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During oncogene-induced senescence (OIS), heterochromatin is lost from the nuclear periphery and forms internal senescence-associated heterochromatin foci (SAHFs). We show that an increased nuclear pore density during OIS is responsible for SAHF formation. In particular, the nucleoporin TPR is necessary for both formation and maintenance of SAHFs. Loss of SAHFs does not affect cell cycle arrest but abrogates the senescence-associated secretory phenotype—a program of inflammatory cytokine gene activation. Our results uncover a previously unknown role of nuclear pores in heterochromatin reorganization in mammalian nuclei and demonstrate the importance of heterochromatin organization for a specific gene activation program.
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- Deanery of Molecular, Genetic and Population Health Sciences - Visitor: Staff Non UK HEI
Person: Affiliated Independent Researcher
- Deanery of Molecular, Genetic and Population Health Sciences - Director of Human Genetics Unit
- MRC Human Genetics Unit
Person: Academic: Research Active