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Genetic Manipulation of Glycogen Allocation Affects Replicative Lifespan in E. coli.

Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M - PLoS Genet. (2016)

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.

View Article: PubMed Central - PubMed

Affiliation: Biozentrum, University of Basel, Switzerland.

ABSTRACT
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.

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Related in: MedlinePlus

Electron micrographs show polar localization of glycogen in csrA mutant cells.Electron micrographs of wild type E. coli cells (A), csrA mutant cells (B) and csrA ΔglgA double mutant cells (C). Three representative pre-divisional cells per strain are depicted. The last image in each row is a magnified view of the first image in this row. Only the csrA mutant (B) displays granular structures indicative of glycogen, and these structures localize to the cell poles (in these experiments, it is not possible to determine which of the two cell poles is the old pole). Cells from the other two strains show no evidence of glycogen granules. Size bars are 1μm.
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pgen.1005974.g002: Electron micrographs show polar localization of glycogen in csrA mutant cells.Electron micrographs of wild type E. coli cells (A), csrA mutant cells (B) and csrA ΔglgA double mutant cells (C). Three representative pre-divisional cells per strain are depicted. The last image in each row is a magnified view of the first image in this row. Only the csrA mutant (B) displays granular structures indicative of glycogen, and these structures localize to the cell poles (in these experiments, it is not possible to determine which of the two cell poles is the old pole). Cells from the other two strains show no evidence of glycogen granules. Size bars are 1μm.

Mentions: We used two approaches to investigate whether and how glycogen localizes in the E. coli strains that we had investigated for their aging phenotype. First, we analyzed cells with electron microscopy, and found that, in the csrA mutant strain, granules that have been interpreted as glycogen [29,30] localized almost exclusively at the cell poles (Fig 2B); E. coli wild type cells and the csrA ΔglgA double mutant did not show evidence for the accumulation of glycogen granules (Fig 2A and 2C). If newly formed poles are initially free of glycogen, and if glycogen continuously accumulates with increasing pole age, this would directly lead to a difference in the amount of cellular glycogen between cells with old and young poles, and thus could explain their different fates if glycogen has a negative effect on the ability to grow and divide. However, in these experiments, we lack information on the pole age of the cells observed, and we are thus not able to determine whether glycogen accumulates specifically at the old cell poles.


Genetic Manipulation of Glycogen Allocation Affects Replicative Lifespan in E. coli.

Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M - PLoS Genet. (2016)

Electron micrographs show polar localization of glycogen in csrA mutant cells.Electron micrographs of wild type E. coli cells (A), csrA mutant cells (B) and csrA ΔglgA double mutant cells (C). Three representative pre-divisional cells per strain are depicted. The last image in each row is a magnified view of the first image in this row. Only the csrA mutant (B) displays granular structures indicative of glycogen, and these structures localize to the cell poles (in these experiments, it is not possible to determine which of the two cell poles is the old pole). Cells from the other two strains show no evidence of glycogen granules. Size bars are 1μm.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4836754&req=5

pgen.1005974.g002: Electron micrographs show polar localization of glycogen in csrA mutant cells.Electron micrographs of wild type E. coli cells (A), csrA mutant cells (B) and csrA ΔglgA double mutant cells (C). Three representative pre-divisional cells per strain are depicted. The last image in each row is a magnified view of the first image in this row. Only the csrA mutant (B) displays granular structures indicative of glycogen, and these structures localize to the cell poles (in these experiments, it is not possible to determine which of the two cell poles is the old pole). Cells from the other two strains show no evidence of glycogen granules. Size bars are 1μm.
Mentions: We used two approaches to investigate whether and how glycogen localizes in the E. coli strains that we had investigated for their aging phenotype. First, we analyzed cells with electron microscopy, and found that, in the csrA mutant strain, granules that have been interpreted as glycogen [29,30] localized almost exclusively at the cell poles (Fig 2B); E. coli wild type cells and the csrA ΔglgA double mutant did not show evidence for the accumulation of glycogen granules (Fig 2A and 2C). If newly formed poles are initially free of glycogen, and if glycogen continuously accumulates with increasing pole age, this would directly lead to a difference in the amount of cellular glycogen between cells with old and young poles, and thus could explain their different fates if glycogen has a negative effect on the ability to grow and divide. However, in these experiments, we lack information on the pole age of the cells observed, and we are thus not able to determine whether glycogen accumulates specifically at the old cell poles.

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.

View Article: PubMed Central - PubMed

Affiliation: Biozentrum, University of Basel, Switzerland.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus