E. coli that are young (blue) and old (red) have distinct properties.


There is no escape. Even the lowly Escherichia coli, which at first glance seems to go on dividing symmetrically and forever, ages over time, according to Eric Stewart, François Taddei (Inserm, Paris, France), and colleagues.

There was hope for E. coli immortality because the bug lacked obvious asymmetries. Organisms that age tend to segregate damaged molecules preferentially into a compromised parent, and that segregation often shows up as a morphological asymmetry. Furthermore, the uncompromised offspring often turns up as a juvenile form that must undergo further development or growth before being competent for reproduction. Signs of such a progression were also lacking in the case of E. coli.

Stewart and colleagues undertook a more comprehensive examination of E. coli division dynamics, using a custom-made, computerized tracking system that followed E. coli divisions as they generated 35,049 cells. Cleavage sites in the middle of the bacterium were defined as “new poles” and those at the distal ends as “old poles.” Thus, as cells divided to form a chain, cells at either end of the chain had particularly “old” poles. These cells had a growth rate 2.2% slower than that of “new pole” cells; they also divided later, produced less biomass, and were more likely to die. The differences increased as poles got increasingly “older” or “younger” (via repeated formation of “new” poles in consecutive divisions).

Stewart says he went into the study an agnostic on whether E. coli would show its age. “I couldn't decide myself, in the beginning,” he says. One reaons is that “people don't know to what extent damage can be fixed,” he says. “Perfect repair could be possible but the cost that would be involved would be high.” E. coli may instead attempt the kind of sorting of damaged contents that is seen during the generation of everything from budding yeast daughter cells to human germline cells. Stewart hopes to visualize any such sorting in E. coli; he is also screening for mutants that age (and thus produce dead cells) more slowly.


Stewart, E.J., et al. 2005. PLoS Biol. doi:.