Requisite Chromatin Remodeling for Myeloid and Erythroid Lineage Differentiation from Erythromyeloid Progenitors.

Cell Reports
Jun WuKyunghee Choi

Abstract

The mammalian SWitch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling BAF (BRG1/BRM-associated factor) complex plays an essential role in developmental and pathological processes. We show that the deletion of Baf155, which encodes a subunit of the BAF complex, in the Tie2(+) lineage (Baf155 (CKO) leads to defects in yolk sac myeloid and definitive erythroid (EryD) lineage differentiation from erythromyeloid progenitors (EMPs). The chromatin of myeloid gene loci in Baf155 CKO EMPs is mostly inaccessible and enriched mainly by the ETS binding motif. BAF155 interacts with PU.1 and is recruited to PU.1 target gene loci together with p300 and KDM6a. Treatment of Baf155 CKO embryos with GSK126, an H3K27me2/3 methyltransferase EZH2 inhibitor, rescues myeloid lineage gene expression. This study uncovers indispensable BAF-mediated chromatin remodeling of myeloid gene loci at the EMP stage. Future studies exploiting epigenetics in the generation and application of EMP derivatives for tissue repair, regeneration, and disease are warranted.

Citations


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Datasets Mentioned

BETA
GSE144243
GSE159381

Methods Mentioned

BETA
scRNA-seq
immunoprecipitation
transfection
dissection
PCR
ChIP
flow cytometry
FACS
reverse transcription PCR
ATAC-seq

Software Mentioned

HOMER
WashU Epigenome Browser
R
GraphPad Prism
MACS2
cutadapt
DiffBind
deepTools
Cell Ranger Single - Cell Software Suite
Cell Range

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