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Personal & societal attitudes to death shape the way we view the inevitable ending of our lives. And experiencing the deaths of others, particularly those close to us, can affect us greatly. But at a much deeper, cellular level, death shapes our very being.

We all begin life as a single cell, a zygote, or fertilised egg. The numerous cell divisions of cleavage see that zygote become a mass of cells (because cleavage results in an increase in cell number but not size, that mass is pretty much the same size as the original single cell). That mass first transforms into a hollow ball of cells & then, through the various events of organogenesis, or organ formation, an embryo takes shape.

But the fine sculpting of the embryo doesn’t result solely from cell division & growth. It’s also dependent on programmed cell death, or apoptosis. This is perhaps most obvious in the development of fingers & toes, which appear as separate digits because cells lying in the regions between those future digits self-destruct (I’ve sometimes seen apoptosis described as cellular suicide). But cell death is also a normal part of body maintenance, destroying cells that have come to the end of their lives or have been infected by a virus, to the tune of billions of cells each day in a healthy individual.

The signals that initiate the death sequence may be internal (in stressed cells, for example) or may come from outside, as when the immune system‘s  ’killer T cells’ stimulate cell death in cells infected by viruses. The process is the same in all apoptosing cells: the cell membrane forms ‘blebs’ – balloon-like outpocketings from the membrane that encloses the cytoplasm & all its contents. These happen as the cell membrane breaks away from its underpinning support structures. (Cells aren’t these tiny unstructured bags of jelly: a ‘cytoskeleton’ of tiny fibres & membrane-walled tubules gives them form & support.) The dying cell shrinks, and first the membrane surrounding its chromosomes, and then the chromosomes themselves, break into fragments. Finally the cell breaks down into a host of smaller fragments, & the immune system’s cleaners, the macrophages or ‘big eaters’, come around & clean up the mess.

So, programmed cell death is essential to the development of complex multicellular organisms like ourselves. But just when did death enter the picture? Do single-celled organisms ‘die’ in the same way? After all, they reproduce largely by binary fission, with the occasional bit of unicellular hanky-panky, so the cell line surely goes on. And on…

It turns out that in the oceans, some single-celled organisms, planktonic algae & cyanobacteria, do an awful lot of dying. Nick Lane points out that these phytoplankton fix as much CO2 into glucose as all land plants combined – ‘yet at any one time they account for just 1% of Earth’s biomass. This means their rate of turnover is huge; on average, the world’s phytoplankton population is replaced once a week’ (Lane, 2008). The usual explanation for this mass mortality is that the tiny cells are gobbled up by slightly less tiny animals, killed by disease, or starve when the nutrient supply runs out. But vast numbers of algae can disappear almost overnight, and some researchers suggest that this speed of dying is best explained by the phenomenon of apoptosis.

It turns out that researchers studying phytoplankton die-offs have found that algal and cyanobacterial cells grown in the lab die in exactly the same way as cells of more complex creatures: blebbing, fragmentation of internal components, & finally dissolution of the cell itself.  What’s more, the enzymes involved in this process are similar to those that guide apoptosis in human cells – and in those of plants & fungi as well. This suggests that the origins of cell death go a very long way back indeed – back perhaps to the origins of those tiny cellular power-houses, the mitochondria. It’s suggested that some of the members of this ancient group of enzymes are ‘part of an ancestral pathway that activates programmed cell death in response to damaging levels of oxidative stress’ (Gallois, cited in Lane, 2008), which in phytoplankton can be caused by things such as UV radiation, a shortage of iron or CO2, or viral infections.

There are obvious benefits to cellular suicide in complex animals: apart from those I mentioned above, it can also help to keep cancerous cells in check. But it’s hard to see the gains for individual plankton in self-destruction. Lane cites research suggesting that ‘the death apparatus is part of an ancient tug of war between viruses and their prey’, given that viruses are rife in seawater & plankton rather susceptible to them. Because plankton reproduce by binary fission they are essentially clones of the parent cells & thus the members of a given species would share most of their genes with each other. If, in the face of a virulent virus, enough cells die off to slow the rate of infection, then maybe a tendency for self-destruction would actually be selected for.

So, if complex organisms acquired the now essential apoptosis enzymes via their mitochondria, then it could indeed be said that at the deepest levels, death has shaped us all.

N. Lane (2008) Origins of death. Nature 453: 583-585