Martincorena et al. estimated synonymous diversity () across 2,930 orthologous gene alignments from 34 Escherichia coli genomes, and found substantial variation among genes in the density of synonymous polymorphisms. They argue that this pattern reflects variation in the mutation rate per nucleotide () among genes. However, the effective population size (N) is not necessarily constant across the genome. In particular, different genes may have different histories of horizontal gene transfer (HGT), whereas Martincorena et al. used a model with random recombination to calculate . They did filter alignments in an effort to minimize the effects of HGT, but we doubt that any procedure can completely eliminate HGT among closely related genomes, such as E. coli living in the complex gut community.
Here we show that there is no significant variation among genes in rates of synonymous substitutions in a long-term evolution experiment with E. coli and that the per-gene rates are not correlated with estimates from genome comparisons. However, there is a significant association between and HGT events. Together, these findings imply that variation reflects different histories of HGT, not local optimization of mutation rates to reduce the risk of deleterious mutations as proposed by Martincorena et al.

Betul Kacar, Eric Gaucher
(Submitted on 23 Sep 2012)

One way to understand the role history plays on evolutionary trajectories is by giving ancient life a second opportunity to evolve. Our ability to empirically perform such an experiment, however, is limited by current experimental designs. Combining ancestral sequence reconstruction with synthetic biology allows us to resurrect the past within a modern context and has expanded our understanding of protein functionality within a historical context. Experimental evolution, on the other hand, provides us with the ability to study evolution in action, under controlled conditions in the laboratory. Here we describe a novel experimental setup that integrates two disparate fields – ancestral sequence reconstruction and experimental evolution. This allows us to rewind and replay the evolutionary history of ancient biomolecules in the laboratory. We anticipate that our combination will provide a deeper understanding of the underlying roles that contingency and determinism play in shaping evolutionary processes.

• “…Selection at intermediate rates of dispersal leads to high niche differentiation between genotypes, allowing greater coverage of the heterogeneous environment & a higher regional productivity.”
• “in situ evolutionary diversification”

Background:

• Two ecological effects considered in relationship betw diversity & productivity – difficult to disentangle
  • Complementarity: niche differentiation, positive interactions (e.g. facilitation) –> more avail. resource can be exploited
  • Sampling: greater richness –> higher probability of containing some high-productivity individuals
• Pop gen & eco models: env heterogeneity & intermediate dispersal considered to be important for emergence & maintenance of polymorphism w/in metapops, species diversity w/in metacomms
• Thus: heterogeneity/dispersal –> diversity –> productivity??

Method:

• Pseudomonas fluorescens: 500 generations, Biolog microplates w/95 diff C sources, 4 dispersal rates
• Optical density taken as measure of productivity

Results:

• Productivity increase greatest at intermed. dispersal – b/c dispersal allows distant specialists to reach more optimal sources
  • Prod lowest at 0% dispersal – only source of variation is local mutation, w/an unhelpfully low eff. pop size
  • Prod @ 100% dispersal slightly lower compared to intermed
  • W/increasing dispersal, move from only bimodal distribution of success on indiv. substrates (i.e. some really good & some really bad eaters) to unimodal over time (all good eaters)
• Ruling out sampling effect:
  • Individual productivity does not increase w/selection - not selecting for individually high-prod genotypes
  • Partitioning variance into G (genotypic variation in productivity), E (variation in growth between substrates – env heterogeneity), GxE (extent to which diff geno react diff to diff substrates – niche variation)
    • further break down GxE into inconsistency (niche differentiation – complementarity – how different are diff genotypes’ responses to substrates?) & responsiveness (diversity of niche breadth w/in metacomm – how narrowly/broadly adapted are diff genotypes?)
    • Inconsistency is the only proportion that varies among dispersal treatments: maximal functional diversity at intermediate dispersal
    • Also find weak positive correlation betw ranked inconsistency & productivity of diff metacomms

Conclusions

• Low/intermed dispersal favors specialists; high dispersal favors generalists (“invasive species” – low inconsistency, high responsiveness [weak data for that]) –> intermediate diversity & productivity
• Inconsistency doesn’t account for all of the correlation betw diversity & productivity – facilitation? potential for which would also be maximized by maximal functional diversity

Great intro to experimental evolution through an interview with Sinead Collins of the University of Edinburgh.

It is a somewhat interesting idea, but note that they are only evolving a single piece of music or a small population, not a program for generating music or rules distinguishing music users like from music users don’t like.  So even after running their experiment for a long time, they only end up with a small amount of music.

They have examples sampled about every 150 generations up to 6000 generations.  I find even the latest generation quite difficult to listen to for more than a minute or so.  Composers need not fear being replaced by this technique any time soon.

Actually, that’s not really true. Biologists generally agree that predators, prey, parasites, and competitors can exert natural selection on the other species they encounter, but we’re still not sure how much those interactions matter over millions of years of evolutionary history.

On the one hand, groups of species that are engaged in tight coevolutionary relationships are also very diverse, which could mean that coevolution causes diversity. But it could be that the other way around: diversity could create coevolutionary specificity, if larger groups of closely-related species are forced into narower interactions to avoid competing with each other.

Part of the problem is that it’s hard to study a species evolving over time without interacting with any other species—how can we identify the effect of coevolution if we can’t see what happens in its absence? If only we could force some critters to evolve with and without other critters, and compare the results after many generations …

Oh, wait. That is totally possible. And the results have just been published.

A team of evolutionary microbiologists has performed exactly the experiment I outlined above. The study’s lead author is Diane Lawrence, a Ph.D. student in the lab of Timothy Barraclough, who is listed as senior author.

For the experiment, the team isolated five bacterial species, of very different lineages, from pools of water at the bases of beech trees—ephemeral pockets of habitat for all sorts of microbes that break down woody debris, dead leaves, and other detritus. They cultured the bacteria on tea made from beech leaves, in vials containing either a single species, or all five species, and let them evolve for eight weeks—several dozens of bacterial generations. In a particularly clever twist on standard experimental evolution methods, they also used nuclear magnetic resonance (NMR) to identify the carbon compounds in sterilized tea that had been “used up” by the bacterial cultures, and compared the compounds in fresh beech tea to determine what the bacteria were eating.

The foot of a beech tree.

And, maybe not surprisingly, the bacterial species’ evolution with company turned out to be quite a bit from their evolution alone. Left alone, most of the species evolved a faster growth rate. This is a common result in experimental evolution, because the process of transferring evolving bacteria to fresh growth medium—”serial transfers” that were performed fifteen times over the course of the experimetn—can create natural selection that favors fast-growing mutants. But, grown all together in the same tube, species that had evolved faster growth rates in the solo experiment evolved slower growth instead.

To find out what had evolved in the multi-species tubes, the team tested the growth of the bacterial species on beech tea that had been used to grow one of the other species, then sterilized. The original, ancestral strains of bacteria generally had negative effects on each others’ growth—they lived on similar compounds in the beech tea, and so their used tea wasn’t very nourishing for the other species. The same thing occurred with the strains that had evolved alone, only stronger, which makes sense in light of the increased growth rates, which would’ve depleted the growth medium faster.

But the interactions among the strains of the different bacterial species that had evolved together was strikingly different. Many of them actually made the tea more nutritious for other species in the evolved community. That is, some of the bacteria had evolved the capacity to eat the waste products of another species that was evolving with them. Using the NMR method to track changes in the presence of different carbon compounds in the tea before and after use provided confirmation that the co-evolved species were using, and producing, complementary sets of resources.

In short, the evolving community didn’t simply become more diverse—it evolved new kinds of mutually beneficial relationships between species that began as competitors.

Beech leaves—yum?

That evolutionary shift toward mutual benefit had a significant impact on the bacterial community as a whole, too. Lawrence et al. assembled new communities of bacteria extracted from the end-point of the group evolution experiment, and compared their carbon dioxide production, a proxy for overall metabolic activity, to that of a community assembled from bacteria extracted from the end point of the solo-evolution experiments. The community of co-evolved bacteria produced significantly more carbon dioxide, suggesting they were collectively able to make more use out of the growth medium.

So that’s a pretty nifty set of results, I have to say. But I’m also left wondering what it tells us more generally. In both Lawrence et al.‘s paper, and in accompanying commentary by Martin Tucotte, Michael Corrin, and Marc Johnson, there’s a fair bit of emphasis on the unpredictability of the result. Lawrence et al. write, in their Discussion section,

The way in which species adapted to new conditions in the laboratory when in monoculture—the setting assumed for many evolutionary theories and experiments—provided little information on the outcome of evolution in the diverse community.

