Nuclear actin structure regulates chromatin accessibility

Buer Sen, Zhihui Xie, Michelle D. Thomas, Samantha G. Pattenden, Sean Howard, Cody McGrath, Maya Styner, Gunes Uzer, Terrence S. Furey and Janet Rubin ()
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Buer Sen: University of North Carolina
Zhihui Xie: University of North Carolina
Michelle D. Thomas: University of North Carolina at Chapel Hill
Samantha G. Pattenden: University of North Carolina at Chapel Hill
Sean Howard: Boise State University
Cody McGrath: University of North Carolina
Maya Styner: University of North Carolina
Gunes Uzer: Boise State University
Terrence S. Furey: University of North Carolina at Chapel Hill
Janet Rubin: University of North Carolina

Nature Communications, 2024, vol. 15, issue 1, 1-15

Abstract: Abstract Polymerized β-actin may provide a structural basis for chromatin accessibility and actin transport into the nucleus can guide mesenchymal stem cell (MSC) differentiation. Using MSC, we show that using CK666 to inhibit Arp2/3 directed secondary actin branching results in decreased nuclear actin structure, and significantly alters chromatin access measured with ATACseq at 24 h. The ATAC-seq results due to CK666 are distinct from those caused by cytochalasin D (CytoD), which enhances nuclear actin structure. In addition, nuclear visualization shows Arp2/3 inhibition decreases pericentric H3K9me3 marks. CytoD, alternatively, induces redistribution of H3K27me3 marks centrally. Such alterations in chromatin landscape are consistent with differential gene expression associated with distinctive differentiation patterns. Further, knockdown of the non-enzymatic monomeric actin binding protein, Arp4, leads to extensive chromatin unpacking, but only a modest increase in transcription, indicating an active role for actin-Arp4 in transcription. These data indicate that dynamic actin remodeling can regulate chromatin interactions.

Date: 2024
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DOI: 10.1038/s41467-024-48580-y

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