If we can put together Boeings and LLMs, we can probably put together computational models of longevity for living beings... even if it's just for Mycoplasma genitalium. But I have never heard of one.
For most unicellular living beings there is no analog of death due to old age, even if their cells may be degraded by adverse environmental conditions, which can lead to the death of those cells before reproduction.
There are a few unicellular organisms that reproduce by an asymmetric division, in which case you could distinguish a "parent" and a "child". In such cases, the "parent" might be able to generate a finite number of "children", before being affected by some kind of senescence that sometimes may lead to death. Only for such unicellular organisms there may exist (or not) a relationship between their "longevity" and that of the multicellular living beings.
Another case of similarity to the aging of multicellular organisms is that for certain unicellular organisms that normally reproduce by simple division (mitosis) it is necessary from time to time to intercalate a syngamy-meiosis pair (i.e. a fusion of 2 cells followed by a division into 4 cells, to achieve the equivalent of a binary division of each of the original 2 cells). Without the intercalated syngamy-meiosis pair, such unicellular organisms seem not able to reproduce by simple division indefinitely. The state of such a cell that has passed through many simple divisions may be related to that of an old cell of a multicellular organism, or not.
Because multicellularity has appeared independently in many groups of living beings, even if most of them exhibit some kind of senescence there is no guarantee that it has the same causes.
Only for simple animals it is pretty certain that their aging mechanisms are related to those of humans.
> Death by old age is mostly a problem of the multicellular living beings (where only a small fraction of their cells are converted into the cells of new young descendants), so it is not something that affects the majority of bacteria.
Yes, and I know that there are multicellular organisms where senescence is pretty much a non-issue (hydra).
Senescence is two processes running in parallel: one is "bad luck" crippling the capabilities of a system. For example, a gene loses functionality after an error during replication. In general, it can happen that a subsystem strands in a part of its state space that it can not exit from, and this could happen even to single-cell organisms. The second process is a response to the first, and it is a set of evolved mechanisms that increases the fitness and/or average life-expectancy of an organism by preemptively shutting down the most fragile subsystems, the ones which are likely to fail early anyway.
Now, these are evolved systems, not designed. They work in an all-is-good-as-long-as-the-species-survives basis. And so comes the heretic question: what happens if the system is engineered? Can we develop and possess algorithms and workflows to design organisms with longer lifespans? Doing so for M. Genitalium is not going to do anything for humans, but once that ball is rolling, we may want to keep pushing the envelope and aiming for bigger and bigger model organisms, until we get to Canis familiaris. Then we pretty-promise to stop.
The mycoplasmas have some of the simplest possible cells, so, as you suggest, they are good candidates for the first cells whose organization and functions will become completely known.
While it is unlikely that understanding a mycoplasma would provide direct information about the causes of senescence in any multicellular organism, there is no doubt that when either a mycoplasma or another of the simplest bacteria will become completely known, that will bring a huge jump in the knowledge about all living beings and from that moment on it will become much easier to discover the causes of senescence and how it might be prevented.
There are bacteria that have extraordinarily efficient mechanisms for DNA repair, so there is no doubt that it should be possible to improve the design of human cells to avoid the accumulation of genetic errors. However, this will not happen in a few years, but in at most a century from now it is very likely that this would be possible.
I always find myself coming back to the dragonfly brain. A dragonfly brain needs exactly sixteen neurons to take input from the 30,000 ommatidia in its eyes, use that information to plot the three-dimensional flight path of airborne prey, compute an intercept course, and send those signals to the wing muscles.
How many transistors do we need for that? Input from 30,000 camera pixels, tracking moving objects in 3D space, computing vectors. Now you have a neuron to transistor efficiency ratio. Now multiply that by 86 billion. One brain. AGI's gonna take a hot minute, folks.
Take that DJI drone. For the sake of argument, let's assume it took 300 000 years to develop: that's for how long we know anatomically modern humans have been around. We could reduce it to 10000 years, to account only for modern estates and concentration of resources in such quality that people get time to do science, invent new things, and imprint all of that in the web of human culture (another information system). Anyhow, humans have developed a thing that flies and has a camera, and the two things are connected, in 300000 years. Insects evolved 2.6 billion years after life appeared on Earth. Is the DJI drone not as amazing as the dragonfly? And if not, but we keep making new versions of it for the next 1000 years, will it be able to catch up to the dragonfly?