The Gates of Immortality

Did biology evolve a way to protect offspring from the ravages of aging by creating a physical barrier that separates the parent from its young?

he idea that every organism must age was a concept that surprised many biologists. For a long time, aging was thought to be a process occurring only in multicellular organisms. The reason for this arguably odd presumption was that we knew somatic cells—such as those that comprise the kidney, brain, and liver—lost their functionality over time: they aged. Furthermore, those cells divided only a limited number of times, around 50, after which they reached the so-called Hayflick limit, stopped proliferating, and died.

Unicellular organisms were thought to be capable of dividing forever, as long as conditions allowed: one generation begetting the next down through time—a sort of immortality. If unicellular organisms were like somatic cells, then they would age as they divide, reach the Hayflick limit, and die.

It wasn’t until the 1950s that researchers who thought about aging began to change their minds. It became clear that the daughter cells of some unicellular organisms seemed to rejuvenate, to start from scratch, while the mother cells accumulated the cellular aberrations that signaled aging. This pattern of aging was seen in such evolutionarily distant organisms like Saccharomyces cerevisiae, known as budding or baker’s yeast, and bacteria such as Caulobacter crescentus and Escherichia coli.1–3 Aging, it seems, is a universal property of all living beings.

For me, that realization begged a more fundamental question, one that as biologists, we are scarcely allowed to ponder: Why do cells allow some mistakes to accumulate? If evolution is such a powerful process—one that finds solutions to all manner of problems—how could there be processes or problems that can’t be fixed?

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