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A Bug's Life: E. coli can't escape old age

Christen Brownlee

Speaking about common characteristics of living things, the Nobel prize–winning biochemist Jacques Monod once said, "What is true for [the bacterium Escherichia] coli is true for the elephant." Now, research has highlighted a new similarity between the two organisms: Like elephants and possibly all other life forms, E. coli is susceptible to the ravages of aging.

A rod-shaped bacterium found in the intestines of people and many other animals, E. coli reproduces asexually in a symmetrical manner—that is, one mother cell divides down the middle to form two identical daughters. Researchers haven't been sure whether symmetrically reproducing organisms ever grow old.

On the other hand, aging seems to occur universally in organisms that reproduce asymmetrically, for example, those whose offspring start out smaller than the parents.

If a mother cell divides symmetrically, many scientists theorized that the offspring inherit cellular components equally ravaged by the experiences of previous generations. Thus, each daughter cell would begin life no more or less worn out than the mother had been.

To test this idea, Eric Stewart at INSERM, the National Institute of Health and Medical Research in Paris, and his colleagues filmed E. coli as they divided into daughter cells. While following the organisms through nine generations, a process that takes about 6 hours, the researchers kept track of the genealogy of every bacterium.

After analyzing the videotapes, Stewart's team found that daughter cells aren't as alike as they look. As each mother cell splits down the middle, each offspring inherits one end-structure, or pole, and develops a new one. At the next division, then, one daughter inherits a pole that's older than the one inherited by the other daughter. According to Stewart's colleague François Taddei, "You can count the age of each cell by the age of its oldest pole."

Bacteria with the older poles showed a reduced growth rate, a decreased rate of reproduction, and an increased risk of dying, compared with cells that inherited newer poles, Stewart and his colleagues report in the February PLoS Biology. The team attributes these detriments simply to old age.

These results "suggest that aging is a fundamental aspect of all cells," comments Martin Ackermann of ETH, the Swiss Federal Institute of Technology in Zurich. Even so, he says, "the next important question should be, Are there any organisms that can't age?"

Taddei notes that he doesn't expect scientists to find a truly immortal form of life. Many researchers suspect that as organisms live, their cells develop subtle flaws that contribute to the aging process. Although cells have a variety of methods to fix these flaws, Taddei says, the self-repairing mechanisms may be too costly to permit cells to maintain themselves in perfect working order.

"It's like if you took your car to the garage every day," says Taddei. "You could replace every component of the car, and we can hope that it wouldn't age, but it would be very expensive."

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References:

Stewart, E.J. … and F. Taddei. 2005. Aging and death in an organism that reproduces by morphologically symmetric division. PLoS Biology 3(February):e45. Abstract.

Further Readings:

Ackermann, M., S.C. Stearns, and U. Jenal. 2003. Senescence in a bacterium with asymmetric division. Science 300(June 20):1920. Full Text.

Kirkwood, T.B.L., and R. Holliday. 1979. The evolution of aging and longevity. Proceedings of the Royal Society of London B 205:531–546.

Nyström, T. 2002. Aging in bacteria. Current Opinion in Microbiology 5(Dec. 1):595–601. Abstract.

Sources:

Martin Ackermann
ETH Zürich
Ecology and Evolution
ETH Zentrum, NW
CH-8092 Zürich
Switzerland

Eric J. Stewart
Génétique Moléculaire Evolutive et Médicale
U571 INSERM
Faculté Necker-Enfants Malades
156 rue de Vaugirard
75730 Paris Cedex 15
France

François Taddei
Génétique Moléculaire Evolutive et Médicale
U571 INSERM
Faculté Necker-Enfants Malades
156 rue de Vaugirard
75730 Paris Cedex 15
France


From Science News, Volume 167, No. 6, February 5, 2005, p. 84.