And, as Corrin et al. note,

These results imply that predictions constructed from single-species experiments might be of limited use given that most species interact with many others in nature.

So … evolution went differently under different conditions? That isn’t exactly a shocking revelation. The fact that this is one of the study’s major conclusions is a symptom of how little experimental work has actually tested the effects of multiple species on evolution. One experiment I’ve discussed previously on my own blog, Denim and Tweed, focused on the joint effects of predators and competitors on microbes that live in pitcher plant pitfalls, similarly emphasized the fact that it wasn’t possible to predict the evolutionary effects of predators and competitors together based solely on their individual effects. Work in this line of inquiry is hanging at the point of establishing that complex conditions lead to complex results.

What I’d really like to know—and I think all the authors of both the paper and the commentary would agree with me on this—is how we can begin to make general predictions about community evolution beyond, “it depends what we put in at the start.” It may be that we’ll need a lot more studies like this current one before we can start to identify common processes, and more interesting trends.◼

References

Turcotte, M., Corrin, M., & Johnson, M. (2012). Adaptive evolution in ecological communities. PLoS Biology, 10 (5) DOI: 10.1371/journal.pbio.1001332

Lawrence, D., Fiegna, F., Behrends, V., Bundy, J., Phillimore, A., Bell, T., & Barraclough, T. (2012). Species interactions alter evolutionary responses to a novel environment. PLoS Biology, 10 (5) DOI: 10.1371/journal.pbio.1001330

For their experiments, they used a pair of old enemies: the common gut bacterium and standard lab microbe E. coli, and one of its viruses, the lambda phage. Phages (or bacteriophages, literally “bacterium eaters”) are viruses that infect bacteria. They are also some of mother nature’s funkiest-looking children. Below is an example, because if you haven’t seen one of them, you really should. I borrowed this electron micrograph of phage T4 from GiantMicrobes, where you can get a cute plushie version

Phages work by latching onto specific proteins in the cell membrane of the bacterium, and literally injecting their DNA into the cell, where it can start wreaking havoc and making more viruses. Meyer et al.‘s phage strain was specialised to use an E. coli protein called LamB for attachment.

The team took E. coli which (mostly) couldn’t produce LamB because one of the lamB gene’s regulators had been knocked out. Their virus normally couldn’t infect these bacteria, but a few of the bacteria managed to switch lamB on anyway, so the viruses could vegetate along in their cultures at low numbers. Perfect setup for adaptation!

Meyer and colleagues performed a lot of experiments, and I don’t want to go into too much detail about them (hey, is that me trying not to be verbose???). Here are some of their intriguing results:

First, the phages adapted to their LamB-deficient hosts. They did so very “quickly” in terms of what we usually think of as evolutionary time scales (naturally, “evolutionary time scales” mean something different for organisms with life cycles measurable in minutes). Mutations in the gene coding for their J protein (the one they use to attach to LamB) enabled them to use another bacterial protein instead. Not all experimental populations evolved this ability, but those that did succeeded in less than 2 weeks on average.

The new protein target, OmpF, is quite similar to LamB, which might explain how the viruses evolved the ability to use it so quickly. But more interesting than the speed is the how of their innovation. Amazingly, all OmpF-compatible viruses shared two specific mutations. Another mutation always occurred in the same codon, that is, it affected the same amino acid in the J protein. A fourth mutation invariably occurred in a short region near the other three. Altogether, these four mutations allowed the virus to use OmpF. Plainly, we are dealing with more than mere convergent evolution here. Often, many different mutations can achieve the same thing (see e.g. Eizirik et al., 2003), but in this case, a very specific set of them appeared necessary. I’ll briefly revisit this point later, but first we have another fascinating result to discuss!

By comparing dozens of viruses that did and didn’t evolve OmpF compatibility, the researchers determined that all four mutations were necessary for the new ability. Three were not enough; there were many viral strains with three of the four mutations that couldn’t do anything with LamB-deficient bacteria. On the surface, this sounds almost like something Michael Behe would say (see Behe and Snokes, 2004), except the requirement for more than one mutation clearly didn’t prevent innovation here. Given the distribution of J mutations, it’s also likely that they were shaped by natural selection, even in virus populations that didn’t evolve OmpF-compatibility. So what did the first three mutations do? What use was, as it were, half a new J protein?

