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Bacterial Time-Turner

May 17, 2015


Bacteria Lab students are wrapping up a paper on “polar aging” of E. coli. What does that mean? Every time a bacterial cell divides, each daughter cell inherits an old pole (preexisting cell division) and a new pole (formed by division). Inevitably, a line of cells inherits an old pole for many generations. In the colony above, the old poles are marked yellow; the new poles are green, and inbetween generations are marked other colors. The white line marks the divide between two half-lineages of the original ancestral cell, for which we don’t know which pole was old or new. A small portion of a colony lineage is diagrammed:


Under certain conditions, the cell with the superannuated pole (yellow) tires out. You can see where the green-yellow cell has given up dividing. The old-pole cell division slows, and the cell eventually dies of old age–despite inheriting a new pole too. It’s like Rowling’s Death Eater that got its head stuck in a time-turner jar, and turned into a baby’s head: half old and half newborn.

Can bacteria ever “reverse” their “polar age”? Not E. coli, we think–but other kinds of bacteria do. Mycobacteria, which cause tuberculosis, grow differently by extending one pole only (Bree Aldridge, Science 2012).

Myco polar

The extending mycobacterial pole makes a newborn cell that accelerates cell division (Age 2) while leaving behind an old-pole cell that pauses (Age 1). But then–in the next generation, the old pole accelerates division–leaving its new pole behind, suddenly old. In effect, a mycobacterium is a time-turner, its young pole growing old and its old pole growing new. Though not an endless loop, the lineage endlessly generates deadly infectious cells showing age-dependent resistance to various antibiotics.

Why do bacteria age? As best we can tell, they age for the same reason humans do. Humans are animals that partition their biomass into an immortal germ line (the sex cells) and a mortal soma (the rest of our body.) The mortal body (the bacterial old pole) “eats death” by inheriting all the mistakes, the misfolded proteins, while keeping the germ line young. In humans, similarly, our brains accumulate the misfolded proteins associated with Parkinson’s and Alzheimer’s. But our germ line (new pole) remains the potential baby, while it’s still part of one’s own body. Like E. coli, we’re all the hapless Death Eater stuck with half a baby.

  1. May 17, 2015 10:40 pm

    I think your analogy to human germ line and soma cells is forced. But I do have a question. HeLa cells should also have old and new poles. Since they don’t stop dividing at the Hayflick limit, but rather are immortal, is there evidence that they do in fact behave more like your E. Coli?

  2. May 17, 2015 11:06 pm

    HeLa cells with unlimited nutrients will divide forever. However, if you apply stress, I predict that some daughter cells will outgrow others (partitioning damage).
    Yeast cells definitely age; a mother cell buds about twenty daughters before dying.
    E. coli ages (partitions damage) under certain conditions but not others. It depends on whether growth rate or biomass accumulation confers greater fitness.

  3. Merriman Hunter permalink
    May 19, 2015 3:09 pm

    Thank you for another great post 🙂 This work really sets one to thinking, in the best way. I wonder how, evolutionarily, analogous phenomena to that that which your students are characterising here would have fit in with the development of multicellular organisms from once-independent unicellular ancestors? I have a cartoon in my head of a colonial proto-metazoan with each of its members trying to pass off the mortality-can to someone else.

    I guess it would be different in eukaryotic cells but, as you say, some daughter cells (Mini-lineages? What do we call smaller subdivisions of cell-lines?) would surely outgrow others. I wonder if/how the damage partitioning is structured in tissue development and maintenance. And I love your use of the ‘eats death’ phrase; so apt!

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