Other Problems With The Classical Ageing Theories
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A raised criticism for all three mainstream theories based on classical evolutionary process concepts is the potential existence of 'deliberate' metabolic mechanisms that work to promote death.
One is apoptosis, or programmed cell death. Apoptosis is responsible for killing infected cells, cancerous cells and cells that are simply in the wrong place during development. There are clear benefits to apoptosis, so the existence of apoptosis isn't a problem for evolutionary theory. The problem is that apoptosis seems to ramp up late in life and kill healthy cells, causing weakness and degeneration. And, paradoxically, apoptosis has been observed as a kind of 'altruistic suicide' in colonies of yeast under stress. This seems to be a direct hint that senescence arose because it conferred a direct evolutionary advantage, rather than some kind of side effect of genes that have other evolutionary advantages (pleiotropy).
A second 'deliberate' mechanism is called replicative senescence or cellular senescence. Metaphorically, a cell may be said to 'count' (with its telomeres) the number of times that it has divided, and after a set number of replications, it languishes and dies. It has been proposed that this mechanism evolved to suppress cancer. Many invertebrates experience replicative senescence, though they never die of cancer. Even one-celled organisms count replications, and will die if they don't replenish their telomeres with conjugation (sex).
More strictly, of course, cells cannot 'count' the number of times they have divided. Telomeres are not a counting mechanism, though they may be used to indicate the number of times a particular chromosome has been replicated. Cellular processes for genetic material replication occurs in both directions along DNA, 5' to 3' and on the other strand, 3' to 5'. As the 3' to 5' end is impossible for DNA polymerase to grab at the 1 base pair mark, a handful of basepairs (10-15) are cut off each replication. Over time, this cutting short of the DNA results in no telomeres, and the cell is unable to replicate that chromosome without cutting into genes.
The dilemma is that classical evolutionary theory says that what is maintained in a lineage is that which ensures the viability of an organism and its offspring. Ageing can only cut off an individual's capacity to reproduce. So, according to classical theory, ageing could only evolve as a side effect, or epiphenomenon of selection. The disposable soma theory and antagonistic pleiotropy theory are examples in which a compensating individual benefit, compatible with classical evolution theory (See neo-Darwinism and modern evolutionary synthesis) is proposed. Nevertheless, there is accumulated evidence that ageing looks like an adaptation in its own right, selected for its own sake.
Semelparous organisms and others that die suddenly following reproduction (e.g. salmon, octopus, marsupial mouse (Brown Antechinus), etc.) also represent instances of organisms who incorporate a life span limiting feature. Sudden death is more obviously an instance of programmed death or a purposeful adaptation than gradual ageing. Biological elements clearly associated with evolved mechanisms such as hormone signalling have been identified in the death mechanisms of organisms such as the octopus.
Read more about this topic: Evolution Of Ageing
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