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Programmed Cell Death Is Vital to Life, but Where’d It Come From?

baby toes.jpg

Not least with today’s terrible headlines in mind, death is a disturbing topic. It’s something we don’t like to talk about, and something we seek to avoid as long as possible. Those who give up their lives for the sake of others are considered heroes, and rightly so. Yet in order for us to develop, to grow from egg to adult, many of our cells have done just that. They gave up their lives for our good.

Scientists call this process of self-sacrifice programmed cell death — apoptosis is the technical term. It is a program of deliberate self-destruction, much like the auto-destruct program in Star Trek episodes, except in this case, once the program is triggered the process rapidly becomes irreversible. The cell shreds its insides. Its DNA goes through a series of stages that break it down into fragments. The cell’s inner structure falls apart and condenses. Then special cells called macrophages clear up the shriveled dead cells.

Cells die for many reasons — they die to give shape to our fingers and toes, they die to produce our nervous system, they die to make sure our immune system can tell friend from foe. If apoptosis failed in part, the result would be deformity. If it failed entirely, we would all die as embryos. 

So how might such a thing evolve? The benefit of such self-sacrifice can only occur when cells begin to collaborate to make a multicellular organism. One paper proposed such collaboration as something like a mutually assured destruction scenario where two cell types each make molecules the other needs, causing a kind of grudging cooperation between them. Withdrawal of those factors causes cell death, presumably by apoptosis. This scenario is circular. Did cooperation evolve because of cell death, or did cell death evolve because of cooperation? Both would seem to need to be in place at the same time for a stable system to occur.

Another paper argues for the evolution of apoptosis through multiple fortunate episodes of horizontal gene transfer, followed by the creation of a few new protein domains and/or cooption of existing proteins to new functions. They go on to say:

The observations described here emphasize the pivotal role of bacterial-eukaryotic HGT [horizontal gene transfer] in the origin of the eukaryotic PCD system and, by implication, of the eukaryotic multicellularity itself. Indeed, much of the glory of eukaryotic ascension to the ultimate complexity of higher plants and animals might owe to a lucky choice of bacteria with complicated differentiation processes as the primary, and perhaps subsequent symbionts. [Emphasis added.]

Does it make sense to say that eukaryotes fortuitously evolved a way to self-destruct, and then became multicellular, which is presumably where the benefit came in? The first steps would seem to be non-adaptive, of no benefit, in addition to being completely improbable.

I might paraphrase all of this: add just the right ingredients, stir well, then pull a dead rabbit out of your hat.

Image source: Olivia @ MooMama/Flickr.

Ann Gauger

Senior Fellow, Center for Science and Culture
Dr. Ann Gauger is Director of Science Communication and a Senior Fellow at the Discovery Institute Center for Science and Culture, and Senior Research Scientist at the Biologic Institute in Seattle, Washington. She received her Bachelor's degree from MIT and her Ph.D. from the University of Washington Department of Zoology. She held a postdoctoral fellowship at Harvard University, where her work was on the molecular motor kinesin.

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