Inner nuclear protein Matrin-3 coordinates cell differentiation by stabilizing chromatin architecture

Hye Ji Cha, Özgün Uyan, Yan Kai, Tianxin Liu, Qian Zhu, Zuzana Tothova, Giovanni A. Botten, Jian Xu, Guo-Cheng Yuan, Job Dekker and Stuart H. Orkin ()
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Hye Ji Cha: Harvard Medical School
Özgün Uyan: University of Massachusetts Medical School
Yan Kai: Dana-Farber Cancer Institute and Harvard Medical School
Tianxin Liu: Harvard Medical School
Qian Zhu: Harvard Medical School
Zuzana Tothova: Dana Farber Cancer Institute
Giovanni A. Botten: University of Texas Southwestern Medical Center
Jian Xu: University of Texas Southwestern Medical Center
Guo-Cheng Yuan: Dana-Farber Cancer Institute and Harvard Medical School
Job Dekker: University of Massachusetts Medical School
Stuart H. Orkin: Harvard Medical School

Nature Communications, 2021, vol. 12, issue 1, 1-19

Abstract: Abstract Precise control of gene expression during differentiation relies on the interplay of chromatin and nuclear structure. Despite an established contribution of nuclear membrane proteins to developmental gene regulation, little is known regarding the role of inner nuclear proteins. Here we demonstrate that loss of the nuclear scaffolding protein Matrin-3 (Matr3) in erythroid cells leads to morphological and gene expression changes characteristic of accelerated maturation, as well as broad alterations in chromatin organization similar to those accompanying differentiation. Matr3 protein interacts with CTCF and the cohesin complex, and its loss perturbs their occupancy at a subset of sites. Destabilization of CTCF and cohesin binding correlates with altered transcription and accelerated differentiation. This association is conserved in embryonic stem cells. Our findings indicate Matr3 negatively affects cell fate transitions and demonstrate that a critical inner nuclear protein impacts occupancy of architectural factors, culminating in broad effects on chromatin organization and cell differentiation.

Date: 2021
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DOI: 10.1038/s41467-021-26574-4

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