Tag Archives: science and religion

Does Behe’s “First Rule” Really Show that Evolutionary Biology Has a Big Problem?

Michael Behe has a new book coming out this month called Darwin Devolves. Nathan Lents, Joshua Swamidass, and I wrote a review of that book for the journal Science. (You can also find an open-access copy of our review here.) It provides an overview of the problems we see with his thesis and interpretations. As our review states, Behe points to many examples of evolution in which genes and their functions have been degraded, but he largely ignores the ways that evolution generates new functions and thereby produces complexity. That’s a severe problem because Behe uses the evidence for the ease of gene degradation to support his overarching implication that the current scientific understanding of the mechanisms of evolution is inadequate and, consequently, the field of evolutionary biology has a “big problem.”

I won’t attempt to summarize Behe’s entire book nor our short review, as people can read those for themselves if they want. Instead, I hope to accomplish three things in this post and two more that will follow. In this first post, I explain why Behe’s so-called “first rule of adaptive evolution” does not imply what he says it does about evolution writ large. In the second post, I’ll discuss whether my long-term evolution experiment (the LTEE for short) does or doesn’t provide strong support for Behe’s position in that regard. In my third post, I’ll explain why I think that Behe’s positions, taken as a whole, are scientifically untenable.

I. Behe’s “First Rule of Adaptive Evolution” Confounds Frequency and Importance

Behe’s latest book is centered around what he calls “The First Rule of Adaptive Evolution: Break or blunt any gene whose loss would increase the number of offspring.” As he wrote in an immediate, dismissive response to our review: “The rule summarizes the fact that the overwhelming tendency of random mutation is to degrade genes, and that very often is helpful. Thus natural selection itself acts as a powerful de-volutionary force, increasing helpful broken and degraded genes in the population.”

Let’s work through these two sentences, because they concisely express the thrust of Behe’s book. The first sentence regarding “the tendency of random mutation” is not too bad, though it is overly strong. I would tone it down as follows: “The tendency of random mutation is to degrade genes, and that is sometimes helpful.” My reasons for these subtle changes are that: (i) many mutations are selectively neutral or so weakly deleterious as to be effectively invisible to natural selection; (ii) while loss-of-function mutations are sometimes helpful to the organism, I wouldn’t say that’s “very often” the case (though it may be in some systems, as I’ll discuss in part II); and (iii) even those degradative mutations that are not helpful on their own sometimes persist and occasionally serve as “stepping stones” on the path toward new functionality. This last scenario is unlikely in any particular instance, but given the prevalence of degrading mutations it may nonetheless be important in evolution. (This scenario does not fit neatly within the old-fashioned caricature of Darwinian evolution as only proceeding by strictly adaptive mutations, but it is certainly part of modern evolutionary theory.)

Behe’s next sentence then asserts the power of the “de-evolutionary” process of gene degradation. This is an unjustifiable extrapolation, yet it is central to Behe’s latest book. (It’s not the sort of error I would expect from anyone who is deeply engaged in an earnest effort to understand evolutionary science and present it to the public.) Yes, natural selection sometimes increases the frequency of broken and degraded genes in populations. But when it comes to the power of natural selection, what is most frequent versus most important can be very different things. What is most important in evolution, and in many other contexts, depends on timescales and the cumulative magnitude of effects. As a familiar example, some rhinoviruses are the most frequent source of viral infections in our lives (hence the expression “common cold”), but infections by HIV or Ebola, while less common, are far more consequential.

Or consider an investor who bought stocks in 100 different companies 25 years ago, of which 80 have been losers. Ouch? Maybe not! A stock can’t lose more than the price that was paid for it, and so 20 winners can overcome 80 losers. Imagine if that investor had picked Apple, for example. That single stock has increased in value by well over 100-fold in that time, more than offsetting even 80 total wipeouts all by itself. (In fact, research on the stock market has shown the vast majority of long-term gains result from a small minority of companies that, like Apple, eventually become big winners.)

In the same vein, even if many more mutations destroy functions than produce new functions, the latter category has been far more consequential in the history of life. That is because a new function may enable a lineage to colonize a new habitat or realm, setting off what evolutionary biologists call an “adaptive radiation” that massively increases not only the numbers of organisms but, over time, the diversity of species and even higher taxa. As one example, consider Tiktaalik or some relative thereof, in any case a transitional kind of fish whose descendants colonized land and eventually gave rise to all of the terrestrial vertebrates—amphibian, reptiles, birds, and mammals. That lineage left far more eventual descendants (including ourselves), and was far more consequential for the history of life on Earth, than 100 other lineages that might have gained a transient advantage by degrading some gene and its function before eventually petering out.

