will adding telomerase to a cell allow the cell to continue to divide?

Answer 1

the short answer is probably yes, though it depends on a lot of things. there is some thinking out there that the length of telomeres tells a cell when to stop dividing, i.e. if the telomeres are too short the cell doesn't divide. some cancer cells have been shown to produce excess telomerase. according to this theory, producing more telomerase may help lengthen the telomeres and keep the cells dividing for longer, but the reality is that many other factors also control cell division, such as external growth factors or contact growth inhibition from other cells. thus experimentally, it probably depends on what kind of system you're using -- e.g. whole mice or some specific type of cells in dishes -- and how you're using that system -- e.g. overproducing it in the entire mouse or just in certain cells. whole mice overproducing telomerase do live longer, their cells live longer, and they seem younger, but they get a lot of cancers.

Answer 2

There is a defect/mutation relating to telomerase that allows tumor cells to divide repeatedly, but there are many different factors that keep this from happening

Telomerase allows us to lengthen the telomeres in our genetic material and they are only used as part of the cell cycle for gametic cells
and it is used for development so babies and children cell's have telomerase

When we get older many of our somatic cells go into a G0 phase and no longer divide

Once we are beyond child bearing age 40 or later for women and 50-70 for men we no longer use telomerase because we produce no gametic cells and many scientist believe shortening of telomeres and aging coincide

But there are many other factors to aging than just telomere length

Answer 3

Telomerase is an enzyme that adds specific DNA sequence repeats ("TTAGGG" in all vertebrates) to the 3' ("three prime") end of DNA strands in the telomere regions, which are found at the ends of eukaryotic chromosomes

Answer 4

It's an enzyme that occurs naturally in eukaryotic cells and serves the function of elongating the telomeres (the ends of chromosomes). It adds the sequence TTAGGG to the ends of eukaryotic chromosomes.

The whole process of DNA replication involves DNA polymerases, RNA primers and an understanding of the leading/lagging strands of DNA. The two strands of DNA are arranged in opposite directions. The directionality is known as 3'(3 prime) - 5' (5 prime) for each strand. So, you will have one strand going 3'-5' which is being transcribed continuously (i.e. the leading strand). Going in the opposite direction (5'-3') is a problem that results in fragments of DNA being produced (Okazaki fragments). RNA primers bind to each fragment position prior to the generation of Okazaki fragments. DNA ligase simply joins the fragments. But the whole process of converting RNA to DNA requires the DNA strand to continue beyond the fragment. RNase enzymes destroy the RNA fragments including the primer attached to the end of the DNA. Ultimately, the ends of the DNA won't be replicated because the end RNA primers will be degraded before they are converted.

Without this elongation, the telomeres will gradually shorten as cells divide until transcription can no longer occur. As a result, cellular division will cease and this has become one of the main explanations of the causes of aging.

Theoretically, adding telomerase to cells has been heralded as a form of therapy to extend the life of cells indefinitely. Dr. Michael Fossel (see source below) claims this to be the case but I personally believe that eventually DNA mutations (from environmental factors: smoking, pollution, foods etc.) would eventually be sufficient enough to induce apoptosis. Several studies have been conducted in the past that point to a link between induction of apoptosis (cell death) and damage to DNA. More specifically, damage to the ends of DNA can be interpreted by the cell as double strand breakages (DSB). I uncovered a few articles on this when I was investigating the effects of microwave frequencies on damage to DNA.

Indeed, somatic cells can enter the G0 phase permanently i.e. the cells become terminally differentiated (note that lymphocytes only temporarily enter this phase....they can be stimulated upon coming into contact with their corresponding antigen).

And that reminds me of another plausible explanation for cessation of normal cellular division: one of my professors was conducting research in this area and claimed cell division has a greater chance of failing due to the shortening of the mitotic spindle fibres that align chromosomes to the metaphase plate during meosis. The result is the formation of cancer cells which appear to be capable of overexpressing telomerase...