Alexey Olovnikov, Elizabeth Blackburn, Carol W. Greider, Joseph G. Gall, Jack W. Szostak genetics |
Telomere
The ends of each chromosome have tiny caps called “telomeres” composed of a sequence of six nonsense nucleotides repeated hundreds of times to protect the ends from deteriorating or from fusing with other chromosomes but that are shortened with each copy. Regular DNA replication stops at the telomeres, so that sometimes the telomeres are broken; therefore, another mechanism, the telomerase enzyme, replenishes the telomeres; however, in humans, telomerase is active only in germ cells, stem cells, and some types of white blood cells. Body cells are on their own and after enough divisions, their shortened telomeres results in damage and senescence.
Fuses
Random genetic mutations are inevitable; having a finite lifetime may prevent cells from going wacko. Shortening telomeres are like fuses; when they burn to the end, their chromosomes blow.
Terminal transferase
Why couldn’t there be an enzyme that guards against growing old? Sadly deteriorating ends of chromosomes need repairs but our own telomerase isn’t active everywhere it’s needed. Let’s admit we’re not perfect, considering we tend to fall apart before we reach a hundred years like a machine that’s never oiled. Let’s say it were possible to lubricate without risking cancerous growths. Why then would we choose to accept imperfections; why not become superhuman? The question is whether being human and being godlike are compatible. Probably not. The scary prospect of death may be nothing compared to living forever.
Not only did these scientists discover the roles performed by telomeres and telomerase, but they also explained how they work and tied this all to the Hayflick limit.
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