Asteroid impacts aren’t common either, but the dinosaurs (among other groups) sure felt the impact of one at the end of the Cretaceous. (There remains some debate about the cause of that mass extinction event, but whatever the cause its consequences were huge.) Luckily for us, though, some early mammals survived. Evolution often leads to dead ends, sometimes as a consequence of exogenous events like asteroids, and other times because adaptations that are useful under a narrow set of conditions (such as those caused by mutations that break or degrade genes) prove vulnerable over time to even subtle changes in the environment. It has been estimated that more than 99% of all species that have ever existed are now extinct. Yet here we are, on a planet that is home to millions of diverse species whose genomes record the history of life.

Summing up, Behe is right that mutations that break or blunt a gene can be adaptive. And he’s right that, when such mutations are adaptive, they are easy to come by. But Behe is wrong when he implies these facts present a problem for evolutionary biology, because his thesis confuses frequencies over the short run with lasting impacts over the long haul of evolution.

[The picture below shows the Tiktaalik fossil discovered by Neil Shubin and colleagues.  It was posted on Wikipedia by Eduard Solà, and it is shown here under the indicated Creative Commons license.]

Tiktaalik

 

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Thirty years is enough

The LTEE has run for over 30 years and almost 70,000 generations. It’s time to shut it down, as of today.

It’s been a hell of a lot of work, and we have almost nothing to show for it. As some astute commentators have noted around the web, the creatures in the flasks are still just bacteria—creatures, just as they were created.

If you read the first LTEE paper*, you’ll see we predicted the bacteria should become yeast by about 5,000 generations, nematodes at 15,000 generations or so, and fruit flies by 30,000 generations, maybe 35,000 at the outside.

After that, we’d have to stop the experiment anyhow, because we wouldn’t be able to freeze and bring them back alive any longer.

Plus, we’d have to get IRB approval for human experimentation if we ran it much past 50,000 generations.

Well, we’ve given the LTEE all this time, and still … they’re just bacteria. I guess we’ve proven that Charles Darwin was wrong after all.

As an astute reviewer pointed out when we submitted that first paper, “I feel like a professor giving a poor grade to a good student …” I should’ve listened and quit way back then. It would’ve saved everyone a lot of time and effort.

Now it’s going to be a hell of a lot of work next week emptying the freezers and autoclaving all those samples.

*Lenski, R. E., M. R. Rose, S. C. Simpson, and S. C. Tadler. 1991. Long-term experimental evolution in Escherichia coli. I. Adaptation and divergence during 2,000 generations. American Naturalist 138: 1315-1341.

 

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What Was I Thinking?

The LTEE has run for over 10,000 days and almost 67,000 generations. It’s time to shut it down, as of today.

It’s been a hell of a lot of work, and we have almost nothing to show for it. As some astute commentators have noted around the web, the creatures in the flasks are still just bacteria—creatures, just as they were created.

If you read the first LTEE paper*, you’ll see we predicted the bacteria should become yeast by about 5,000 generations, nematodes at 15,000 generations or so, and fruit flies by 30,000 generations, maybe 35,000 at the outside.

After that, we’d have to stop the experiment anyhow, because we wouldn’t be able to freeze and bring them back alive any longer.

Plus, we’d have to get IRB approval for human experimentation if we ran it much past 50,000 generations.

Well, we’ve given the LTEE all this time, and still … they ’re just bacteria. I guess we’ve proven that Charles Darwin was wrong after all.

As an astute reviewer pointed out when we submitted that first paper, “I feel like a professor giving a poor grade to a good student.”  I should’ve listened and quit way back then. It would’ve saved everyone a lot of time and effort.

Now it’s going to be a hell of a lot of work next week emptying the freezers and autoclaving all those samples.

* Lenski, R. E., M. R. Rose, S. C. Simpson, and S. C. Tadler. 1991. Long-term experimental evolution in Escherichia coli. I. Adaptation and divergence during 2,000 generations. American Naturalist 138: 1315-1341.

