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generation. Since the selection pressure that drives evolution selects whole organisms that
reproduce most successfully, the genotypes that encourage somatic cell death for the good
of making a body that reproduces most efficiently will triumph over those that protect
somatic cells and, by doing so, make a less efficient body. Occasionally, mutations arise
that do allow somatic cells to survive and proliferate for their own sakes rather than in
a way that is regulated by the rest of the body; indeed, such cells often end up regulating
other body systems (for example, blood supplies) to serve them. The neoplasias that this
behaviour produces are a major cause of mortality in the developed world. The only reason
that these mutations are not less common than they are is probably that they tend to happen
after the reproductive years so would not be selected against.
The initial evolution of elective cell death is thought to have been in the context of defence
and of starvation.
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Autophagy that does not proceed all the way to cell death is a means of
starving cells recycling dispensible components to keep vital systems running. Selection for
this, which would apply even to unicells, may have placed many of the components of
autophagy cell death in place. Apotosis can be triggered by viral infection and some other
sources of cell stress: in a population of genetically related cells, even independent unicells,
it would make evolutionary sense for an infected cell to kill itself before its infection multi-
plied and spread to all of its sisters. In the context of metazoan behaviour, JBS Haldane
famously remarked 'I would [lay down my life] for two brothers or eight cousins'
d
a calcu-
lation based on what fraction of these relatives' DNA would be identical to his own. In
crowded cultures of thousands of sister amoebae grazing on bacteria under some rotten
log, elective cell death of one infected cell to save the herd would make even more sense.
The use of death in development of multicellular bodies is merely an extension of this prin-
ciple: the genes that drive it ensure their more efficient multiplication even when this means
the sacrifice of some of the cells that contain copies of them.
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