How does telomerase prevent chromosome shortening

Theories abound : is it oxidative stress damaging our DNA? Is glucose to blame? Are our cells just following a pre-programmed biological timetable regardless of any other factors?

One theory suggests that the ageing process is at least partly linked to our telomeres. These are little protective caps at the ends of the DNA molecules that make up our chromosomes. Their job is to stop the ends of chromosomes from fraying or sticking to each other, much like the plastic tips on the ends of shoelaces.

Telomeres also play an important role in making sure our DNA gets copied properly when cells divide. DNA strands get shorter and shorter with every cell division. This maintenance of the telomeres ensures the genetic information is continually protected and the cell can continue to divide normally.

It may be that the telomeres are inherently shorter. Or it could be that the telomere shortening process is accelerated. In fact, it could be a combination of these factors. Perhaps the telomerase enzyme is not working correctly to maintain a healthy telomere length or the telomere protective structure is defective. In Telomere Biology Disorders or TBDs the extension, replication or maintenance of telomere length or structure is affected. Without telomeres, the ends of chromosomes would look like broken DNA, and the cell would try to fix something that wasn't broken.

That also would make them stop dividing and eventually die. Before a cell can divide, it makes copies of its chromosomes so that both new cells will have identical genetic material. To be copied, a chromosome's two DNA strands must unwind and separate. An enzyme DNA polymerase then reads the existing strands to build two new strands. It begins the process with the help of short pieces of RNA.

When each new matching strand is complete, it is a bit shorter than the original strand because of the room needed at the end for this small piece of RNA. It is like someone who paints himself into a corner and cannot paint the corner. An enzyme named telomerase adds bases to the ends of telomeres. In young cells, telomerase keeps telomeres from wearing down too much. But as cells divide repeatedly, there is not enough telomerase, so the telomeres grow shorter and the cells age. Telomerase remains active in sperm and eggs, which are passed from one generation to the next.

If reproductive cells did not have telomerase to maintain the length of their telomeres, any organism with such cells would soon go extinct.

Structure of the catalytic subunit of telomerase, TERT. As a cell begins to become cancerous, it divides more often, and its telomeres become very short. If its telomeres get too short, the cell may die. Often times, these cells escape death by making more telomerase enzyme, which prevents the telomeres from getting even shorter. Many cancers have shortened telomeres, including pancreatic, bone, prostate, bladder, lung, kidney, and head and neck.

Measuring telomerase may be a way to detect cancer. And if scientists can learn how to stop telomerase, they might be able to fight cancer by making cancer cells age and die. In one experiment, researchers blocked telomerase activity in human breast and prostate cancer cells growing in the laboratory, prompting the tumor cells to die.

But there are risks. Blocking telomerase could impair fertility, wound healing, and production of blood cells and immune system cells. Can you spare minutes to tell us what you think of this website? Open survey. In: Facts In the Cell. Telomeres are sections of DNA found at the ends of each of our chromosomes.

They consist of the same sequence of bases repeated over and over. This sequence is usually repeated about 3, times and can reach up to 15, base pairs in length. Telomere caps Image credit: U.