Well, the story goes that somatic cells have a mitotic clock, which is based on shortening of telomeres every time a cell divides. Once telomeres are very short, normal cells senesce and cannot divide anymore. Thus, normal (human) somatic cells are not immortal. Even adult (human) stem cells loose telomeric sequence, when they multiply, although at a slower pace. That seems to be the reason, why we age.
It has been known for more than 70 years (thanks to Barbara McClintock) that once telomeres are broken, chromosome ends become sticky and fuse with other chromosome ends. During cell divisions breakage-fusion-bridge cycles occur. The consequence is aneuploidy.
Chromosome healing is the only way out. And it seems the enzyme telomerase is involved. So, if normal human cells multiply beyond a limit (Hayflick), telomeres become critically short, subsequently chromosomes undergo breakage-fusion-bridge-cycles and finally the activation of chromosome healing mechanisms (possibly based on high telomerase levels) results in zombie cells, which are immortal and often transformed.
Well, the story goes that somatic cells have a mitotic clock, which is based on shortening of telomeres every time a cell divides. Once telomeres are very short, normal cells senesce and cannot divide anymore. Thus, normal (human) somatic cells are not immortal. Even adult (human) stem cells loose telomeric sequence, when they multiply, although at a slower pace. That seems to be the reason, why we age.
It has been known for more than 70 years (thanks to Barbara McClintock) that once telomeres are broken, chromosome ends become sticky and fuse with other chromosome ends. During cell divisions breakage-fusion-bridge cycles occur. The consequence is aneuploidy.
Chromosome healing is the only way out. And it seems the enzyme telomerase is involved. So, if normal human cells multiply beyond a limit (Hayflick), telomeres become critically short, subsequently chromosomes undergo breakage-fusion-bridge-cycles and finally the activation of chromosome healing mechanisms (possibly based on high telomerase levels) results in zombie cells, which are immortal and often transformed.
First, continuous cell lines are almost always derived from cancer cells, which are typically aneuploid. Second, aneuploidy in normal tissues may actually be more prevalent than usually appreciated because it takes a certain degree of monoclonality to appreciate aneuploidy; cultured cells are often derived from single cells, hence are monoclonal, or become essentially monoclonal or oligoclonal with time, unlike cells within normal tissues. Third, cells in culture are artificially subjected to continuous growth stimuli, increasing the likelihood of mitotic errors that can lead to polyploidy and subsequent aneuploidy; even cultures of normal human fibroblasts, as they age, develop a certain degree of aneuploidy
Hi Reinhard, thank you for your answer. I have one more question for you. What determines whether a particular cell at senescence goes to apoptosis or repairs itself through chromosome healing ?
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