What does telomerase do to the length of your telomeres?
Telomerase actively lengthens the ends of chromosomes, thereby counteracting the natural telomere shortening that occurs with each cell division. In most ordinary body cells, however, the enzyme is barely active, meaning telomeres still gradually shorten with age.
Telomerase is a specialised enzyme that lengthens the ends of chromosomes, known as telomeres. With each cell division, a small piece of the telomere is lost, because the DNA copying process cannot replicate the very last sections. Telomerase compensates for that loss by repeatedly adding the same short DNA sequence (TTAGGG) to the end, using an internal RNA template that the enzyme carries with it. Without this replenishment, every cell division would make telomeres slightly shorter.
In most ordinary body cells (somatic cells), telomerase is barely active. As a result, those telomeres shorten as a person ages. Once a telomere reaches a critical minimum length, the cell permanently stops dividing, a state called cellular ageing or senescence. This is seen as a biological brake: it prevents damaged cells from continuing to multiply, but at the same time limits the self-repair capacity of tissues.
Telomerase does not act randomly. It has a preference for the shortest telomeres in a cell, so that the balance in length within that cell is preserved. Not every telomere is extended at every division; the weakest links receive priority. This guidance ensures that the overall telomere profile remains balanced, and that one chromosome end does not grow endlessly while others become too short.
Telomerase is also not the only player. The enzyme lengthens only one strand of the DNA (the 3' end). A second molecular machine, the CST-Pol-alpha/Primase complex, fills in the other, complementary strand. That same complex also limits how far telomerase can extend. Telomere length is therefore the outcome of an interplay between multiple molecular machines, not purely the work of telomerase alone.
When genes encoding telomerase or associated proteins are damaged by hereditary mutations, people can develop serious diseases referred to as telomeropathies. A hallmark of these conditions is abnormally rapid telomere shortening, with consequences for tissues that depend on rapid cell renewal, such as bone marrow and the lungs.
There is also a downside to telomerase activity. In many forms of cancer, telomerase is reactivated in cells that do not normally do so. This allows cancer cells to maintain their telomere length and keep dividing without the natural brake of senescence. The presence of telomerase activity in tumour cells is therefore an active area of research, both as a biological marker and as a potential target for treatment.
All claims are based on the provided PMIDs (24993696, 18432920, 16741708, 21429730, 40609992, 37495394, 38890299). The basic action of telomerase (elongation, senescence in its absence) is strongly supported. The balancing role of the CST complex and the preference for the shortest telomeres are moderately supported. The link with cancer is associative and moderately supported.