Single‐cell RNA analysis of chromodomain‐encoding genes in mesenchymal stromal cells of the mouse dental pulp

Author:

Becker Timothy James1,Enkhmandakh Badam2,Bayarsaihan Dashzeveg23ORCID

Affiliation:

1. Department of Computer Science Connecticut College New London Connecticut USA

2. Department of Reconstructive Sciences Center for Regenerative Medicine and Skeletal Development, University of Connecticut Health Center Farmington Connecticut USA

3. Institute for System Genomics University of Connecticut Storrs Connecticut USA

Abstract

AbstractThe chromodomain helicase DNA‐binding (CHD) and chromobox (CBX) families of proteins play crucial roles in cell fate decisions, differentiation, and cell proliferation in a broad variety of tissues and cell types. CHD proteins are ATP‐dependent epigenetic enzymes actively engaged in transcriptional regulation, DNA replication, and DNA damage repair, whereas CBX proteins are transcriptional repressors mainly involved in the formation of heterochromatin. The pleiotropic effects of CHD and CBX proteins are largely dependent on their versatility to interact with other key components of the epigenetic and transcriptional machinery. Although the function and regulatory modes of CHD and CBX factors are well established in many cell types, little is known about their roles during osteogenic differentiation. A single‐cell RNA‐sequencing analysis of the mouse incisor dental pulp revealed distinct spatiotemporal expression patterns of CHD‐ and CBX‐encoding genes within different clusters of mesenchymal stromal cells (MSCs) representing various stages of osteogenic differentiation. Additionally, genes encoding interaction partners of CHD and CBX proteins, such as subunits of the trithorax‐COMPASS and polycomb chromatin remodeling complexes, exhibited differential co‐expression behaviors within MSC subpopulations. Thus, CHD‐ and CBX‐encoding genes show partially overlapping but distinct expression patterns in MSCs, suggesting their differential roles in osteogenic cell fate decisions.

Funder

University of Connecticut

Publisher

Wiley

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