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On the Evolution of Citrate Use

Those who follow the long-term evolution experiment (LTEE) with E. coli know that the most dramatic change we have observed to date is the origin of the new ability to grow on citrate. It’s dramatic for several reasons including the fact (external to the LTEE) that E. coli has been historically defined as a species based in part on its inability to grow on citrate in oxic environments and the fact (internal to the LTEE) that it was so difficult for the bacteria to evolve this ability that only one of the populations did so, and that it took over 30,000 generations even though an abundance of citrate has been present in the medium throughout the LTEE. Even after 64,000 generations, only the Ara–3 population has evolved that new ability.

Zachary Blount, formerly a graduate student and now a postdoc in my lab, has spent the last decade studying the evolution of this population and its new ability. His two first-authored papers in PNAS (2008) and Nature (2012) demonstrated, respectively, that (i) the origin of the ability to grow on citrate in the LTEE was contingent on one or more “potentiating” mutations that happened before the “actualizing” mutation that conferred the new function first appeared, and (ii) the actualizing mutation was a physical rearrangement of the DNA that brought together a structural gene, citT, that encodes a transporter and a previously unconnected regulatory region to generate a new module that caused the phenotypic transition to Cit+. These papers presented and discussed much more than these two points, of course, but they are the key findings. More recently, Zack was a coauthor on a paper in eLife (2015) by Erik Quandt, Jeff Barrick, and others that identified two mutations in the gene for citrate synthase—one that potentiated the evolution of citrate utilization, and another that subsequently refined that new function.

So we were keenly interested when we saw a new paper titled “Rapid evolution of citrate utilization by Escherichia coli by direct selection requires citT and dctA” by Dustin Van Hofwegen, Carolyn Hovde, and Scott Minnich. The paper is posted online as an accepted manuscript by the Journal of Bacteriology. What follows here are some overall impressions of their paper that Zack and I put together. We may follow these impressions later with some further analysis and comments.

* * * * *

Let’s begin by saying that it’s great to see other groups working on interesting systems and problems like the evolution of citrate utilization in E. coli.

Moreover, the actual science that was done and reported looks fine and interesting, though we have a few quibbles with some details that we will overlook for now. By and large, the work confirms many of the findings that were reported in our papers cited above:

(i) the ability to grow on citrate in the presence of oxygen can and does evolve in E. coli (Blount et al., 2008);

(ii) when aerobic growth on citrate evolves, it does not do so quickly and easily (Blount et al., 2008) but instead takes weeks or longer—more on that below;

(iii) all strains that have evolved this new ability have physical rearrangements that involve the citT gene and appear also to involve a so-called “promoter capture” whereby a copy of this transporter-encoding gene acquires a new upstream regulatory region (Blount et al., 2012); and

(iv) genetic context matters—the strain one uses affects the likelihood of evolving the Cit+ function (Blount et al., 2008) and the resulting ability to grow on citrate (Blount et al., 2012; Quandt et al., 2015).

The problem, then, is not with the experiments and data. Rather, the problem is that the results are wrapped in interpretations that are, in our view, flawed and fallacious.

“No new genetic information”

The authors assert repeatedly (last sentence of their Importance statement, and first and last paragraphs of their Discussion) that “no new genetic information evolved.” However, that statement flatly contradicts the fact that in their experiments, and ours, E. coli gained the new ability to grow on citrate in the presence of oxygen. We would further add (which we have not emphasized before) that these Cit+ strains can grow on citrate as a sole carbon source—when E. coli grows anaerobically on citrate, it requires a second substrate for growth in order to use the citrate (a phenomenon called “co-metabolism”).

The claim that “no new genetic information evolved” is based on the fact that the bacteria gained this new ability by rearranging existing structural and regulatory genetic elements. But that’s like saying a new book—say, Darwin’s Origin of Species when it first appeared in 1859—contains no new information, because the text has the same old letters and words that are found in other books.

In an evolutionary context, a genome encodes not just proteins and patterns of expression, but information about the environments where an organism’s ancestors have lived and how to survive and reproduce in those environments by having useful proteins, expressing them under appropriate conditions (but not others), and so on. So when natural selection—that is, differential survival and reproduction—favors bacteria whose genomes have mutations that enable them to grow on citrate, those mutations most certainly provide new and useful information to the bacteria.

