Fig. 8: Schematic illustration of the role of LEMD3 in organizing the 3D chromatin architecture to maintain the contractile phenotype of vascular smooth muscle cells (VSMCs). | Nature Communications

Fig. 8: Schematic illustration of the role of LEMD3 in organizing the 3D chromatin architecture to maintain the contractile phenotype of vascular smooth muscle cells (VSMCs).

From: The inner nuclear membrane protein LEMD3 organizes the 3D chromatin architecture to maintain vascular smooth muscle cell identity

Fig. 8: Schematic illustration of the role of LEMD3 in organizing the 3D chromatin architecture to maintain the contractile phenotype of vascular smooth muscle cells (VSMCs).

Inner nuclear membrane protein LEMD3 binds to CBX3, a principal reader of H3K9me3, subsequently anchoring heterochromatin at the nuclear periphery. Lemd3 depletion causes the repositioning of heterochromatin from the nuclear periphery toward the interior in VSMCs. Furthermore, Lemd3 depletion alters the genome conformation as the increase of inter-TAD interactions at the boundaries of A and B compartments, which correlates with the repression of  VSMC contractile gene expression. Overall, LEMD3 organizes the 3D chromatin architecture by anchoring heterochromatin at the nuclear periphery to maintain the VSMC contractile identity.

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