Lucky in Life, Prologue

I’ve been meaning to write for a long time about the role of chance … luck … whatever you want to call it … in life, from the grand sweep of evolution to our individual existence.

Well, just this morning, I came pretty close to demise by random genetic drift. Almost every weekday, I walk to and from work at Michigan State University. It’s a pleasant walk through pretty neighborhoods and the beautifully landscaped MSU campus.

Today was not much different from most other days. It had been sprinkling lightly, but no wind or anything out of the unusual.

I walked the route I usually take, crossing the streets by habit in more or less the same spots every time, I guess. The only moderately big road I cross is Grand River Avenue, where it intersects with Bogue Street. No problem on Grand River.

I walk down Bogue on the east side or the west side of the street depending on the traffic light, where cars are, on whimsy I guess. I was walking on the east side, though I would have to cross over to the west to get to the building where I work.

At this point in my walk, I’d guess that’s the side I’m still on maybe 80% of the time. Lucky today was one of those days. I heard a loud crack on the other side of the street. A tree limb snapped and crashed hard on the sidewalk.

Maybe half a second from snap to crash? And the limb was big and bifurcating, with two main branches, each maybe a foot in diameter. It came down straight, square and hard against the sidewalk. Even if you had an instant to react, it wouldn’t be clear which way to run to avoid one branch and not get smacked by the other.

I wasn’t the only lucky one. No one was there to get hit. A student was walking toward the spot, maybe 100 feet away. I called out something like “That was crazy, lucky you weren’t there.” He nodded and crossed to my side of the street.

It was only in walking the next couple hundred feet that I realized I had been lucky, too, to be walking this morning on the east side and not the west side of the road.

Indeed, each of us is incredibly lucky just to be here—the product of billions of generations of parents who were not only fit enough to survive and reproduce, but also lucky enough to have escaped the random drift of life and death.

[Both photos: Richard E. Lenski.]

Added November 1:  The second tree to come after me this autumn … or maybe I should say this fall.  This one was much smaller but fell just a few steps behind me on my morning run!

[Photo: Madeleine Lenski]

A Wild Weekend

My wife Madeleine and I had a wild Memorial-day weekend.

Late Saturday afternoon, a dog found a baby squirrel, perhaps 5 or 6 weeks old, and chased it through our fence. The poor squirrel appeared to be in shock—its back was wet; it had probably been mouthed by the dog—but otherwise unharmed. We tried putting the baby squirrel on a protected tree branch in hopes that its mother would come and rescue it, but that did not happen and it did not budge … and nighttime was approaching.

So we brought the squirrel inside, and placed him in a secure container with rags to keep warm overnight. We hoped he would survive.

Indeed, the next morning, little “Nutcase” was dry and warm and, while still scared, on close inspection he seemed healthy and acting much stronger. You can see me holding him in the picture below.

On Sunday, we found a local wildlife rescue shelter that already had 20 other baby squirrels. There’s evidently been a bumper crop of the little fellas this year. Rearing them with others of their species, and with appropriate food and shelter, gives the foundlings a better chance of surviving when they are released back into the wild. Good luck, little Nutcase!

That wasn’t the end, though, of our wild weekend. On Monday, as Madeleine helped our daughter clean a garden shed, they disturbed a mother deer mouse living in a lawn-care bag with seven nursing pups.

The bag had been moved outside the shed before the mice were discovered. Mama mouse ran and, along with one of the pups, she hid right next to the bag inside a dense roll of wire fencing, the type used to protect young trees from browsing deer. But mama mouse did not abandon her pups!

We moved the other six pups and the nesting material into a more suitable container back inside the shed. We also carried the roll of wire fencing, along with mama mouse and that one pup, back into the shed. The next challenge—and it took us a couple of hours—was to coax mama mouse and that pup out of the fencing and into the container with the other six pups.

Success! Mama mouse was reunited with all her babies, and she promptly set out to nurse them. We gave her some bits of fruit and nuts, and a jar lid with water, to help her get over her stress and back to her work raising her family.

It’s amazing how invested one gets in helping wildlife survive, especially after meeting them “in person.”

Infectiously Fun Science

Science is sometimes frustrating. The work is often repetitive and even tedious. It can be hard to explain to our friends and families—and sometimes even to peers—what we’re doing and why we think it’s important and interesting. The current state of the academic job market is terrible.

But science is also often fun. There’s the joy of discovery, which grows out of the quieter excitement of seeing data come together to support or refute an existing idea and, perhaps, to generate a brand-new idea. If we’re lucky, we enjoy the recognition of our peers that comes when a paper is accepted, a grant funded, or a talk well received.

For those of us who study evolution, the frustrations can be magnified by critics and trolls who aren’t interested in evidence or reason, having already closed their minds to even the idea of evolution based on their narrow, literal reading—or, more often, someone else’s reading—of texts written in other languages long before science provided an evidence-based way to understand the world in which we live.

