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Polycomb repressive complex 1.1 coordinates homeostatic and emergency myelopoiesis.
Nakajima-Takagi, Yaeko; Oshima, Motohiko; Takano, Junichiro; Koide, Shuhei; Itokawa, Naoki; Uemura, Shun; Yamashita, Masayuki; Andoh, Shohei; Aoyama, Kazumasa; Isshiki, Yusuke; Shinoda, Daisuke; Saraya, Atsunori; Arai, Fumio; Yamaguchi, Kiyoshi; Furukawa, Yoichi; Koseki, Haruhiko; Ikawa, Tomokatsu; Iwama, Atsushi.
Afiliación
  • Nakajima-Takagi Y; Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Oshima M; Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Takano J; Laboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
  • Koide S; Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Itokawa N; Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Uemura S; Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Yamashita M; Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Andoh S; Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Aoyama K; Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Isshiki Y; Department of Cellular and Molecular Medicine, Chiba University, Chiba, Japan.
  • Shinoda D; Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Saraya A; Department of Cellular and Molecular Medicine, Chiba University, Chiba, Japan.
  • Arai F; Department of Stem Cell Biology and Medicine, Kyushu University, Fukuoka, Japan.
  • Yamaguchi K; Division of Clinical Genome Research,Advanced Clinical Research Center, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Furukawa Y; Division of Clinical Genome Research,Advanced Clinical Research Center, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
  • Koseki H; Laboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
  • Ikawa T; Division of Immunobiology, Research Institute for Biomedical Sciences, Tokyo University of Science, Chiba, Japan.
  • Iwama A; Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Elife ; 122023 Jun 02.
Article en En | MEDLINE | ID: mdl-37266576
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 ß-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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Mielopoyesis / Complejo Represivo Polycomb 1 Límite: Animals Idioma: En Revista: Elife Año: 2023 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Mielopoyesis / Complejo Represivo Polycomb 1 Límite: Animals Idioma: En Revista: Elife Año: 2023 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Reino Unido