. Here we show that PRC1.1 serves as an epigenetic switch that coordinates homeostatic and emergency hematopoiesis. PRC1.1 maintains balanced output of steady-state hematopoiesis by restricting C/EBPα-dependent precocious myeloid differentiation of HSPCs and the HOXA9- and β-catenin-driven self-renewing network in myeloid progenitors. Upon regeneration, PRC1.1 is transiently inhibited to facilitate formation of granulocyte-macrophage progenitor (GMP) clusters, thereby promoting emergency myelopoiesis. Moreover, constitutive inactivation of PRC1.1 results in unchecked expansion of GMPs and eventual transformation. Collectively, our results define PRC1.1 as a novel critical regulator of emergency myelopoiesis, dysregulation of which leads to myeloid transformation.

Indexed as

MyelopoiesisPolycomb Repressive Complex 1AnimalsCell DifferentiationHematopoietic Stem CellsHistonesMiceHistonesPolycomb Repressive Complex 1emergency myelopoiesishematopoietic stemmousemyelopoiesispolycomb repressive complex 1.1progenitor cellregenerative medicinestem cells

Identifiers

PMID37266576
PMCPMC10287155
OpenAlexW4379094655

What Socratic 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 Socratic graph.