DNMT3A R882 mutants interact with polycomb proteins to block haematopoietic stem and leukaemic cell differentiation

Junji Koya; Keisuke Kataoka; Tomohiko Sato; Masashige Bando; Yuki Kato; Takako Tsuruta-Kishino; Hiroshi Kobayashi; Kensuke Narukawa; Hiroyuki Miyoshi; Katsuhiko Shirahige; Mineo Kurokawa

doi:10.1038/ncomms10924

Nature Communications (Mar 2016)

DNMT3A R882 mutants interact with polycomb proteins to block haematopoietic stem and leukaemic cell differentiation

Junji Koya,
Keisuke Kataoka,
Tomohiko Sato,
Masashige Bando,
Yuki Kato,
Takako Tsuruta-Kishino,
Hiroshi Kobayashi,
Kensuke Narukawa,
Hiroyuki Miyoshi,
Katsuhiko Shirahige,
Mineo Kurokawa

Affiliations

Junji Koya: Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1, Hongo, bunkyo-ku
Keisuke Kataoka: Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1, Hongo, bunkyo-ku
Tomohiko Sato: Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1, Hongo, bunkyo-ku
Masashige Bando: Laboratory of Genome Structure and Function, Research Center for Epigenetic Disease, Institute for Molecular and Cellular Biosciences, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku
Yuki Kato: Laboratory of Genome Structure and Function, Research Center for Epigenetic Disease, Institute for Molecular and Cellular Biosciences, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku
Takako Tsuruta-Kishino: Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1, Hongo, bunkyo-ku
Hiroshi Kobayashi: Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1, Hongo, bunkyo-ku
Kensuke Narukawa: Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1, Hongo, bunkyo-ku
Hiroyuki Miyoshi: Subteam for Manipulation of Cell Fate, RIKEN BioResource Center, 3-1-1, Koyadai
Katsuhiko Shirahige: Laboratory of Genome Structure and Function, Research Center for Epigenetic Disease, Institute for Molecular and Cellular Biosciences, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku
Mineo Kurokawa: Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1, Hongo, bunkyo-ku

DOI: https://doi.org/10.1038/ncomms10924
Journal volume & issue: Vol. 7, no. 1
pp. 1 – 14

Abstract

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DNMT3A mutations are known to cause acute myeloid leukaemia. Here, Koya et al. show that DNMT3A R882H mutation causes monoblastic transformation and haematopoietic stem cell accumulation in a methylation-independent manner, by suppressing the polycomb repressive complex 1, causing transcriptional silencing.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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