That’s how evolution works—it’s not as though new genes and functions somehow appear out of thin air. As the bacterial geneticist and Nobel laureate François Jacob wrote (Science, 1977): “[N]atural selection does not work as an engineer works. It works like a tinkerer—a tinkerer who does not know exactly what he is going to produce but uses whatever he finds around him, whether it be pieces of string, fragments of wood, or old cardboards; in short, it works like a tinkerer who uses everything at his disposal to produce some kind of workable object.”

To say there’s no new genetic information when a new function has evolved (or even when an existing function has improved) is a red herring that is promulgated by the opponents of evolutionary science. In this regard, it seems relevant to point out that the corresponding author, Scott Minnich, is a fellow of the Discovery Institute and was an expert witness for the losing side that wanted to allow the teaching of “intelligent design” as an alternative to evolution in public schools in the landmark Kitzmiller v. Dover case.

“Rapid evolution of citrate utilization”

In the title of their paper and throughout, Van Hofwegen et al. emphasize that, in their experiments, E. coli evolved the ability to grow aerobically on citrate much faster than the 30,000 generations and ~15 years that it took in the LTEE. That’s true, but it also obscures three points. First, we already demonstrated in replay experiments that, in the right genetic background and by plating on minimal-citrate agar, Cit+ mutants sometimes arose in a matter of weeks (Blount et al. 2008). Second, rapid evolution of citrate utilization—or any evolution of that function—was not a goal of the LTEE. So while it is interesting that Van Hofwegen et al. have identified genetic contexts and ecological conditions that accelerate the emergence of citrate utilization (as did Blount et al., 2008), that in no way undermines the slowness and rarity of the evolution of this function in the context of the LTEE (or, for that matter, the rarity of Cit+ E. coli in nature and in the lab prior to our work). Third, the fastest time that Van Hofwegen et al. saw for the Cit+ function to emerge was 19 days (from their Table 1), and in most cases it took a month or two. While that’s a lot faster than 15 years, it’s still much longer than typical “direct selections” used by microbiologists where a readily accessible mutation might confer, for example, resistance to an antibiotic after a day or two.

So while we commend the authors’ patience, we do not think the fact that their experiments produced Cit+ bacteria faster than did the LTEE is particularly important, especially since that was not a goal of the LTEE (and since we also produced them much faster in replay experiments). However, in a manner that again suggests an ulterior nonscientific motive, they try to undermine the LTEE as an exemplar of evolution. The final sentence of their paper reads: “A more accurate, albeit controversial, interpretation of the LTEE is that E. coli’s capacity to evolve is more limited than currently assumed.” Alas, their conclusion makes no logical sense. If under the right circumstances the evolution of citrate utilization is more rapid than it is in the LTEE, then that means that E. coli’s capacity to evolve is more powerful—not more limited—than assumed.

“Speciation Event”

To us, one of the most interesting facets of the evolution of the citrate-using E. coli in the LTEE is its implications for our understanding of the evolutionary processes by which new species arise. Part of the reason for this interest—and the one that’s most easily stated in a popular context—is that the inability to grow on citrate is part of the historical definition for E. coli as a species, going back almost a century. But the deeper interest to us lies not in labeling a new species or debating where to draw the line between species—various criteria are used by different scientists, and inevitably there are many cases that lie in grey areas. Rather, as evolutionary biologists, we are most interested in the process of speciation—the ecological and genetic dynamics that lead to changing biological forms that, over time, are more and more like a new species until, eventually, perhaps far in the future, there is no doubt that a new species has evolved.

In short, speciation is not an event. As Ptacek and Hankison (2009, in Evolution: The First Four Billion Years) put it, “[S]peciation is a series of processes, with a beginning stage of initial divergence, a middle stage wherein species-specific characteristics are refined by various forces of evolution, and an end point at which a new species becomes a completely separate evolutionary lineage on its own trajectory of evolutionary change with the potential for extinction or further diversification into new lineages.” We realize that scientists (ourselves included) often use shorthand and jargon instead of writing more carefully and precisely. We have no doubt that one can find solid scientific papers that talk about speciation events; but except for cases that involve hybridization leading to polyploids that are reproductively isolated in a single generation (as sometimes occurs in plants), this is simply an imprecise shorthand.