The answer would delight the late Stephen Jay Gould: the new function was a blatant example of exaptation. Exaptations are traits that originally had one function, but were later co-opted for another. While three mutations predisposed the J gene to OmpF-compatibility, they also improved its ability to bind its original target. Thus, there was a selective advantage right from the first mutation. And, in essence, this is what we see over and over again when we look at novelties. Fish walk underwater, non-flying dinosaurs cover their eggs with feathered arms, and none of them have the first clue that their properties would become success stories for completely different reasons.

In the paper, there is a bit of discussion on co-evolution and how certain mutations in the bacteria influenced the viruses’ ability to adapt to OmpF, but I’d like to go back to the convergence/necessity point instead. I have a few half-formed thoughts here, so don’t expect me to be coherent

We’ve seen cases where the same outcome stems from different causes, like in the cat colour paper cited above. Then there is this new function in a virus that seems to always come from (almost) the same set of mutations. Why? I’m thinking it has to do with (1) the complexity of the system, (2) the type of outcome needed.

Proteins interact with other proteins through very specific interfaces. Sometimes, these interactions can depend on as little as a single amino acid in one of the partners. If you want to change something like that, there is simply little choice in what you can do without screwing everything up. On the other hand, something like coat colour in mammals is controlled by a whole battery of genes, each of which may be amenable to many useful modifications. And when it comes to even more complex traits like flying (qv. aside discussing convergence and vertebrate flight/gliding in the mutations post), the possibilities are almost limitless.

So there’s that, and there is also what you “want” with a trait. There may be more ways to break a gene (e.g. to lose pigmentation) than to increase its activity. When the selectively advantageous outcome is something as specific as a particular protein-protein interaction, the options may be more restricted again. (To top that, the virus has to stick to the bacterium with a very specific part in its structure, or the whole “inject DNA” bit goes the wrong way.) Now that I read what I wrote that sounds like there will be very few “universal laws” of evolutionary novelty (exaptation being one of them?). Hmm…

References

Behe MJ and Snoke DW (2004) Simulating evolution by gene duplication of protein features that require multiple amino acid residues. Protein Science 13:2651-2664

Eizirik E et al. (2003) Molecular genetics and evolution of melanism in the cat family. Current Biology 13:448-453

Meyer JR et al. (2012) Repeatability and contingency in the evolution of a key innovation in phage lambda. Science 335:428-432

One of these major questions that can cause someone to drool on their shirt in amazement of evolution is the transition of life from unicellular, sovereign entities to cooperative multicellular organisms. A recent paper by Ratcliff et al. (2012) from the University of Minnesota posits that the first step towards multicellular organisms is cellular clustering; they then proceed to evolve clustering in unicellular yeast and ask questions about the clusters.

RECIPE FOR EVOLVING MULTICELLULAR CLUSTERS FROM UNICELLULAR YEAST

Premise: Bigger things settle in solution faster than smaller things.

(Oversimplified) Materials: Unicellular yeast (Saccharomyces cerevisiae), test tubes, solution that the yeast can eat, time

Step 1: Suspend unicellular yeast in solution in a test tube.

Step 2: Wait 45 minutes.

Step 3: Transfer the cells at the bottom of the tube to a new tube with fresh solution.

Step 4: Return to Step 2 60 times.

Step 5: Look in microscope.

How to go from one cell to multicellular clusters. Photos from Figure 1 of Ratcliff et al. (2012).

That on the right is the snowflake phenotype (their name for the multicellular clusters); every experimental replicate that Ratcliff et al. did produced it. The selection imposed by (1) gravity and (2) time was strong enough for the yeast to repeatedly evolve the snowflake (they experimentally determine the snowflake had a 34% fitness advantage over the unicellular phenotype).

The first major question the authors wanted to answer was how the clusters were forming. Were they unrelated cells sticking together (aggregation) or was a single cell producing baby cells without fully dividing (thus forming clusters of genetically related cells or “postdivision adhesion”)? Turns out, it’s the latter – the cells within a snowflake are related. The reason this makes pretty good evolutionary sense is discussed below.

