Discover the shocking secret of unit-construction to bacterial aging and the idea that eukaryotic singularity is not immune from temporal depreciation. Learn about the delicate and unknown biological characteristics that explain their extraordinary robustness and why bacterial aging research is an essential step toward scientific and medical evolutions.
You are Not an Immortal Decedent of the Bacteria
We once thought that single-celled organisms such as bacteria were immune to the effects of aging. This was based on the idea that these organisms divided symmetrically and created offspring identical to their parents, a reproduction method known as binary fission.
But research from 2005 turned that assumption on its head. Surprisingly, two types of cells were found in the common bacterium Escherichia coli (E. coli), despite the fact that they look the same under a microscope. What researchers discovered from closely watching the division process was that, while older cells were replaced over time, they demonstrated reduced growth rate and offspring production with a higher chance of dying compared to their sprightlier young counterparts.
But, the way I see it, having bacterial aging is an evolutionary advantage.
The realisation that bacteria too age has revealed much about the evolutionary sense of it all. Asymmetrical division, in which the parent cell is older than its offspring, is recognised as an essential strategy to preserve population diversity and increase overall fitness.
A different way of looking at the data yields the age bias — but closer inspection reveals that it benefits a bacterial colony as a whole, rather than an individual cell. This makes environmental conditions less influential to cause harm to the population due to its gene pool or type as Type 2.* Variance within a gene pool can make it easier for populations to withstand changing environmental conditions. The reason being natural selection can function better on a gene pool that has greater diversity thereby increasing the total fitness of the population.
In addition, asymmetric division can also alleviate the burden of protein aggregates—a prime cause of aging in both bacterial and eukaryotic cells. By contrast, old cells could externalize these age-related damages and sprout off progeny that appears “younger” at a molecular level.
Conclusion
If the ancient wisdom is that bacteria are immortal, modern science has been forced to concede that these single-celled creatures can in fact age. The finding is much more than just an exponent of the basic mechanisms of aging, as its implications extend to progress in areas that range from antibiotic development to human disease therapy. Appreciating the nuances involved in the life cycle of bacteria may reveal novel areas for discovery that benefit the microbial kingdom and our own.
