Although some DNA damage signaling and repair proteins associate with telomeres during and/or immediately following their replication [15], [16], telomeres function to protect chromosome ends from being continually recognized as double-stranded DNA breaks throughout the rest of the cell cycle.
Telomeres are bound by conserved protein machineries acting to protect chromosomal ends from being recognized as double-strand breaks.
(2) They protect the ends from being recognized as double-strand breaks and from being attacked by nucleases.
For example, TRF2 protects telomeres from being recognized as double-strand breaks (DSBs) by repressing ataxia-telangiectasia-mutated (ATM) signaling (Karlseder et al., 1999; Denchi & de Lange, 2007).
Telomere sequences stabilize chromosomal ends by binding to proteins that prevent them from being recognized as double-stranded breaks by repair enzymes (de Lange 1992).
Dual analysis was introduced using a quadrant dot plot, in which necrotic cells were identified as single PI-positive, early apoptotic cells were Annexin V-FITC-positive only, and cells in late apoptosis were recognized as double-positive for annexin V-FITC and propidium iodide.
In combination with the binding of telomeric proteins, this structure is thought to hide the ends of the chromosomes from being recognized as double-strand breaks needing repair by NHEJ, which would form dicentric chromosomes and cause a mitotic catastrophe [ 7, 8].
However, disclosure to one's sexual partner has been recognized as a double edged sword [74]- it has the potential to yield much needed social support [35] but may also result in stigmatization, discrimination, and potentially abandonment [74], [76], [77].
Telomeres have a critical function as they serve as protective caps, preventing the chromosomal ends to be accidently recognized as DNA double strands by the DNA damage repair system, and activation of the p53 or p16INK4a pathway, which eventually leads to senescence or apoptosis.
Telomeres are nucleoprotein structures at the ends of chromosomes that protect them from being recognized as DNA double-strand breaks, thus preventing chromosomal end-to-end fusions1.
