Telomeres are the terminal
portions of the chromosomes, made up of long repetitive sequences of TTAGGG
associated with proteins and act as a protection cap of the chromosomes. They
serve as a physical barrier against fusion, recombination and degradation of
chromosomes. When a somatic cell reaches a time when it loses its capacity of
replicating, it has reached the replication senescence - event that happens
when a cell has lost enough telomere that it can't replicate anymore, this
happens because the cell can only replicate so much telomere each cell cycle [1].
This point is also called 'Hayflick limit', discovered in the 1960s, which is
the limit of replications that an in vitro
diploid cell can undergo [2].
Ageing
is then, related to cell divisions and when the cell reaches that point, it
goes through biochemical and morphological changes that lead to senescence.
Something that is under scientific interest is ageing reversal, in other words,
putting a halt in replicative senescence. This is where telomerase comes in -
an enzymatic ribonucleoprotein complex that regulates telomeres. When it is
active, it performs telomere maintenance, so that when the cell replicates, it
doesn't lose telomere parts, leading to a state where the cell doesn't reach
replicative senescence anymore [1, 3].
Image 1. Telomere (Source: http://upload.wikimedia.org/)
References:
[1] Wai LK. (2004).
Telomeres, Telomerase, and Tumorigenesis -- A Review. MedGenMed 6(3): 19.
[2] Shay JW, Wright WE. (2000). Hayflick, his
limit, and cellular ageing. Mol Cell Biol;1:72-76.
[3] Reddel
RR. (2000). The role of senescence and immortalization in carcinogenesis. Carcinogenesis 121(3): 477-84
Licenciatura em Biologia Aplicada, 2º ano
PL3 - Grupo 10
Daniel Figueiredo
Domingos Gomes
Leandro Lopes
Sofia Beatriz Silva