PDS5A and TOP2B cooperate for chromatin recruitment via CTCF.

Catalytically active TOP2B increases PDS5A occupancy genome wide at CTCF-bound chromatin, with cooperative recruitment driven by CTCF’s amino-terminal 95–116 region.

• Why it matters: How cohesin regulators and DNA topology enzymes coordinate at CTCF boundaries to shape transcription and genome architecture remains unclear, especially in glioma contexts.
• What they did: The study tested cooperative recruitment of PDS5A and TOP2B to CTCF-bound chromatin, mapped CTCF amino acids 95–116 as the PDS5A-interacting region, and used inducible PDS5A knockdown to measure TOP2B occupancy and gene expression.
• The result: Loss of the CTCF 95–116 region dysregulated gene expression and mildly reduced chromatin loops, while PDS5A knockdown reduced TOP2B occupancy and altered expression, linking PDS5A–TOP2B function to glioma drug sensitivity.

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