Apoptosis refers to a form of programmed cell death that occurs in multicellular organisms, characterized by a series of biochemical events leading to cell changes and death. We can think of it as a self-elimination of cells, self-induced death.
The apoptosis is a very crucial need for cellular organisms to control their cell populations and remove cells that are damaged, potentially harmful, or no longer needed. This need is particularly acute in multicellular organisms, where the coordination of cell growth and death is essential for the organism’s development and survival. However the initial observation of the self-destruction is traced back to the single-celled organisms — the first eukaryote, or cell bearing a nucleus and mitochondria — that seem to have evolved it as a social behavior.
There are two main pathways to the “kill yourself” command:
- In the extrinsic pathway, the signal for apoptosis comes from outside the cell. This external signal binds to death receptors on the cell surface, which triggers a cascade of events leading to the activation of caspases (protease enzymes). These caspases then proceed to dismantle the cell’s internal structures, leading to cell death.
- In the intrinsic pathway, the signal for apoptosis originates from within the cell itself, often due to internal stress or damage, such as DNA damage. This internal distress causes the mitochondria to release apoptotic factors into the cytosol of the cell. These factors lead to the activation of caspases, which then carry out the cell’s destruction.
There is an important question to be asked here. On the ladders of the evolution, at which step did the cellular organism come up with the idea of killing its cells to control the cell populations and remove cells that are damaged, potentially harmful, or no longer needed? Seems like there are some theories to explain it:
- Endosymbiotic Hypothesis: This hypothesis suggests that apoptosis evolved due to antagonistic interactions between the protoeukaryotic host and protomitochondrial endosymbionts. According to this model, protomitochondria produced both toxins (apoptotic factors) and antitoxins (antiapoptotic factors), similar to the addiction molecules of extant phages and plasmids. Over time, these toxins were transformed into the apoptotic factors recognized today.
- Predator/Prey Dynamics: Another hypothesis argues that early protoeukaryotes were predators that relied on bacterial prey. These bacteria, in response to predation, produced toxins as a defense mechanism. Over time, as bacteria were domesticated to serve as mitochondria within eukaryotic cells, their toxins evolved into apoptotic factors.
- Kin Selection and Altruistic Suicide: In unicellular organisms, apoptosis can be seen as a form of altruistic suicide, where a cell dies to benefit its clonal relatives. This behavior could be maintained by kin selection, where the genetic fitness of related individuals is favored.
- Antagonistic Pleiotropy: Apoptotic factors often have additional, nonapoptotic functions. Cell death in unicellular organisms is sometimes accidental and caused by the nonapoptotic activity of apoptotic factors. This concept of antagonistic pleiotropy suggests that genes can have both beneficial and detrimental effects, which may have contributed to the maintenance of apoptotic mechanisms.
Thinking about these hypotheses, it feels like the random mutation of the DNA that resulted into a better fit for the cellular organism to have complex interplay with other cellular organisms and their environments, including interactions with other cells and endosymbiotic relationships might explain the whole thing here.