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

doi:10.1016/j.isci.2022.105554

Chromatin reconstruction during mouse terminal erythropoiesis

iScience. 2022 Nov 11;25(12):105554. doi: 10.1016/j.isci.2022.105554. eCollection 2022 Dec 22.

Authors

Honghao Bi^{1

2}, Ye Hou^{2

3}, Juan Wang^{2

3}, Zongjun Xia^{1

2}, Dongmei Wang^{1

2}, Yijie Liu^{1

2}, Haiyan Bao^{1

4}, Xu Han^{1

2}, Kehan Ren^{1

2}, Ermin Li^{1

2}, Feng Yue^{2

3}, Peng Ji^{1

2}

Affiliations

¹ Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Ward 3-230, Chicago, IL60611, USA.
² Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA.
³ Department of Biochemistry and Molecular Genetics, Feinberg School of Medicine, Northwestern University, 303 East Superior, Simpson Querrey 7-518, Chicago, IL60611, USA.
⁴ Department of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.

Abstract

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.

Keywords: Cell biology; Structural biology.

Abstract

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