In our first paper on the citrate-using E. coli that arose in the LTEE, we clearly emphasized that becoming Cit+ was only a first step on the road to possible speciation (Blount et al., 2008). One criterion that many biologists would apply to investigate speciation is whether a later form merely replaced an earlier form (evolution without speciation) or, alternatively, one lineage split into two lineages that then coexisted (incipient speciation). In fact, we showed that, after the new function evolved, the Cit+ and Cit lineages coexisted (and their coexistence was confirmed using genomic data in Blount et al., 2012). We concluded the 2008 paper by asking explicitly: “Will the Cit+ and Cit– lineages eventually become distinct species?” (emphasis added) and discussing how we might assess their ongoing divergence.

By contrast, Van Hofwegen et al. dismiss the idea of speciation out of hand, not only by calling it an event but by treating the issue as though it hinges, literally, on the individual mutations that produced a Cit+ cell. For example, they write: “[B]ecause this adaptation did not generate any new genetic information … generation of E. coli Cit+ phenotypes in our estimation do not warrant consideration as a speciation event.” And in the penultimate sentence of their paper, they say: “[W]e argue that this is not speciation any more than any other regulatory mutant of E. coli.” (We also note that this is a rather bizarre generalization, as though the gain of function that gave access to a new resource is equal in regards to its speciation potential to, say, the loss of regulation of a function that is no longer used by a lineage in its current environment. Both might well be adaptations, but one seems much more likely to begin the process of speciation.)

In conclusion, Van Hofwegen, Hovde, and Minnich have done some interesting experiments that shed further light on the nature of the mutations and ecological conditions that allow E. coli cells to evolve the ability to grow aerobically on citrate, a function that this species cannot ordinarily perform. However, they misunderstand and/or misrepresent the relevance of this system for evolutionary biology in several important respects. 

And the meaning of historical contingency

The paper by Hofwegen et al. is accompanied by a commentary by John Roth and Sophie Maisnier-Patin. Their abstract begins: “Van Hofwegen et al. demonstrate that E. coli rapidly evolves ability to use citrate when long selective periods are provided. This contrasts with the extreme delay (15 years of daily transfers) seen in the long-term evolution experiments of Lenski and coworkers. Their idea of ‘historical contingency’ may require reinterpretation.”

Historical contingency is a complicated notion, but it essentially means that history matters. In Blount et al. (2008), we made it clear what we mean by historical contingency in the context of the evolution of the Cit+ lineage in one of the LTEE populations. Was this an extremely rare event that could have happened at any time? Or did it instead depend on the occurrence of a sequence of events, a particular history, whereby an altered genetic context evolved—a potentiated background—in which this new function could now evolve?

Roth and Maisnier-Patin’s suggestion that our idea of “historical contingency” may require reinterpretation reflects a false dichotomy between historical contingency, on the one hand, and the effects of different selection schemes, on the other. The fact that evolution might be fast and not contingent on genetic background (though the evidence of Van Hofwegen et al. is, at best, ambiguous in this regard) in one set of circumstances has no bearing on whether it is contingent in another set of circumstances. The historical contingency of Cit+ evolution is not mere conjecture. We showed that the evolution of this new function in the LTEE was contingent. In replay experiments, Blount et al. (2008) showed that that the Cit+ trait arises more often in later-generation genetic backgrounds than in the ancestor or early-generation backgrounds. Moreover, Blount et al. (2012) performed genetic manipulations and showed that a high-copy-number plasmid carrying the evolved module that confers the Cit+ function had very different phenotypic effects when put in a Cit clone from the lineage within which Cit+ evolved than when placed in the ancestor or even other late-generation lineages not on the line of descent leading to the emergence of the Cit+ bacteria. In the clone on the line of descent, this module conferred strong, immediate, and consistent growth on citrate. In the other genetic backgrounds, growth on citrate was weak, delayed, and/or inconsistent.

The hypothesis of historical contingency is not mutually exclusive with respect to causal factors of an ecological or genetic nature—it simply says that factors that changed over time were important for the eventual emergence of Cit+. Moreover, historical contingency was invoked and demonstrated in a specific context, namely that of the emergence of Cit+ in the LTEE—it does not mean that the emergence of Cit+ is historically contingent in other experimental contexts, nor for that matter that other changes in the LTEE are historically contingent—in fact, some other evolved changes in the LTEE have been highly predictable and not (or at least not obviously) contingent on prior mutations in the populations (e.g., Woods et al., PNAS, 2006). [For more on historical contingency and the LTEE, you can download a preprint of Zack’s latest paper from his website: Blount, Z. D. A Case Study in Evolutionary Contingency. Studies in the History and Philosophy of Biology and Biomedical Sciences.]