At the same time—and perhaps driven in part by the controversy surrounding evolution and religion—the field of evolution has long been blessed with great writers and speakers who are willing and able to engage the public. Twenty years before he published On the Origin of Species, Charles Darwin had already cemented his place in the public eye with his travelogue The Voyage of the Beagle. As a result, the Origin was an instant best seller on both sides of the Atlantic. And while Darwin shied away from speaking in public about his discoveries, Thomas Henry Huxley was a gifted orator who became “Darwin’s Bulldog” in public lectures and debates.

That tradition continues to this day. Some of my favorites include The Selfish Gene by Richard Dawkins, Wonderful Life by the late Stephen Jay Gould, Darwin’s Dangerous Idea by Daniel Dennett, and Your Inner Fish by Neil Shubin. Experts argue about scientific issues, minor and even major, contained in these books. But it’s hard for me to imagine an open-minded reader, someone interested in science and evolution, who would not find these books highly stimulating—even infectious in the sense of wanting to share them and the ideas they contain with others.

And speaking of infectious, new ways of communicating science have burst onto the scene since the printing press. For example …

Baba Brinkman is a rapper who raps about science, literature, public policy, and more. For your scientific enjoyment, here are three of my favorites from The Rap Guide to Evolution:

Performance, Feedback, Revision

Creationist Cousins

I’m A African

Here’s another from The Rap Guide to Human Nature:

Short Term Mating Dance

And here’s a brand-new one—on microbiology and disease—with a cameo appearance by yours truly and three students who work in my lab:

So Infectious

Whether you’re a scientist or not, I hope you’ll agree that these are worth sharing with your students, friends, and families!

[Image source: music.bababrinkman.com/album/the-rap-guide-to-evolution]

Chao and Levin, 1981, PNAS

This is the third in my series of must-read papers.  It’s an elegant paper that sits right at the interface of ecology, evolution, and behavior.  And like the last paper that I wrote about, this one is superb for teaching and capturing the interest of students.

Chao, L., and Levin, B. R.  1981. Structured habitats and the evolution of anticompetitor toxins in bacteria.  Proc. Natl. Acad. Sci. USA 78, 6324-6328.

Short summary:  Some bacterial strains produce and release toxins that kill members of their own species – except, that is, close kin that possess a linked immunity function.  The production of the toxins is also lethal to the small fraction of cells that actually do so in any given generation.  Lin Chao and Bruce Levin sought to understand when and how this trait would be beneficial.  When killer and sensitive strains competed in liquid, the killer strain prevailed, but only if it started out above a threshold frequency.  That raised the question of how the killer strain could reach that frequency, because it was at a disadvantage when it was below that threshold.  When the same strains competed in a structured environment (a gel-like matrix), this conundrum was resolved—the killer strain could invade a population of sensitive cells even if the killers started at an arbitrarily low frequency.  The difference arises because, in the structured environment, the resources made available by the killers accrue disproportionately to the killers’ kin.  This paper was ahead of its time, but it set the conceptual stage for the now-blossoming field that uses microbes to study the evolution of social traits and interactions.

Some additional background and explanation:  Many bacteria can produce and release toxins that kill other members of the same species.  These toxins are called bacteriocins in general; those studied by Chao and Levin are also called colicins because they are produced by, and used against, E. coli.  The toxin production and immunity functions are tightly linked in a genetic module, and such modules are often located on extra-chromosomal elements called plasmids.  Interestingly, the production of the toxin is lethal to the individual cell that does so, because the cell must lyse to release the toxin.  However, only a small proportion (maybe 1%) of the potential killers that carry the toxin/immunity module actually produce toxin in a given generation, while the others constitutively express the immunity function.

How can a function evolve that is lethal to the individual organism that expresses it?  Chao and Levin began by competing two otherwise identical E. coli strains—one that carries the toxin/immunity module, the other sensitive to the toxin—in a well-mixed liquid medium.  Let’s call the strains K and S for killer and sensitive, respectively.  If there were enough K cells (above ~2% in their experimental conditions), then K rose in frequency and drove the S type extinct.  Although the K population experienced some deaths from the production of the toxin, the resulting toxin concentration was so high that the death rate of S exceeded its growth rate.

But if the initial frequency of the K type was below that ~2% threshold, then the outcome was reversed—the S population rose in frequency, and the K population declined, although the exclusion played out more slowly than when K started out above the threshold.  What’s happening here?  The K cells still had the extra cell deaths caused by the release of toxin, but the concentration of toxin was not sufficient to wipe out the S population.  Some S cells were killed, and their resources—those released upon their death plus those they could no longer consume—became available to other cells.  Because the competition environment was well mixed, any cell—whether K or S—had equal access to the freed-up resources.  If the death rate of the K type (the proportion that produces toxin and then lyses) were greater than the kill rate of the S type, then K would decline in frequency because the resulting benefit—the extra resource that became available—was equally available to all survivors, regardless of whether they had the K or S genotype.

From an ecological standpoint, it’s a nice example of a dynamically unstable equilibrium between two competitors.  However, it raises a problem from an evolutionary perspective.  If possession of the toxin/immunity module is beneficial when it is common in a population, but disadvantageous when it is rare, then how can it go from being rare to common?

