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    What do you think could happen, if all our cells expressed Telomerase to keep all the chromosomal telomeres at their original length.

    Think of consequences of that in a multicellular organisms, such as ourselves
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    (Original post by samzz_033)
    What do you think could happen, if all our cells expressed Telomerase to keep all the chromosomal telomeres at their original length.

    Think of consequences of that in a multicellular organisms, such as ourselves
    There is a minimum length for chromosomal telomeres. If this minimum is falling below, the cells to those telomeres cannot be divided. That leads to cell death (apoptosis) as a rule. To prevent this, the enzyme telomeres keep the original length of those telomeres of a cell.

    Imagine what happened to stem cells (cells in 'developmental stage' without belonging to tissues and organisms first) or cancer cells if they are not dying, as they keep the original length of the telomers and go on in dividing themselves.*
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    (Original post by Kallisto)
    There is a minimum length for chromosomal telomeres. If this minimum is falling below, the cells to those telomeres cannot be divided. That leads to cell death (apoptosis) as a rule. To prevent this, the enzyme telomeres keep the original length of those telomeres of a cell.

    Imagine what happened to stem cells (cells in 'developmental stage' without belonging to tissues and organisms first) or cancer cells if they are not dying, as they keep the original length of the telomers and go on in dividing themselves.*
    Cells that have reached their hayflick limit, and hence DNA replication can no longer occur, do not necessarily undergo apoptosis. Instead, some cells may become senescent, that is, they no longer divide. But yes, stem cells and cancer cells have high teloemerase activitiy while hepatocytes (liver cells) also have some telomerase activity.
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    (Original post by Jpw1097)
    Cells that have reached their hayflick limit, and hence DNA replication can no longer occur, do not necessarily undergo apoptosis. Instead, some cells may become senescent, that is, they no longer divide. But yes, stem cells and cancer cells have high teloemerase activitiy while hepatocytes (liver cells) also have some telomerase activity.
    Just some questions to your statement in bold print:

    But as a rule cells undergoes apoptosis as the cells are not able to divide no longer and have reached a critical length? And what about a senescent cell, so indivisible cell, which are not working no longer, so losing the function in a tissue or organ? does this has to lead to apoptosis necessarily? or do some of them become to skin cells, as they have to be regarded as dead cells, so apoptosis does not come off?

    Thanks for answers in advance! *
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    (Original post by Kallisto)
    Just some questions to your statement in bold print:

    But as a rule cells undergoes apoptosis as the cells are not able to divide no longer and have reached a critical length? And what about a senescent cell, so indivisible cell, which are not working no longer, so losing the function in a tissue or organ? does this has to lead to apoptosis necessarily? or do some of them become to skin cells, as they have to be regarded as dead cells, so apoptosis does not come off?

    Thanks for answers in advance! *
    A senescent cell does not undergo apoptosis, neither do senescent cells necessarily lose function, they are still metabolically active as far as I know. The problem is that, since senescent cells are no longer able to undergo mitosis, they cannot replace cells which suffer DNA damage (and consequently undergo apoptosis or become senescent themselves) as well as other types of damage. Hence, eventually the number of cells that are fully functional decline as senescent cells are unable to replace damaged cells, and hence tissue function also declines.
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    (Original post by Jpw1097)
    A senescent cell does not undergo apoptosis, neither do senescent cells necessarily lose function, they are still metabolically active as far as I know. The problem is that, since senescent cells are no longer able to undergo mitosis, they cannot replace cells which suffer DNA damage (and consequently undergo apoptosis or become senescent themselves) as well as other types of damage. Hence, eventually the number of cells that are fully functional decline as senescent cells are unable to replace damaged cells, and hence tissue function also declines.
    I see. So to prevent that those cells with DNA damage are creating carcinoma by mitosis, they have to become senescent or undergo apoptosis. That is quasi an 'emergency measure' for cells. Very interesting.

    Just another question (maybe it is the last one): is there an equilibrium between undergoing apoptosis and getting senescent in terms of cells with DNA damage?
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    (Original post by Kallisto)
    I see. So to prevent that those cells with DNA damage are creating carcinoma by mitosis, they have to become senescent or undergo apoptosis. That is quasi an 'emergency measure' for cells. Very interesting.

    Just another question (maybe it is the last one): is there an equilibrium between undergoing apoptosis and getting senescent in terms of cells with DNA damage?
    Yes, there are a few options for a cell that has DNA damage: firstly, DNA damage may activate DNA repair mechanisms which attempt to repair the DNA. If the DNA damage is too extensive however, the cell becomes senescent or undergoes apoptosis. DNA damage could lead to mutations which could enable cells to bypass checkpoints in the cell cycle which could lead to uncontrolled cell division which could result in the formation of tumours or cancers.

    As for a balance between apoptosis and senescence, I'm not really sure in all honesty.

    Also, I'd just like to add that carcinomas are cancers that originate from epithelial cells. There are many different types of cancers such as lymphomas, sarcomas, leukaemia, melanoma and so on.
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    (Original post by Jpw1097)
    Yes, there are a few options for a cell that has DNA damage: firstly, DNA damage may activate DNA repair mechanisms which attempt to repair the DNA. If the DNA damage is too extensive however, the cell becomes senescent or undergoes apoptosis. DNA damage could lead to mutations which could enable cells to bypass checkpoints in the cell cycle which could lead to uncontrolled cell division which could result in the formation of tumours or cancers.

    As for a balance between apoptosis and senescence, I'm not really sure in all honesty.

    Also, I'd just like to add that carcinomas are cancers that originate from epithelial cells. There are many different types of cancers such as lymphomas, sarcomas, leukaemia, melanoma and so on.
    I just thought it has to be, because if there are too many senescent cells, there are too many cells which are not able to divide anylonger what may cause a desaster. Look: If there are cells which undergo apoptosis, they have to substitude by another cells. But if there are too many senescent cells, it is hard to create new (substitute) cells by mitosis. That is why the question for equilibrium.

    By all means, you get my reputation points. You did more than enough for that. *
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    (Original post by Kallisto)
    I just thought it has to be, because if there are too many senescent cells, there are too many cells which are not able to divide anylonger what may cause a desaster. Look: If there are cells which undergo apoptosis, they have to substitude by another cells. But if there are too many senescent cells, it is hard to create new (substitute) cells by mitosis. That is why the question for equilibrium.

    By all means, you get my reputation points. You did more than enough for that. *
    That's it, eventually you get to a stage where you have to replace damaged cells or cells that were destroyed by apoptosis but you don't have enough actively dividing cells to replace them as so many cells have become senescent. This is, as far as I'm aware, one of the theories that explain the deterioration of tissues with age.
 
 
 
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