Some other major findings first: the snowflakes produced baby snowflakes (instead of unicellular offspring, which some organisms apparently do).  Also, the snowflake phenotype was stable even when the selective pressures were removed – they didn’t revert to populations of single celled yeast when transferred 35 times without gravitational selection. Furthermore, the authors found snowflakes had a juvenile phase and an adult phase. This means that reproduction was delayed until a minimum size was reached. Additionally, the snowflakes had determinate growth – once they got to a certain size, they grew no more.

When the gravitational selection was strengthened, the snowflakes settled faster. The strong-selection snowflakes grew larger, contained more cells and delayed the adult phase. Because stronger selection caused these phenotypic changes in the snowflakes, the authors conclude that selection is acting on the snowflake as a single unit instead of acting on the cells that comprise the snowflake.

Another aspect of multicellularity the authors investigate is that of “division of labor”. In humans, different cells in our bodies do different things. How did THAT evolve? (Would you call it cooperation?) The authors show that the snowflakes do a version of cellular differentiation. Some of the cells undergo apoptosis (cell death) for the benefit of the whole. This is a pretty interesting concept, if you ask me, and it’s the reason that the cells being related makes sense. In order for division of labor to be favored in this way (some cells forgoing reproduction and instead undergoing cell death), two things must occur. Cells that die must be genetically related to cells that reproduce and the benefit of the death must exceed the cost of one more cell not reproducing. The authors use propagule size and number to determine if these conditions are met; the reason some cells undergo apoptosis is to create breaks in the snowflake that allow the baby snowflakes to be released into the world. This is adaptive because it allows more babies to be made than if the snowflakes used traditional cell divisions.

In summary: Selection for larger size (as determined by gravity) caused multicellular clustering to evolve in unicellular yeast. The resulting “snowflakes” were clusters of genetically related cells that produced little baby snowflakes, sometimes at the expense of individual cells dying. And the kicker: seems like it was pretty easy, right? I’m like two supplies and a billion dollar microscope short of doing this in my kitchen tonight!

 Ratcliff WC, Denison RF, Borrello M & Travisano M. 2012. Experimental evolution of multicellularity. PNAS (Early Edition). DOI: 10.1073/pnas.1115323109

Other kinds of nerds have discovered what beer geeks have known for a long time: Brewers yeast is an amazing little critter.  In the world of brewing, yeast is a major factor in the character and potency of a beer.  In the world of science, it is an industrious single-cell organism that is sometimes called upon to help humans unravel the underpinnings of life on Earth.

The most recent example of this comes from the University of Minnesota, where a couple of experimental evolution geeks (Post doc researcher William Ratcliff and his adviser Michael Travisano) were trying to figure out the coolest thing they could do in their lab. They didn’t have the resources to play around with the origins of life, so they decided the next best alternative was to explore the origins of multicellular life. 

Multicellular life isn’t a simple thing to create.  It took our primordial ancestors about three billion years to evolve from single-cell organisms, and billions more to morph into the collection of 100 trillion cells (with over 200 varieties working in concert) that makes up today’s average web-surfing American.  Of course with all the brain cells we burn on cable TV and alcohol, our cell count is probably closer to 90 trillion, but I digress. 

Ratcliff and Travisano weren’t looking to create anything as complex as a human.  Instead, they aimed to create primitive multicellular creatures, and decided brewers yeast was great place to start.  Brewers yeast lives a simple existence – it floats in fluid, eating sugar and budding off daughter cells who float away and in turn do the same thing.

William Ratcliff, Uber Nerd

Ratcliff and Travisano placed brewers yeast in flasks full of broth, which were shaken for a day and allowed to settle.  They then extracted a small sample of yeast from the bottom of the flask and put it in a fresh broth and repeated this process again and again.

By doing this, they isolated the cells that dropped the quickest, favoring the cells that were the most dense.  After a couple of weeks, they noticed that the yeast was sinking very fast and forming a cloudy layer at the bottom of the flasks.  When they looked at it under the microscope, they were greeted with snowflake-shaped clusters of multicellular yeast.  This wasn’t that a bunch of single-cell critters that were stuck together – these were bonafide multicellular organisms, each with hundreds of cells.  Brewers yeast managed to accomplish in a couple of weeks what took our single-cell ancestors billions of years to do.

