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A CHAF1B-Dependent Molecular Switch in Hematopoiesis and Leukemia Pathogenesis

Andrew Volk1, Kaiwei Liang2, Praveen Suraneni1

  • 1Division of Hematology/Oncology, Northwestern University, 303 East Superior Street, 5-123, Chicago, IL 60611, USA.

Cancer Cell
|November 14, 2018
PubMed

CHAF1B is the p60 subunit of the chromatin assembly factor (CAF1) complex, which is responsible for assembly of histones H3.1/H4 heterodimers at the replication fork during S phase. Here we report that CHAF1B is required for normal hematopoiesis while its overexpression promotes leukemia. CHAF1B has a pro-leukemia effect by binding chromatin at discrete sites and interfering with occupancy of transcription factors that promote myeloid differentiation, such as CEBPA. Reducing Chaf1b activity by either heterozygous deletion or overexpression of a CAF1 dominant negative allele is sufficient to suppress leukemogenesis in vivo without impairing normal hematopoiesis.

Keywords:
CAF1CHAF1BMLL-AF9hematopoiesis

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