Enhanced Diagnostic Tools
The mechanism by which telomeres prevent end-to-end fusion has remained elusive. Here, we show that human telomeric protein TRF2 plays a key role in the protective activity of telomeres. A dominant nega- fusions detectable in metaphase and anaphase cells. Telomeric DNA persisted at the fusions, demonstra- ting that TTAGGG repeats per se are not sufficient for telomere integrity. Molecular analysis suggested that the fusions represented ligation of telomeres that have senes their single-stranded G-tails. Therefore, TRF2 may protect chromosome ends by maintaining the correct structure at telomere termini. In addition, expression of mutant forms of TRF2 induced a growth arrest with characteristics of senescence. The results raise the possibility that chromosome end fusions and senes- cence in primary human cells may be caused by loss by TRF2 from shortened telomeres.
If you need any literature regarding
any of our products or services, please do not hesitate to submit a request.