Cells can respond to cancer-driving oncogenes by triggering an irreversible cell cycle arrest called senescence.
Senescent cells activate a gene expression programme that leads to the secretion of inflammatory proteins that can affect how tumours grow.
The team investigated what triggers this inflammatory gene expression programme and discovered an unexpected link between TPR - located at the pores used to transport material into and out of the nucleus - and chromatin re-organisation and loss of structural integrity at the edge of the nucleus, during these early stages of oncogene-induced senescence.
This loss of structural integrity results in bits of the genome breaking off from the nucleus and ending up in the cytoplasm where it triggers the cellular machinery that normally senses viral infection.