Question

Why do cells have telomeres?

Why do telomeres get shorter every time a cell divides? What counteracts this shortening?

What role do telomeres play in aging?

If telomerase makes cancer cells immortal, could it prevent normal cells from aging?

Do you think we could extend the average lifespan by preserving or restoring the length of telomeres with telomerase? If so, does that raise a risk the telomerase also will cause cancer?

Answer 1

1. ANS: Telomere is a RNA dependent DNA polymerase, which was present as a part in the chromosome. Chromosome is the condensed genetic material present inside nucleus of each and every cells containing DNA. Telomere is the repetitive nucleotide sequences present at the end of a chromosome. The sequence in case of vertebrates is TTAGGG. During replication the replication of telomere occurs in different way. The key enzyme present in telomere is telomerase.

Function:

Telomere protects the chromosome from becoming sticy ended.

It determines the age of a cell

The length of telomere shortens as age is increased.

2. ANS: Telomere shortening:

The cells contain telomerase because DNA polymerase cannot make the end part of chromosome which is a long non-coding nucleotide tail and protein complex. Only telomerase has the capacity of developing the long poly-A or G tail. It is needed to maintain the balance of natural DNA which has a long telomere and its replicate doesn’t contain. The polymerase enzyme sense poly-A sequence and stop its process, so the further process is completed by telomerase.

Telomere shortening occurs due to the replication process in lagging strand of DNA. DNA polymerase can copy the fragment in 5’ to 3’ direction. In lagging strand it needs RNA primer for replication. After replication of lagging strand all RNA primer gets copied into new DNA. These new fragments attach to lagging strand. Only last primer at the site where telomere starts cannot copy into DNA; this results into lost of telomere into lagging strand. The other reason is high guanine content in DNA genome; this is highly susceptible to oxidative stress.

3. ANS: Telomere role in ageing:

This degeneration is related to aging because aging is caused when cells lose their functions. Human liver loses yearly 55 base pairs of telomeric DNA. This type of shortening is related to almost every tissue and organ. If this shortening appears fast then it terms as dyskeratosis congenital. This is the disease of pre aging. Such shortening on continuing leads to senescence, oncogenic transformation of somatic cells or apoptotic cell death.

4. ANS: In theory, I think should be possible telomerase to prevent normal cells form aging, because if we are capable of halting or prolonging our telomerase from shortening that will prevent the aging of our cells and increase may in fact increase our lifespan. Recent research shows that “increased telomerase expression is associated with a higher susceptibility to develop cancer both in mice and humans” (Bernardes de Jesus, Vera, Schneeberger, Tejera, Ayuso, Bosch, & Blasco, 2012). I find this not to be a viable solution to prolonging youth as there is literature showing that such genetically restoring telomeres may increase the increase the risk of developing cancer. Critically short telomeres act as a barrier to the development of cancer and if we prevent this shortening the human being will be at increased risk of cancer growth. (Bernardes de Jesus, Vera, Schneeberger, Tejera, Ayuso, Bosch, & Blasco, 2012) pointed out that preserving the length of just enough to extend critically short telomeres in old cells. “This would prevent precancerous cells from proliferating continuously, but might give normal cells a temporary boost to maintain tissue function for a few more years”

References:

Bernardes de Jesus, B., Vera, E., Schneeberger, K., Tejera, A., Ayuso, E., Bosch, F., & Blasco, M. (2012). Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer. EMBO Molecular Medicine, 4(8), 691-704. doi:10.1002/emmm.201200245.