When one of these cells was plucked off the organism and allowed to reproduce, its babies went right about the business of forming clusters of cells.  This showed that the organism had indeed mutated into a multicellular creature.  When allowed to grow to adulthood (which takes just a few hours), these new multicellular organisms would expand the arms of their snowflakes until they pressed together, breaking one away, which would then form into its own snowflake and repeat the process.

Ratcliff tells the New York Times that “Forming clusters isn’t a freaky yeast thing.” It is the way that many animals and plants began their climb to what we see today, so this is indeed a peek at how multicellular life got its start, with single cell organisms mutating through the process of natural selection.  In the case of this brewers yeast, the survivors were the critters at the bottom of the flask, in nature it was the ones who best responded to their environment and propagated successfully.

Ratcliff and company are still playing around with the evolution of yeast cells, but won’t say where they’re headed until they publish their results.  All Ratcliff would tell the Times is that, “We’re getting really interesting things happening now.”

This got me to thinking about what might be happening in the two carboys full of homebrew that have been sitting in my master bathroom tub for several months.  If Ratcliff and his colleagues got multicellular organisms to form a couple of weeks, I imagine by now my beer has opposable thumbs!

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Red flour beetles mating. Photo by Lukasz Michalczyk.

Female red flour beetles (Tribolium castaneum) shouldn’t want to mate more than once. They get enough sperm from a single male to fertilize all their eggs, and mating with multiple males can actually harm them. So why do many red flour beetle females mate multiple times?

New research published this week in Science provides one answer to this question. Red flour beetles often go through population ‘bottlenecks’: the population can get nearly wiped out, so only a few individuals survive to produce the next generation. This leads to lots of inbreeding. And inbreeding can lead to lots of problems.

The solution? Mate more.

The researchers forced 33 different populations of beetles to inbreed by brother-sister mating for 8 generations. They also had a large population of beetles that didn’t inbreed during this time. After the 8 generations, inbred females that only mated with one male had only half the number of offspring as females that weren’t inbred. But if you let them mate with 5 males, they were back to cranking out babies.

So, they showed that being promiscuous was a good thing for inbred females. But, were they actually more likely to be promiscuous than normal females?

The next experiment tested just that: give inbred females and noninbred females the chance to mate with 10 healthy males and see who takes advantage most of this wonderful opportunity. It’s easy to tell when female red flour beetles don’t want to mate. They run away, roll over on their sides or back, and generally just make it really difficult for even the most ambitious male to work his charm.

By the way, this experiment was done 15 generations after inbreeding stopped. Females from the populations that had been inbred were way more likely to mate with lots of males than the females whose ancestors weren’t inbred. They started mating faster, mated longer, and had more total matings than the never-been-inbred ladies. In fact, they spent almost 40% of their time having sex, compared to less than 20% for the control females.

The authors of the paper suggest that inbreeding makes natural selection work in overtime, because the changes in mating behavior were very dramatic and happened very quickly (in evolutionary time). Living in an inbred population means that females are more likely to mate with a close relative who carries the same bad mutations as she does. Females who mate with many males have a better chance of finding a guy with compatible genes that she can pass on to healthy offspring.

Who knew that keeping it all in the family could be such an aphrodisiac?

Reference:

Michalczyk, L., Millard, A., Martin, O., Lumley, A., Emerson, B., Chapman, T., & Gage, M. (2011). Inbreeding Promotes Female Promiscuity Science, 333 (6050), 1739-1742 DOI: 10.1126/science.1207314

C. maculatus penis. Image via Wikipedia.

Male seed beetles (Callosobruchus maculatus) have long spikes covering their penises (or adeagus, if you want to be scientific about it). These spikes are thought to have evolved in response to female promiscuity, as a way of increasing the male’s chances of fertilizing a female’s eggs. Females, in response to the spikes, have evolved every man’s worst nightmare: spikes inside her vagina. Talk about a rocky relationship.

This is what evolutionary biologists call sexual conflict. Males and females of a species have a common goal: to pass on their genes to the next generation. Sometimes, however, males and females have conflicting best strategies for getting that done. Females may benefit by spreading out their relatively small supply of eggs across multiple males. Males, on the other hand, tend to benefit most when they mate with many females, and each female uses only his sperm to fertilize her eggs.

