Steve the telomere

Hello fellow biologists and apparently Zach too! I'm back after what seems like an eternal sabbatical, and it must have seemed longer for you guys, because I know how much you love reading my random and often overly opinionated thoughts on biological processes. Doing 4 A-levels is tough ok, and the majority of the school Biology syllabus is so dull. More epidemiology or epigenetic mechanisms are required please Edexcel. Anyways, today I'm going to tell you guys a story, with a biological twist. Once upon a time, in a nucleus far, far away there lived a chromosome. This chromosome was young and healthy, no mutations or replication errors, just enjoying life in the nucleolus, surrounded by friendly histones and its other chromosomal buddies. But what keeps our young chromosome friend mutation free? you may ask. Telomeres, my dear Wattson (I know that doesn't work, just humor me). Telomeres are areas of repeated nucleotide sequences, TTAGGG repeated 2,500 times in humans, at the the end of each chromatid on a chromosome, which protect the chromosome from potential mutations, as well as stopping neighboring chromosomes or fragments from randomly fusing with each other (they're such a friendly bunch). Due to the nature of semi-conservative DNA replication in eukaryotic organisms, the ends of the chromatids cannot be copied by DNA polymerase, and so instead of the base sequence being ruined by this flaw in our DNA replication mechanism, the telomeres are there to valiantly defend the chromosome from damage. I may be romanticising slightly here, but I can't stress enough how valuable telomeres are to our genome. After 'taking one for the team' so to speak, an enzyme called telomerase, a reverse transcriptase kind of enzyme, synthesises new repeating sequences to replenish the telomere 'cap' on the chromatids, so they can continue to protect the chromosome from damage. At this point you would be forgiven for thinking that, if we could maintain the telomeres in our multipotent bone marrow (hematopoietic if you're a sucker for the biological terminology like me) stem cells for example, we could extend our lifespans. But actually, telomere shortening in cellular senescence (biological word for aging) is an essential process in the reduction of cancer risk, we think. Telomere shortening in humans can induce replicative senescence, a mechanism which prevents instability within our genetic material and thus the development of cancer in the older body cells produced, by limiting the number of cell divisions they can undergo before apoptosis. However, shortened telomeres can also impair the immune system, and that might increase cancer susceptibility. The telomere shortening process is the very definition of a double edged sword, as it may protect our most vital genetic information from the corruption of cancer, but it is also the root of just about every age-related disease you can think of. So next time you're having an existential crisis about your place in the universe, remember that Steve the telomere has always got your back.