AI Article Synopsis

  • This study examines how survivin interacts with the polycomb repressive complex 2 (PRC2), which plays a key role in silencing gene expression by modifying histone proteins.
  • Researchers found that different levels of survivin in CD4 T cells correlate with varying expressions of PRC2 subunits, and studies indicated that survivin binds with PRC2 along DNA.
  • Inhibiting survivin leads to increased trimethylation of histone 3 at lysine 27, suggesting that survivin may block PRC2's ability to silence genes effectively.

Article Abstract

This study investigates the role of survivin in epigenetic control of gene transcription through interaction with the polycomb repressive complex 2 (PRC2). PRC2 is responsible for silencing gene expression by trimethylating lysine 27 on histone 3. We observed differential expression of PRC2 subunits in CD4 T cells with varying levels of survivin expression, and ChIP-seq results indicated that survivin colocalizes with PRC2 along DNA. Inhibition of survivin resulted in a significant increase in H3K27 trimethylation, implying that survivin prevents PRC2 from functioning. Peptide microarray showed that survivin interacts with peptides from PRC2 subunits, and machine learning revealed that amino acid composition contains relevant information for predicting survivin interaction. NMR and BLI experiments supported the interaction of survivin with PRC2 subunit EZH2. Finally, protein-protein docking revealed that the survivin-EZH2 interaction interface overlaps with catalytic residues of EZH2, potentially inhibiting its H3K27 methylation activity. These findings suggest that survivin inhibits PRC2 function.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10391610PMC
http://dx.doi.org/10.1016/j.isci.2023.106976DOI Listing

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