Abstract
Telomere, the nucleoprotein structure at the end of eukaryotic linear chromosomes is indispensable for maintaining the genome stability. Telomeric DNA loss is apparent with each cell division, which marks an endpoint to the indefinite replication of the cell by causing replicative senescence that may lead to the programmed cell death. The loss of telomere is normal in cell division and as such after 20 - 40 divisions, telomere becomes too short to facilitate the capping function. Telomere uncapping or chromosomal free end causes a potential threat to the genomic stability and thus leads to the accumulation of chromosomal abnormalities that have been known to play a role in aging and cancer. Telomerase, the ribonucleoprotein complex, and its accessory proteins are required to maintain the telomere sequence. Telomerase plays a key role in maintaining the length of telomere by adding G-rich repeat sequences. Its activity has been found to be quite high in the gametes, stem cells and most importantly tumor cells. Almost 85% of tumor cells compensate for telomere loss aided by telomerase-associated protein complex and shelter in complex or telosome. However, 5% - 10% of the cells undergo telomerase-independent mechanism. This review presents the molecular view of the telomere and telomerase along with its associated complex structures. It also discusses its contrasting role in causing cellular senescence and promoting tumorigenesis.
Highlights
Telomeres are chromatin structures that cap and protect the end of chromosomes
Telomere uncapping or chromosomal free end causes a potential threat to the genomic stability and leads to the accumulation of chromosomal abnormalities that have been known to play a role in aging and cancer
This review presents the molecular view of the telomere and telomerase along with its associated complex structures
Summary
Telomeres are chromatin structures that cap and protect the end of chromosomes. Progressive telomere shortening affects the chromosomal cap, which further leads to chromosomal instability, end-to-end fusion and cell death [1] [6]. The gradual loss of telomeric repeats at the chromosomal ends affects cell function during aging. Human chromosome ends have 2 - 10 kilobase pairs of detectable telomere repeats depending on the type of tissue, the age of the donor and the replicative history of the cells. The dramatic effect of the telomere loss is often conspicuous in cancer cells wherein gradual telomere loss is considered as DSBs (Double-stranded breaks) This situation results from the loss of tumor suppressor alleles and leads the cells towards a state of immortality [12]. One remarkable feature of nucleoprotein structure located at the end of the chromosomes is to protect the chromosomal ends and prevent them from being considered as double-stranded breaks (DSBs)
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