Chao and Levin recognized that a physically structured environment might be important, because it would change the distribution of the freed-up resources to the two cell types.  So they repeated the competitions between K and S strains, again varying the initial frequency of the K type, except now in a semi-solid medium called “soft agar.”   (The procedures get more complicated here; to propagate the competing cell types, each day they had to free the cells from the soft-agar matrix and transfer them into a new matrix.)  When the two types competed in this structured environment, the unstable equilibrium disappeared, and the K strain could invade and take over from an arbitrarily low initial frequency.  That is, the K genotype could now go from being rare to common.

Why this difference between the liquid and semi-solid environments?  In the structured environment, the bacteria grew as colonies, not as individuals floating about at random.  As a consequence, the extra resources made available by the killers flowed disproportionately to their own kin.  Here a picture is worth a thousand words; I show a figure from Chao and Levin below that makes this point graphically.  In a sea of crowded S colonies, there’s one K colony.  The K colony is larger than most of the S colonies.  Each colony began from a single cell; the fact that the K colony is larger than most means that it got more than its share of resources.  Even more strikingly, the K colony is surrounded by a large zone that is entirely devoid of colonies—the toxins released by the small proportion of K cells that lysed have diffused into this zone and prevented growth of S cells.  The resources diffused randomly, but the K colony sat alone in the middle of this zone of inhibition that it generated, and so indeed it got more than its share of resources.

The figure above is from Chao and Levin, 1981, Proc. Natl. Acad. Sci. USA; it is shown here under the doctrine of fair use.  The image is centered on a single colony of toxin-producing bacteria surrounded by an inhibition zone and, further out, by colonies of sensitive bacteria.  The scale bar is 0.5 mm.

A Later, Related Paper:  There’s another nice paper by Ben Kerr, Peg Riley, Marc Feldman and Brendan Bohannan (2002, Nature) that builds on the work by Chao and Levin.  Kerr et al. added a third “player”—a third strain—into these experiments, one that was resistant to the toxin but did not produce it.  In a physically structured environment, the toxin-producing killer strain could invade and displace the sensitive strain, just as Levin and Chao saw.  However, the resistant strain could invade and displace the toxin-producer, because the physiological cost of resistance was less than the combined costs of toxin-production and immunity.  And the sensitive strain could invade and displace the resistant strain, because the sensitive strain did not pay the cost of resistance.  In other words, the pairwise interactions were non-transitive, just like the game of rock-paper-scissors.  But although each pairwise interaction had a winner and a loser, the three types could coexist indefinitely in a spatially structured environment provided different spatial regions were out of phase—in effect, the three populations chased one another around in space and time.

Why I like this paper so much:  First, the paper by Chao and Levin beautifully illustrates how population biologists frame, dissect and analyze a complex problem—one that involves frequency-dependent effects, tradeoffs, spatial structure, and genetic relatedness along with both scramble and interference competition.  Out of all these complications, there comes that “Aha!” moment when it all makes sense—just like the feeling one gets from the Luria and Delbrück experiment.

Second, there’s been a boom in the study of the evolution of social behaviors using microbes over the last 15 years or so.  The current phase began with papers by Paul Tuner and Lin Chao on interactions among viruses infecting the same cell leading to a Prisoner’s Dilemma (Nature, 1999); by Greg Velicer, Lee Kroos, and myself on cheating during multicellular fruiting-body development in the bacterium Myxococcus xanthus (Nature, 2000); and by Joan Strassmann, Yong Zhu, and David Queller on cooperation and cheating in aggregations of the social amoeba Dictyostelium discoideum (Nature, 2000).  Today, there are many groups around the world who study quorum sensing, fruiting-body formation, biofilms, toxin degradation, and other microbial behaviors from an evolutionary perspective.  The 1981 paper by Chao and Levin showed that microbial systems could serve as model systems for studying social evolution while being fascinating in their own right.  (It’s also fitting to note that John Bonner, who pioneered the study of D. discoideum, served as the editor for Chao and Levin’s paper.)

Third, Bruce Levin was my postdoctoral mentor, and Lin Chao did his graduate work with Bruce.  Lin had moved on to a postdoc position before I joined the lab, but this paper was one of my formative exposures to the conceptual elegance and experimental power of using microbes to study population dynamics.  Lin and Bruce had also written two papers on the dynamics of interactions between bacteria and phage (Levin et al., 1977, Am. Nat.; Chao et al., 1977, Ecology), and those papers were the ones that first led me to write Bruce about the possibility of joining his group as a postdoc.

Finally, this paper provides a sobering reminder that we humans are not as special as we often imagine, even in warfare.  Mindless bacteria were killing each other billions of years before we came on the scene.  Perhaps we can use our minds to suppress the worst of our primal urges.

[ADDED 13 Sept. 2013] Lin Chao emailed me that “The inspiration of that work was a lecture that Bruce gave in his Pop Biology class at UMass where he discussed the limitations of Lotka Volterra equations for interference competition.  That sat in my mind for a couple of years until it became a real project.” So this must-read paper also provides a nice example of the productive interplay between teaching and research.