Genetic Manipulation of Glycogen Allocation Affects Replicative Lifespan in E. coli.
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.
Biozentrum, University of Basel, Switzerland.|Philipps-Universität Marburg, LOEWE-Zentrum für Synthetische Mikrobiologie, Marburg, Germany.
Alex
A
Boehm
Institute of Biogeochemistry and Pollutant Dynamics, Department of Environmental Systems Science, ETH Zurich, Switzerland.|Department of Environmental Microbiology, Eawag, Dübendorf, Switzerland.|Department of Physics, University of California, San Diego, La Jolla, United States of America.
Markus
M
Arnoldini
Institute of Biogeochemistry and Pollutant Dynamics, Department of Environmental Systems Science, ETH Zurich, Switzerland.|Institute of Science and Technology Austria, Klosterneuburg, Austria.
Tobias
T
Bergmiller
Institute of Biogeochemistry and Pollutant Dynamics, Department of Environmental Systems Science, ETH Zurich, Switzerland.|Department of Environmental Microbiology, Eawag, Dübendorf, Switzerland.
Thomas
T
Röösli
Institute of Biogeochemistry and Pollutant Dynamics, Department of Environmental Systems Science, ETH Zurich, Switzerland.|Department of Environmental Microbiology, Eawag, Dübendorf, Switzerland.
Colette
C
Bigosch
Institute of Biogeochemistry and Pollutant Dynamics, Department of Environmental Systems Science, ETH Zurich, Switzerland.|Department of Environmental Microbiology, Eawag, Dübendorf, Switzerland.
Martin
M
Ackermann
D002455:Cell Division / Q000235:genetics* / Q000502:physiology; D004926:Escherichia coli / Q000235:genetics / Q000254:growth & development* / Q000378:metabolism*; D029968:Escherichia coli Proteins / Q000235:genetics*; D005809:Genes, Regulator; D006003:Glycogen / Q000235:genetics; D016601:RNA-Binding Proteins / Q000235:genetics*; D012097:Repressor Proteins / Q000235:genetics*; D013997:Time Factors
C093587:CsrA protein, E coli; D029968:Escherichia coli Proteins; D016601:RNA-Binding Proteins; D012097:Repressor Proteins; D006003:Glycogen