SETD1A function in leukemia is mediated through interaction with mitotic regulators BuGZ/BUB3.


Journal

EMBO reports
ISSN: 1469-3178
Titre abrégé: EMBO Rep
Pays: England
ID NLM: 100963049

Informations de publication

Date de publication:
09 10 2023
Historique:
revised: 11 07 2023
received: 02 03 2023
accepted: 18 07 2023
pmc-release: 03 08 2024
medline: 10 10 2023
pubmed: 3 8 2023
entrez: 3 8 2023
Statut: ppublish

Résumé

The H3K4 methyltransferase SETD1A plays a crucial role in leukemia cell survival through its noncatalytic FLOS domain-mediated recruitment of cyclin K and regulation of DNA damage response genes. In this study, we identify a functional nuclear localization signal in and interaction partners of the FLOS domain. Our screen for FLOS domain-binding partners reveals that the SETD1A FLOS domain binds mitosis-associated proteins BuGZ/BUB3. Inhibition of both cyclin K and BuGZ/BUB3-binding motifs in SETD1A shows synergistic antileukemic effects. BuGZ/BUB3 localize to SETD1A-bound promoter-TSS regions and SETD1A-negative H3K4me1-positive enhancer regions adjacent to SETD1A target genes. The GLEBS motif and intrinsically disordered region of BuGZ are required for both SETD1A-binding and leukemia cell proliferation. Cell-cycle-specific SETD1A restoration assays indicate that SETD1A expression at the G1/S phase of the cell cycle promotes both the expression of DNA damage response genes and cell cycle progression in leukemia cells.

Identifiants

pubmed: 37535603
doi: 10.15252/embr.202357108
pmc: PMC10561176
doi:

Substances chimiques

Cyclins 0
Cell Cycle Proteins 0
BUB3 protein, human 0
Poly-ADP-Ribose Binding Proteins 0

Banques de données

GEO
['GSE159146', 'GSE189894']

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e57108

Subventions

Organisme : NCI NIH HHS
ID : R01 CA204396
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States

Informations de copyright

© 2023 The Authors.

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Auteurs

Sarah Perlee (S)

Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Gerstner Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Sota Kikuchi (S)

Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Tomoyoshi Nakadai (T)

Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY, USA.

Takeshi Masuda (T)

Laboratory of Pharmaceutical Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Institute for Advanced Biosciences, Keio University, Tsuruoka, Japan.

Sumio Ohtsuki (S)

Laboratory of Pharmaceutical Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.

Makoto Matsumoto (M)

Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Bahityar Rahmutulla (B)

Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Masaki Fukuyo (M)

Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Paolo Cifani (P)

Molecular Pharmacology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Alex Kentsis (A)

Molecular Pharmacology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Robert G Roeder (RG)

Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY, USA.

Atsushi Kaneda (A)

Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Takayuki Hoshii (T)

Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.

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Classifications MeSH