Biochemical controls: why apoptosis? (Introduction)

by David Turell @, Wednesday, March 06, 2024, 18:16 (260 days ago) @ David Turell

Cells kill themselves on purpose:

https://www.quantamagazine.org/cellular-self-destruction-may-be-ancient-but-why-20240306/

"[When] a mitochondrion receives a signal, and its typically placid proteins join forces to form a death machine.

They slice through the cell with breathtaking thoroughness. In a matter of hours, all that the cell had built lies in ruins. A few bubbles of membrane are all that remains.

"Apoptosis, as this process is known, seems as unlikely as it is violent. And yet some cells undergo this devastating but predictable series of steps to kill themselves on purpose. ...although it turned out that apoptosis is a vital creative force for many multicellular creatures, to a given cell it is utterly ruinous. How could a behavior that results in a cell’s sudden death evolve, let alone persist? (my bold)

***

"Apoptosis can be traced back to ancient forms of programmed cell death undertaken by single-celled organisms — even bacteria — that seem to have evolved it as a social behavior.

"The findings of one study, suggest that the last common ancestor of yeast and humans — the first eukaryote, or cell bearing a nucleus and mitochondria — already had the tools necessary to end itself some 2 billion years ago. And other research, including a key paper published last May, indicates that when that organism was alive, programmed cell death of some kind was already millions of years old.

***

"The theory involves the mitochondrion — an organelle that was once a free-living bacterium. It is the cell’s energy producer. It also crops up again and again in apoptosis pathways. Guido Kroemer, who studies the role of mitochondria in apoptosis, dubbed them “the suicide organelles.”

“'Many call it,” Nedelcu said, “the central executioner of cell death.”

***

"Bacteria are single-celled, and may live among their kin. Can they also die for some greater good? There are hints that under the right conditions, bacteria infected with a virus may kill themselves to arrest the spread of disease. These revelations have reshaped how researchers think about programmed cell death, and Aravind recently discovered another piece of the puzzle.

"It involves protein regions called NACHT domains, which appear in some animal apoptosis proteins. NACHT domains also exist in bacteria. In fact, in the wild, the microbes that have the most NACHT domains sometimes partake of what looks very much like multicellular living, Aravind said. They grow in colonies, which makes them especially vulnerable to contagion and especially likely to benefit from each other’s self-sacrifice.

***

"These preserved domains tell a story of apoptotic origins, according to Aravind. “You already had a premade cell-death apparatus that was there in certain bacteria,” he said. Then, at some point, some lineages of eukaryotic cells picked up this toolkit, which eventually endowed cells in multicellular organisms with a way to die for the greater good.

"He no longer believes the evidence points to the mitochondrion as the only bacterial source of apoptosis proteins. The mitochondrion is the primary bacterial leftover still living within most eukaryotic cells, and 25 years ago it was the logical candidate for these mysterious genes, he said. In the years since, however, something else has become clear: The mitochondrion probably wasn’t alone.

"Eukaryotic genomes, researchers have gradually realized, bear many traces of bacterial genes, remnants of a silent parade of other creatures that left their marks on us. They may have been symbionts, like the mitochondrion, that popped in and out of various eukaryotic lineages, leaving genes behind. “We should now realize that this situation probably continued all through eukaryotic evolution,” Aravind said."

Comment: designed to die for the greater good shows purpose at work. The article contains the usual presumptions about how mitochondria appeared. A designer at work is very reasonable.


Complete thread:

 RSS Feed of thread

powered by my little forum