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Loss of Asxl2 leads to myeloid malignancies in mice.

Abstract：

:ASXL2 is frequently mutated in acute myeloid leukaemia patients with t(8;21). However, the roles of ASXL2 in normal haematopoiesis and the pathogenesis of myeloid malignancies remain unknown. Here we show that deletion of Asxl2 in mice leads to the development of myelodysplastic syndrome (MDS)-like disease. Asxl2-/- mice have an increased bone marrow (BM) long-term haematopoietic stem cells (HSCs) and granulocyte-macrophage progenitors compared with wild-type controls. Recipients transplanted with Asxl2-/- and Asxl2+/- BM cells have shortened lifespan due to the development of MDS-like disease or myeloid leukaemia. Paired daughter cell assays demonstrate that Asxl2 loss enhances the self-renewal of HSCs. Deletion of Asxl2 alters the expression of genes critical for HSC self-renewal, differentiation and apoptosis in Lin-cKit+ cells. The altered gene expression is associated with dysregulated H3K27ac and H3K4me1/2. Our study demonstrates that ASXL2 functions as a tumour suppressor to maintain normal HSC function.

journal_name

Nat Commun

journal_title

Nature communications

authors

Li J,He F,Zhang P,Chen S,Shi H,Sun Y,Guo Y,Yang H,Man N,Greenblatt S,Li Z,Guo Z,Zhou Y,Wang L,Morey L,Williams S,Chen X,Wang QT,Nimer SD,Yu P,Wang QF,Xu M,Yang FC

doi

10.1038/ncomms15456

subject

Has Abstract

pub_date

2017-06-08 00:00:00

pages

15456

issn

2041-1723

pii

ncomms15456

journal_volume

8

pub_type

杂志文章

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