Do bacteria age? Most biology textbooks will say that they don’t. However, research challenged that view for the first time in 2005, and a debate has ensued over the past 6 years. But a new model, published today (October 27) in Current Biology, re-examines earlier experiments and suggests that aging may have evolved early on as a mechanism that protects new generations from damages accrued by the parent.
When researchers look at aging in another single-celled organism, budding yeast, it's easy to see that cell division is asymmetrical, with a large parent producing offspring that are much smaller in size. (The second, larger cell that results from cell division is still considered the parent.) Asymmetry in division is an important aspect of aging because it allows an organism to partition damaged proteins—the accumulation of which is a widely accepted proxy for cellular age—into one cell, the older cell, while giving the new cell a clean slate. In bacteria, however, a mother divides into two identical-looking daughters through what was assumed to be symmetric division.
In 2005, Eric Stewart and colleagues, then at INSERM in France, showed that dividing bacteria produce two daughters that replicate at different rates—the first solid evidence for asymmetric division. When he first read the paper, Chao said, "it changed the way I looked at the world." The finding implied that one offspring was taking a hit, retaining the damaged proteins that prevented it from replicating as quickly as the other, "renewed" daughter cell. In other words, it was aging. Chao started creating mathematical models to try to explain aging and produce predictions that could be tested to further validate Stewart and colleagues's data. But last year, another paper, published by some of the same researchers and led by Suckjoon Jun from Harvard University, came out that contradicted part of the 2005 findings, and Chao wondered if his model might be able to explain both observations. Jun's group had developed a system in which single E. coli bacterium could be grown and tracked on a microfluidics channel. They concluded that a "mother" bacterium could divide a hundred time and not show signs of aging. E. coli, he wrote in the article, had "a robust mechanism of growth that is decoupled from cell death."
When Chao re-analyzed both studies, he realized both sets of data fit his mathematical model. The offspring of a mother that divided asymmetrically into faster and slower-growing daughters would have a higher overall fitness than a mother that divided symmetrically. In addition, while some offspring would reproduce faster than others, they would only speed up to a certain point—an equilibrium point. The slow reproducing offspring, likewise wouldn't decrease reproduction rate indefinitely; they would never stop dividing altogether. So the lineage produced by the exponential divisions of a single cell could "reach a immortal state" despite the fact that it was dividing asymmetrically, and producing daughter cells that "age," said Chao.
Jun said that the model is interesting, but that it explains only a portion of his group's data. He also questioned the validity of comparing the data since the two groups grew the bacteria under quite different experimental conditions.
While the model has yet to be tested and verified experimentally, it proposes "interesting" ideas, and "makes testable predictions," said Stewart, who is now at Northeastern University, and was not involved in the research. The model suggests that aging may be an ancient phenomenon that confers a higher fitness to a lineage. "The implication is that when a cell cannot repair all of the damage, it gets rid of the damage," by dividing asymmetrically, said Stewart.
C.U. Rang et al., "Temporal Dynamics of Bacterial Aging and Rejuvenation," Current Biology, doi:10.1016/j.cub.2011.09.018, 2011.