Genetic Manipulation of Glycogen Allocation Affects Replicative Lifespan in E. coli.
Bottom Line: We found that certain changes in the regulation of the carbohydrate metabolism can affect aging.These results demonstrate how manipulations of nutrient allocation can lead to the exclusion of the chromosome and limit replicative lifespan in E. coli, and illustrate how mutations can have phenotypic effects that are specific for cells with old poles.This raises the question how bacteria can avoid the accumulation of such mutations in their genomes over evolutionary times, and how they can achieve the long replicative lifespans that have recently been reported.
Affiliation: Biozentrum, University of Basel, Switzerland.
In bacteria, replicative aging manifests as a difference in growth or survival between the two cells emerging from division. One cell can be regarded as an aging mother with a decreased potential for future survival and division, the other as a rejuvenated daughter. Here, we aimed at investigating some of the processes involved in aging in the bacterium Escherichia coli, where the two types of cells can be distinguished by the age of their cell poles. We found that certain changes in the regulation of the carbohydrate metabolism can affect aging. A mutation in the carbon storage regulator gene, csrA, leads to a dramatically shorter replicative lifespan; csrA mutants stop dividing once their pole exceeds an age of about five divisions. These old-pole cells accumulate glycogen at their old cell poles; after their last division, they do not contain a chromosome, presumably because of spatial exclusion by the glycogen aggregates. The new-pole daughters produced by these aging mothers are born young; they only express the deleterious phenotype once their pole is old. These results demonstrate how manipulations of nutrient allocation can lead to the exclusion of the chromosome and limit replicative lifespan in E. coli, and illustrate how mutations can have phenotypic effects that are specific for cells with old poles. This raises the question how bacteria can avoid the accumulation of such mutations in their genomes over evolutionary times, and how they can achieve the long replicative lifespans that have recently been reported.
Related in: MedlinePlus
Mentions: While the existence of bacterial aging is thus in line with the evolutionary theory of aging, there is a puzzling quantitative discrepancy between expectation and observation: bacteria live much longer than a simple theoretical consideration would suggest. Two studies—one with Caulobacter crescentus , the other with E. coli –followed single cells for long times, and reported that individual bacterial cells can survive and divide for more than one hundred divisions. The observation with E. coli is particularly surprising, as can be shown with a simple argument: in bacterial populations where cells with different pole ages are exposed to the same external conditions, the distribution of pole ages is exponential: 50% of the cells have a pole of age one, 25% have a pole of age two, and so on (for a definition of the pole age of a bacterial cell see Fig 1A). More formally, the fraction of cells with a pole age n is 2-n; i.e. only about one in a million cells has a pole age of 20 or more. Therefore, there is virtually no selection for cells to remain viable once their cell pole is 40 or 50 divisions old (this argument assumes that the process of aging in this case depends on replicative rather than chronological age). Importantly, the pole age distribution in a bacterial population in which all cells are exposed to the same external conditions and extrinsic mortality is stable and not dependent on the growth dynamics of the population [9,10].