Age: Issue 3
Bacteria: The origins of aging
March 21, 2021
Hello friend! Welcome to Age, a bi-weekly special edition of Scrap Facts.
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Bacteria: The origins of aging
In conversation with Lin Chao, a computational geneticist at the University of California San Diego.
Lin Chao didn’t mean to study the origins of aging. Instead, he wanted to study evolution. It’s hard to do in species with long life cycles (such as humans) because it simply takes too long (literal decades). But for bacteria—specifically, a species called E. coli—a new generation buds in 30 minutes. Humans have been around for roughly 10,000 generations, says Chao. For E. Coli, that same number of generations are born in less than a year.
An electron microscope image of E. Coli, courtesy of the US National Institute of Allergy and Infectious Diseases
Chao planned to study the rate at which bacteria evolves. But instead, he discovered something else: Aging as we know it originated in bacteria—which means all the consequences of aging we see in multi-cellular creatures have an evolutionary basis in our single-celled friends.
To explain this a little more, we first have to actually define aging. Most scientists would agree that it’s the collection of damaged proteins and mutations our cells accumulate over time.
Because bacteria only have one cell, they don’t collect genetic mutations over time. (In fact, because they have less DNA than we have, bacteria actually mutate less generation-to-generation than humans do! Bacteria introduce random mutations roughly once every 100 offspring. Though human have a unique combination of their parents’ DNA, they usually have one completely random mutation per generation.)
But bacteria do accumulate damaged proteins the longer they’re around. And there’s where things get fascinating. When a mother bacterium replicates, it keeps all of its damaged proteins to itself. This way, the daughter bacterium it produces is as healthy as can be. (“Mother” is the terminology for any parent bacteria, and “daughters” are their offspring, even though bacteria is genderless. I like to think it’s a matriarchy, though.)
Chao and his team noticed that as bacteria replicate, they don’t simply clone themselves like scientists had thought for decades. Instead, they elongate their cylindrical bodies as they double their cytoplasm (the jelly inside cells), their organelles (like organs within a cell), and their genetic material. Then, as beings twice their normal size, they slice themselves down the middle. One bacterium becomes two.
The longer the mother bacteria is a live, however, the more damaged proteins it accumulates. These proteins are a result of exposure to oxygen, which is the catch-22 of life. On the one hand, most life needs oxygen to convert sugar into cellular fuel, but on the other, oxygen rips up proteins cells need to stay alive.
As they elongate, mother bacteria have these damaged proteins spread out through themselves. But before they break off their daughters, they shuffle all the damaged goods to one side. This way, the daughter bacterium is squeaky clean as it starts to bud off daughters of its own. Though it will accumulate damaged proteins over time, too, it’ll have started off as healthy as possible. Conversely, as mother bacteria hoard more and more damaged proteins over time, they start to slow down.
Mother bacteria could just pass along damaged proteins for their daughters. They’d have a much easier time in life if they did. But it’s a tradeoff they make for their offspring. “Aging is the price parents pay to have vigorous offspring,” Chao says.
If you think about it, we see the same pattern in most species: Parents don’t pass on any damage they acquire in life to their children. (Coral, of course, is the exception I wrote about last time.) Because single-cell organisms like bacteria were the first to evolve, we can say that aging and its inherent protection of offspring is as old as life itself.
But here’s the final twist to this odd tale: Whereas the accumulation of these damaged proteins in most life eventually results in death, it’s not fatal to bacteria—at least in a lab setting. Under ideal circumstances (right temperature, right food, no threats), bacteria are immortal. They reach a critical mass of damaged proteins and then they seem to stop. Chao and his colleagues aren’t sure how, but it seems like they’re able to pass on trace amounts of these damaged proteins to their daughter cells, but not enough to detect using their current electron microscopy. It’s a field of future study for this group.
Immortality doesn’t mean being able to survive anything. Antibiotics, Chao pointed out, can disfigure enough bacterial proteins to put them beyond that critical mass so that they do die. You can also starve them of resources, like agar (sugary microbe snacks), or burn them with UV light or heat.
In any case, bacteria’s immortality causes a heated debate among aging researchers. Can we really call the process of accumulating damaged proteins aging if it doesn’t lead to death? That is a question above my pay grade, I can tell you—but it does make me think that if it isn’t aging, then what is?
That’s all for now—stay curious, friend ❤️
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Top image by Rachel Couch; headshot by Matt Anzur.