Molecular Biology: DNA Structure and Replication

Telomeres, protective caps at the ends of chromosomes, gradually decrease in length with each cell division throughout a human's lifetime.

The enzyme telomerase, crucial for maintaining telomere length, is composed of two essential components: hTERT (human telomerase reverse transcriptase) and hTR (human telomerase RNA component).

When telomeres shorten too much in somatic cells, the cells enter a state of irreversible growth arrest, known as replicative senescence, limiting their ability to divide further.

Senescent cells contribute to the ageing process by accumulating and releasing harmful substances that damage surrounding tissues, accelerating age-related decline.

Inappropriate activation of telomerase in human cells can lead to uncontrolled cell division and the development of cancer, as telomeres are no longer shortened, allowing cells to replicate indefinitely.

Individuals with Werner syndrome (WS) have shorter than normal telomeres, contributing to premature ageing and increased age-related disease susceptibility.

hTR (human telomerase RNA component) acts as a template RNA within telomerase, providing the pattern for adding repeating DNA sequences to maintain telomere length.

Shortened telomeres impede a cell's ability to replicate. This can lead to a halt in cell division, as the protective caps become too short, signaling an 'end of line' for the cell.

A strong correlation exists between the length of telomeres and the lifespan of a cell. Longer telomeres generally translate to longer cell lifespans, enabling cells to divide more times before entering senescence.

Disruption of the D loop structure, a critical feature of telomere maintenance, triggers irreversible cell cycle exit. Cells with compromised D loops are unable to progress through the cell cycle, ultimately leading to their senescence.