The replication always takes place from 5&; to 3&; direction in the new strand. The DNA polymerase enzyme is not able to synthesize the new strand at the 5&; end of the new strand. In other words, a small poion (about 300 nucleotides) in the 3&; ends of the parent strands could not be replicated (Fig. 40.19).This end piece of the chromosome is called telomere. Therefore, another enzyme, telomere terminal transferase or telomerase takes up this job of replication of the end piece of chromosomes.After the normal replication, there is only single strand in this region; so this poion is degraded by exonucleases. This broken end leads to aberrant recombinations or end to end fusions. Unless there is some mechanism to replicate telomeres, the length of the chromosomes will go on reducing at each cell division (genes loss). The stability of the chromosome is thus lost.The shoening of the telomere end is prevented by an enzyme telomere terminal transferase or telomerase. It contains an essential RNA component, which provides the template for telomerase repeat synthesisTelomerase acts like a reverse transcriptase. Telomerase recognizes 3&; end of the telomere, and then a small DNA strand is synthesized.Terminal restriction fragments from 70-year old donors are shoer than those from 20-year old ones. Thus, in old age, the telomerase activity is lost; leading to chromosome instability and cell death.As a general rule, cancer cells have continued presence of telomerase, and the chromosome length equilibrium is maintained, leading to continued cell division. As cancer cells have increased and persistent activity of telomerase, the cancer cells become immoal. Premature shoening of telomeres is seen in some types of aplastic anemia.Ref: DM VASUDEVAN, page no: 480