Chromatin reconstruction during mouse terminal erythropoiesis
Honghao Bi,
Ye Hou,
Juan Wang,
Zongjun Xia,
Dongmei Wang,
Yijie Liu,
Haiyan Bao,
Xu Han,
Kehan Ren,
Ermin Li,
Feng Yue,
Peng Ji
Affiliations
Honghao Bi
Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Ward 3-230, Chicago, IL60611, USA; Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA
Ye Hou
Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA; Department of Biochemistry and Molecular Genetics, Feinberg School of Medicine, Northwestern University, 303 East Superior, Simpson Querrey 7-518, Chicago, IL60611, USA
Juan Wang
Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA; Department of Biochemistry and Molecular Genetics, Feinberg School of Medicine, Northwestern University, 303 East Superior, Simpson Querrey 7-518, Chicago, IL60611, USA
Zongjun Xia
Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Ward 3-230, Chicago, IL60611, USA; Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA
Dongmei Wang
Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Ward 3-230, Chicago, IL60611, USA; Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA
Yijie Liu
Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Ward 3-230, Chicago, IL60611, USA; Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA
Haiyan Bao
Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Ward 3-230, Chicago, IL60611, USA; Department of Hematology and Oncology, Children’s Hospital of Soochow University, Suzhou, China
Xu Han
Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Ward 3-230, Chicago, IL60611, USA; Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA
Kehan Ren
Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Ward 3-230, Chicago, IL60611, USA; Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA
Ermin Li
Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Ward 3-230, Chicago, IL60611, USA; Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA
Feng Yue
Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA; Department of Biochemistry and Molecular Genetics, Feinberg School of Medicine, Northwestern University, 303 East Superior, Simpson Querrey 7-518, Chicago, IL60611, USA; Corresponding author
Peng Ji
Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Ward 3-230, Chicago, IL60611, USA; Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA; Corresponding author
Summary: Mammalian terminal erythropoiesis involves chromatin and nuclear condensation followed by enucleation. Late-stage erythroblasts undergo caspase-mediated nuclear opening that is important for nuclear condensation through partial histone release. It remains unknown the dynamic changes of three-dimensional (3D) genomic organization during terminal erythropoiesis. Here, we used Hi-C to determine the chromatin structural change during primary mouse erythroblast terminal differentiation. We also performed RNA-sequencing and ATAC-sequencing under the same experimental setting to further reveal the genome accessibility and gene expression changes during this process. We found that late-stage terminal erythropoiesis involves global loss of topologically associating domains and establishment of inter-chromosomal interactions of the heterochromatin regions, which are associated with globally increased chromatin accessibility and upregulation of erythroid-related genes.
