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Telomere Protein Found Researchers have discovered the telomere protein TRF2 on DNA fragments associated with inflammation in cells that have stopped dividing. In several models of human cells, scientists observed DNA fragments with TRF2 - a protein that protects telomeres, the ends of chromosomes - in the cytoplasm. These fragments showed signs of DNA damage and cGAS, a protein that recognizes DNA in the cytoplasm. The nucleus normally keeps chromosomes inside the cell. When DNA enters the cytoplasm, cGAS perceives it as a danger signal and triggers an inflammatory response. In senescent cells, this response supports the SASP mode, in which the cell releases cytokines and other substances that change the environment around it. These experiments build on the work of Renuki Kandhaya-Pillai's group from 2017, which found that prolonged exposure to TNFα - an inflammatory signaling molecule - converted endothelial cells into senescence and maintained cytokine release through STAT proteins. The new study asked what DNA might be the source of the cGAS signal in the same model. Researchers compared dividing cells with cells that had entered senescence due to repeated divisions or TNFα, as well as with fibroblasts from people with inherited premature aging syndromes or LMNA gene mutations. In these models, TRF2 was detected on cytoplasmic fragments near γH2AX - a protein marker of DNA damage. Prolonged TNFα treatment reduced the level of lamin B1, a nuclear envelope protein, and authors observed breaks in the envelope and the release of nuclear DNA into the cytoplasm. 🔗 Read original →