APOPTATE?

I've been trying to figure out the verb form of apoptosis. To apoptote? The cell apoptoted?The cell will apop? The cell had apoptated. I know the grammatically correct form is, "to undergo apoptosis" but I don't like that. Boring. Apoptote.

The word apoptosis is derived from Greek. Apo- away. Ptosis- falling.

Apoptosis is crucial for the survival of an organism. Apoptosis rids us of undesirable cells, prevents cancerous tumors, and more.

But how does it happen? Apoptosis is induced either by external or internal factors. Factors within a cell can induce apoptosis, including irreparable DNA damage, issues to the mitochondria, and more. Internal cell stress leads to the activation of initiator caspases, and then, executioner caspases...

Below is caspase 9, one of the most important caspases. Executioner caspases form tetramers with a large and small subunit. As you can see, caspase 9 is a dimer with two active sites and a loop joining the two dimers together; this loop is the linker loop. Caspases have a cysteine residue and cleave at aspartic acids, earning them the name cysteine aspartic acid proteases, or caspases!

One of the primary methods of caspase activation is via cytochrome C. Now, as we all know, the mitochondrion is the powerhouse of the cell. Thus, when the mitochondrion is messed up, the cell puts itself out of its own misery. When mitochondria release cytochrome C, an essential part of the electron transport chain, into the cytoplasm, the cytochrome is recognized by Apaf-1 and ATP, later binding to pro-caspase 9 and forming the apoptosome. With the apoptosome having been formed, pro-caspase 9 dimerises to form caspase 9, and finally cleaves caspase 3.

This dimerisation involves a region of the initiator caspase called the death fold. Proteins bind to the death fold to initiate the dimerisation of initiator caspases. In caspase 9, this death fold is called CARD (caspase recruitment domain).

Caspase 3 is the actual functional caspase. In this situation, caspase 9 is an initiator caspase, and caspase 3 is an executioner caspase....

When one initiator caspase is activated, many executioner caspases end up activated, resulting in the degradation of cellular components in apoptosis. Executioner caspases cause the cleavage and proteolysis of lots of cellular components and induce cytoskeleton degradation, chromatin condensation, nuclear envelope degradation.

Cytoskeleton degradation will result in cell shrinkage, and compaction of cellular components in general. Chromatin will condense along the nuclear envelope in the process of pyknosis, and endonucleases will cut up chromatin bits. Nuclear envelope degradation is known as karyorrhexis, and little bits of nuclear envelope will be scattered around the cell.

As the cell meets a timely fate, blebbing (yes, this is a real science word...) and apoptopodia will form.

Blebbing is a bulge in plasma membrane resulting from the loss of cytoskeleton. With nothing to hold it together, the plasma membrane breaks off. At first, these blebs hold a little bit of cytoplasm. But as time goes on, more and more blebs contain nuclear envelope. Blebbing prevents inflammatory responses in other cells, and I choose to think of blebbing as a noble act on the part of a cell.

Apoptopodia, despite the podia, are taking the cell nowhere. These feet are false, and rather, are just projected spiky bits of cytoskeleton jutting out of the cell. When a cell dies, its membrane undergoes a shuffling. Scramblases (once again, a real science word) will put phosphatidylserine, one of the phospholipids usually on the inner layer of the membrane, on the outside. Thus, the cell signals that it has met its end.

The presence of apoptopodia, phosphatidylserine, and blebbing will trigger the phagocytosis of an apoptoted cell: and so, the cell leaves life unceremoniously, uncelebrated.

I shall choose to picture each dying cell as Vespasian: "Vae, puto deus fio."