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Class notes BI644 Biology of Ageing Week 6
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Class notes for BI644 Biology of Ageing Week 6
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6.1Age Related Disease and Cellular SenescenceThere is a wide range of things that can go
wrong as we get older.
Ageing is a risk factor for a lot of different
disease types. One of these is cancer. From
the graph, we can see that as age
increases, the incidence of cancer
increases, as well as in the other diseases.
Hallmarks of Ageing
A lot of different things that have
been noted to play a role in the
ageing process.
This section will cover cellular
senescence and telomere attrition.
So far, there has been a lot of
discussion about organismal
ageing. But it is useful to think
about an organism in terms of
several distinct compartments; it is
made up of organ systems with different tissues in each.
It is not a given that all ageing happens at the same rate in every single one of those compartments.
It may be that one compartment, organ or tissue is more limiting for ageing or longevity than others.
Some of the mechanisms of ageing and longevity may be the same in all compartments. But some
may be different: For example, only dividing cells are susceptible to hyper-proliferative diseases –
such as cancer.
Adult worms and adult flies have almost no dividing cells in them, so by studying these organisms we
completely miss the aspect of ageing specific to dividing cells. Replicating somatic cells, which are
more common against longer lived organisms, have the capacity to renew and repair tissues which is
likely to contribute to longevity.
But a disadvantage in having mitotic cells is the susceptibility to hyper-proliferative disease, such as
cancer. The fact that worms and flies do not have these dividing cells in their somatic tissue, means
that they will not develop cancer and it is quite hard to model cancer in model organisms. You can
model aspects of it, but not the whole disease. Post-mitotic cells do not give rise to cancer, which is
almost certainly why C. elegans and Drosophila do not get cancer.
The Hayflick Limit
In the 60s Leonard Flick was thinking about how cells divide – could they divide infinitely or was
there a limit on the number of times they could do this. He looked at a cell type called fibroblasts,
and these are connective tissue cells which can be taken from the skin, for example.
, He isolated cells from human tissue and put them in a culture flask with a nutrient medium. The cells
were able to divide, and they formed a confluent layer on the bottom of the flask. Once this
confluent layer, he disrupted the layer, spun the cells in a centrifuge and discarded half of the cells.
The other half of the cells are put back into a new flask with fresh medium and restart the process.
This is known as one passage. He continued to passage the cells to see how long he could keep them
replicating – he did not add any fresh cells to the medium.
He found that cell replication slows and stops after 50 ± 10 passages. Cells have reached what is now
known as the Hayflick limit and undergone replicative senescence. This means they cannot divide
anymore.
One question in the ageing field is whether replicative senescence is a cause of ageing in cells.
The Hayflick limit seems to represent a sort of ageing clock which might set the timer on the length
of adult life. People have been interested in the sort of biological mechanisms that would underlie
such a clock.
Mechanism of DNA Replication
For mitosis to happen, and
for cells to divide, cells
need to replicate their
DNA. They do this quite
efficiently.
The DNA double helix splits
in two and the DNA
polymerase fits in the gaps
and replicates the DNA.
However, on the original
template, there is always a
small amount of DNA that
doesn’t replicate
effectively. This is called
the lagging strand.
End Replication Problem
There is always a small gap on the end of the 3’ UTR of the
DNA. It is not possible to replicate end of lagging strand. With
each round of replication, chromosome ends become shorter
and shorter.
It is possible that this could lead to cellular senescence.
Telomeres
Telomeres are found on either free end of a chromosome. They act as caps to keep the sticky ends
of chromosomes from clumping together.
They are bits of repetitive DNA (TTAGGG) and proteins in a complex.
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