Erik Quandt offers this analogy to illustrate our point that contingency depends on context: “It’s kind of like the difference between being an average person attempting to dunk a basketball when all by yourself, with unlimited time, and maybe even with a trampoline versus having to get to the rim in a game with LeBron James and the Cavs playing defense. Just because you can do it by yourself under optimal conditions, does this negate the difficulty of doing it in an NBA game or say anything about the kind of history (training and/or genetics) that you would need for that situation?”

* * * * *

LTEE lines centered on citrate #11

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Through the Wormhole with Science Communication

As a scientist, I spend a lot of my time trying to communicate subtle ideas and complex results to other scientists who, to a first approximation, share my interests and vocabulary. When I’m not doing that, I also spend a fair bit of time teaching students who are learning about science and, in some cases, trying to become scientists.

But it can be fun and interesting to step outside the usual communication channels by trying to explain our scientific research to people who aren’t scientists or students.

Last fall, I was invited to explain our research on the show Through the Wormhole with Morgan Freeman. The show’s director Tony Lund spoke with me at length by phone, asking questions about scientific concepts, our work, my personal interests, etc.

Based on our conversation, Tony came up with several ideas for scenes to film, both inside and outside the lab. The people in my lab group organized the props and materials that we would need to film the scenes, and several of them also had cameo roles in the various scenes.

Tony then came to MSU, along with veteran cameraman Max Miller. They spent over 12 hours with me, filming scenes in a studio and the lab, and asking countless questions on and off camera. I was impressed by the combination of creativity and attention to detail they brought to this work. For me, it was both exciting and exhausting.

Tony then had to take the hours of film and edit it all down to just a few minutes, while adding interesting visuals and preparing the script for the distinctive style and perspective of the show’s host and narrator, Morgan Freeman.

You can see the fruit of everyone’s labor here, in this four-minute segment: Evolution is Like Poker.

My lab’s portion of the show ran a bit longer than this clip, but this is the bulk of it. A lot of time and effort went into making those few minutes of the show, but I think it was well worth it. I understand the show has over a million viewers, and I hope some of them will have a better understanding of evolution, our place in nature, and the joy of science.

So thanks Tony Lund, Max Miller, Morgan Freeman, Kim Ward in MSU’s communication office, everyone who helped with logistics and production, and all the members of the team, past and present, who have kept the LTEE going … and going … and going.

 

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Science Communication: Where Does the Problem Lie?

When concerns arise about the public’s understanding of science—say, on the efficacy of vaccines vs. their risks—I see many articles, tweets, etc., bemoaning poor scientific communication. Communication involves multiple parties and several steps. The science must be published, discussed widely, explained openly, and eventually stated in terms that non-specialists can understand. It also must be heard—and not merely heard, but fairly considered, carefully weighed, and then accepted, rejected, or put on hold by the intended receiver. That’s not all, of course. There are generally intermediaries—including teachers, reporters, doctors, business interests, politicians, religious leaders, and others—who must also convey the scientific information, but who may block, change, confuse, or distort the message either accidently or deliberately. And none of this is a one-way flow of information. There are multiple voices, and there are feedbacks as questions are asked, answered in new words or with new evidence, and so on. So it’s a complex problem, too complicated for a poll to shed much light. And of course, a poll here will get a highly non-random sample—mostly scientists, students, and others with an interest in science. But perhaps some professional pollster or organization interested in the communication of science can develop a proper poll along these lines (with information about a respondents’ professions, ages, affiliations, etc.), and with proposals about how to improve the situation at the various roadblocks. (Or maybe similar polls already exist. Please feel free to suggest useful references in the comments.) It might also be interesting to run the same poll except with prompts about different issues such as vaccinations, global change, and evolution. So here’s the poll: If you had to say, which one of the following groups shoulders the greatest blame, and thus has the greatest room for improvement, when it comes to the problems of communicating science?

  • Scientists
  • Professional intermediaries such as teachers, reporters, and doctors
  • Other intermediaries such as businesses, politicians, and religious leaders
  • The public

[The image below is from the British Council / BBC World Service site on teaching English. It is shown here under the doctrine of fair use.]

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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]

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