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Thank you for the feedback! DNA isn't the only thing that has to stay mutation free for an organism to not age. Could we draw a list? Your example on prion i

Thank you for the feedback! DNA isn't the only thing that has to stay mutation free for an organism to not age. Could we draw a list? Your example on prion is incorrect as prion are misfolded proteins made by buggy DNA genes. https://en.m.wikipedia.org/wiki/Prion https://en.m.wikipedia.org/wiki/Prion Another thing that I identify as contributing to aging other than cell DNA is mitochondrial DNA (it's weird to realize we have two different DNA in each cells) Does other organelles apply? I fking don't know and how could I? :(

COGlory 7y ago
Prion pathophysiology isn't completely understood, and there's some literature to suggest certain types are caused by environmental factors. Regardless, curing cell aging is only the first step in "curing" aging. Some cell types simply stop dividing as a natural part of the lifecycle, and it isn't necessarily telomere related. Additionally, the only cells that don't shorten telomeres over time are cancer cells. Aging is a complicated process we don't understand.
- The_rationalist 7y ago
  Some cell types simply stop dividing as a natural part of the lifecycle https://en.m.wikipedia.org/wiki/Hayflick_limit https://en.m.wikipedia.org/wiki/Hayflick_limit It's because they have too much DNA damage. Aging is a complicated process we don't understand. I mostly disagree, while it is unknown how much of ageing is not a cause of DNA damage, I expect by far most of it come from DNA damage. Btw: are organelles just protein complexes? If so organelles are made by DNA too.
  - COGlory 7y ago
    The hayflick limit isn't the only cause of senescence. There are many biochemical processes that can induce senescence, and a variety of reasons the cell might do that. Oncogenic stress from reactive oxygen species, double stranded DNA breaks, enzymes like p53 tumor suppressor (this is a big one) and histone deacetylase inhibitors can all lead to senescence. Also, the hayflick limit has little to do with DNA damage per se, but rather is about telomere shortening. DNA is replicated in a ssomewhat asymmetrical fashion, and at the end of the chromosome, and needs the telomere to act as a buffer. Eventually you run out of buffer because every replication loses a little bit. But there's no innate damage to the DNA related to telomere shortening - all of the generic code still is maintained. >Btw: are organelles just protein complexes? If so organelles are made by DNA too. No... Not even close. There are some proteins in them and proteins interact with them but organelles are extremely complex. They are structures made of lipids, proteins, minerals, RNA, etc.

COGlory 7y ago

Prion pathophysiology isn't completely understood, and there's some literature to suggest certain types are caused by environmental factors. Regardless, curing cell aging is only the first step in "curing" aging. Some cell types simply stop dividing as a natural part of the lifecycle, and it isn't necessarily telomere related. Additionally, the only cells that don't shorten telomeres over time are cancer cells. Aging is a complicated process we don't understand.

The_rationalist 7y ago
Some cell types simply stop dividing as a natural part of the lifecycle https://en.m.wikipedia.org/wiki/Hayflick_limit https://en.m.wikipedia.org/wiki/Hayflick_limit It's because they have too much DNA damage. Aging is a complicated process we don't understand. I mostly disagree, while it is unknown how much of ageing is not a cause of DNA damage, I expect by far most of it come from DNA damage. Btw: are organelles just protein complexes? If so organelles are made by DNA too.
- COGlory 7y ago
  The hayflick limit isn't the only cause of senescence. There are many biochemical processes that can induce senescence, and a variety of reasons the cell might do that. Oncogenic stress from reactive oxygen species, double stranded DNA breaks, enzymes like p53 tumor suppressor (this is a big one) and histone deacetylase inhibitors can all lead to senescence. Also, the hayflick limit has little to do with DNA damage per se, but rather is about telomere shortening. DNA is replicated in a ssomewhat asymmetrical fashion, and at the end of the chromosome, and needs the telomere to act as a buffer. Eventually you run out of buffer because every replication loses a little bit. But there's no innate damage to the DNA related to telomere shortening - all of the generic code still is maintained. >Btw: are organelles just protein complexes? If so organelles are made by DNA too. No... Not even close. There are some proteins in them and proteins interact with them but organelles are extremely complex. They are structures made of lipids, proteins, minerals, RNA, etc.