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The human telomere, a simple repeating sequence of six bases, TTAGGG located at the ends of chromosomes (Moyzis et al, 1988) protect them from degeneration, reconstruction, fusion, and loss. It is believed that this shortening becomes critical for a telomere on a particular chromosome, which becomes unstable and the cell stops dividing.

Nevertheless, as human dermal fibroblasts of 100-years-old individuals still have a telomere length of 6–7 kb and retain proliferative capacity for about 20 doublings (Allsopp et al, 1992). They have not reached the limit of their proliferative capacity or of telomere shortening even at such an advanced age. The telomere length of human peripheral blood lymphocytes decreases with age and shortens to about 5 kb in some individuals after age 60 years, but no individuals have been found with a mean telomere length of less than 5 kb, even among 100-years-olds. (Vaziri et al, 1993) (Iwama et al,1998)

Does this Telomere length shortening actually cause our cells to age and malfunction?

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Yes

"all somatic cells have a molecular clock that leads them to develop a senescence phenotype" Ruiz et al. 2022

Short telomeres cause replicative senescence. Senescent cells upregulate survival factors and do not undergo apoptosis (although they should). Senescence is accompanied by SASP (senescence-associated secretory phenotpye). A cell with SASP will secrete inflamatory (and cytotoxic) factors that attract immune cells, maybe in order to be killed and removed from the tissue. If senescent cells aren't removed (due to a high burden of senescent cells), these inflamatory factors also damage surrounding cells. This accumulation of tissue damage is pretty much what "aging" is.

However, there are other mechanisms that cause senescence/aging: There is also DNA-damage, mitochondrial DNA-damage (causes production of reactive oxygen species), accumulation of protein aggregates, chronic inflammation, etc.

Note that cellular stress (drug therapy, genotoxic stress, irradiation, inflammatory stress, etc.) can accelerate telomere shortening. For example, smoking during pregnancy reduces telomere length of the unborn child (Mirzakhani et al. 2017)

But still, telomere length is only a "rough estimate of aging rate and can hardly be regarded as a clinically important risk marker for age-related pathologies and mortality" (Vaiserman & Krasnienkov 2021)

Further reading: Chaib et al. 2022

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Yes.

This was demonstrated by showing that re-activation of telomerase (which lengthens telomeres) prevents cell senescence.

The immortal nature of cancer cells can be attributed in large part to their constitutive expression of telomerase.

The mechanisms by which short telomeres lead to / are linked to senescence, aneuploidy, etc. occurs have been pretty well worked out.

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Yes, it's true in eukaryotes after every cell division telomeres shorten by many base pairs. Telomerase is not found in prokaryotes as their chromosomes are circular. So, no DNA is left out for copying.

In eukaryotes, telomerase is found in stem cells. Note: There are different types of stem cells that exist in humans at every point of their lifetime. But none of them are totipotent(those have the ability to create a full organism)

Thus, telomerase ensures the safety of genetic information by elongating the telomeres. Mechanism of telomere regeneration given in AP biology...I m posting the link below

https://openstax.org/books/biology-2e/pages/14-5-dna-replication-in-eukaryotes

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