This was first shown in a model organism, the ciliate Tetrahymena, and subsequently in lots of other organisms. The telomeres consist, first, of a DNA scaffold composed of a tract of quite simple repeated DNA sequences. In the case of people, the repeat sequence T2AG3 is repeated, in tandem, 1000’s of occasions at the end of every chromosome.
That sequence tract supplies a molecular scaffold on which binds a set of proteins, about which much is understood. These proteins include DNA sequence-particular binding proteins and different proteins that collectively, in impact, sheathe the chromosome finish.
Furthermore, the underlying DNA is also dynamic, for two causes. One motive is that, as was predicted in the 1970s, the known mechanism of DNA polymerase prevents complete DNA replication all the way in which to the ends of the chromosome at every round of replication. Thus, incomplete replication of the chromosome ends occurs, which, if left unchecked by any compensatory mechanism, results in a problem of sustaining the complete-length of chromosomal DNA molecules.
The chromosome ends change into progressively shorter, which was predicted eventually to steer, by some unknown mechanism, to cells ceasing to divide. The answer to this theoretical problem was the enzyme telomerase. Carol Greider and I identified the telomerase enzyme first in the ciliated protozoan Tetrahymena. We used this organism as a result of it has numerous telomeres and is a relatively wealthy source of telomerase.
Telomerase accommodates an RNA element. The RNA has a brief template sequence that’s copied into DNA, which extends, and thus lengthens, the chromosomal DNA. We were able to show that this also occurs in vivo. It is that this addition of telomeric DNA in increments to the ends of chromosomes that offsets and counterbalances the shortening of chromosome ends.
Dr. Blackburn was quick to level out that these correlations don’t necessarily mean that there is a direct cause and effect relationship. In reality, rising telomerase levels ought to lengthen telomeres (see more at Epitalon website) however within the case of most cancers, too much telomerase can be simply as unhealthy as too little telomeres.