The spikes on seed beetle penises may have evolved from this kind of sexual conflict. To test this hypothesis, researchers Luis Catyetano, Alexei Maklalov, Robert Brooks and Russell Bonduriansky forced seed beetles to be monogamous for many generations. They then looked to see whether the male’s penises became less spiky, or if the the female’s vaginal spikes changed at all. They found that forced monogamy did reduce male spikes, but not female ones. The research was published in the current issue of Evolution.

Seed beetles mating. Ouch! Photo by F. de Crespigny.

The penis of the male seed beetle punctures the female’s reproductive tract and, eventually, all those injuries will kill her. Females even have to kick the male constantly during mating to lessen the severity of the injuries–but she still won’t be deterred from hooking up again.

Why would male beetles want to harm females like this?

The current best guess is that the harm is just a side effect. The spikes appear to act as an “anchor”, keeping the female from getting away before he’s finished. The fact that they also puncture her and cause her permanent harm is just collateral damage.

So what about this idea that the male evolved the spikes in response to females sleeping around? The authors of the study found that larger males had bigger spikes on their penises–bigger than would be expected if spike size and body size were linearly correlated. These large males had more potential to harm their mates. Under forced monogamy, the authors expected large males in particular to evolve smaller spikes.

Why? Well, there’s no longer any reason for those spines. They aren’t in competition with any other males, so it’s not like the female is going to stop mating and hook up with Mr. Hot Beetle on the next seed over. Perhaps more importantly, any harm the male inflicts on the female will now harm him to the same degree. His reproduction is now directly tied to hers, and only hers. So it’s in the male’s best interest to make sure she is healthy enough to pump out lots and lots of eggs.

The experimental evolution in this paper was a success. After only 18-21 generations, the authors saw changes in the spike length, bringing the ratio of body size to spike length closer to 1. This wasn’t enough time to see changes in female genital spikes. Since these probably evolved in response to male spikes in the first place, you would expect a lag period for her to respond to shorter male spike length.

But while we’re on the topic of sharp penises that harm females, I thought I would throw in a little bed-bug action as well. Bed-bugs mate using what is known as “traumatic insemination”. Males bypass the female genitals entirely and pierce them in a specialized location on their bellies. They then ejaculate into the female sperm storage organ directly.

A: Bed-bug penis. B: The female "sweet spot" where the male penetrates her. Figure from Stutt and Siva-Jothy.

As you might imagine, this has some costs for the female. Females don’t fight back–they basically let any male mate with them that comes along. And males? Well, in one experiment, “males moved through the culture copulating with any engorged adult females they encountered.” Do the females benefit at all from letting all those males pierce their exoskeleton? Apparently not. Females that only mated twice in an experimental setting had just as many offspring as females that were continuously mated, as they would be in nature (i.e.: your bed). But those females who were constantly being mated died much sooner than the females that only did it twice.

Seems like males have the advantage in this species. Maybe there just isn’t enough selective pressure for females to evolve defenses–after all, they’re still having lots and lots of babies whether they die sooner rather than later. And, honestly, I don’t feel so bad for them. Bed-bugs suck.

If you want to be freaked out, check out this video by Isabella Rossellini where she explains how bed-bugs do it, in her own unique way.

References

Cayetano, L., Maklakov, A., Brooks, R., & Bonduriansky, R. (2011). EVOLUTION OF MALE AND FEMALE GENITALIA FOLLOWING RELEASE FROM SEXUAL SELECTION Evolution, 65 (8), 2171-2183 DOI: 10.1111/j.1558-5646.2011.01309.x

Stutt, A. (2001). Traumatic insemination and sexual conflict in the bed bug Cimexlectularius Proceedings of the National Academy of Sciences, 98 (10), 5683-5687 DOI: 10.1073/pnas.101440698

Related articles

• Will male cottony cushion scales survive their own mating strategy?(nittygrittyscience.com)
• Love is (sometimes) a battlefield (nittygrittyscience.com)
• Why do male Callosobruchus maculatus harm their mates? (Behavioral Ecology)
• The Spiky Penis Gets the Girl (Sciencemag.org)
• Why Humans No Longer Have Spiky Penises (newser.com)

In this post I will be as clear as I can about the simple idea that can give you this power.

So what then is wrong with the perspective that most science and all of medicine uses that makes it all so confusing and contradictory? Let me tell a few stories and I think you will see.

Imagine that she is you.

You see your GP. She of course sends you to a dermatologist. After all, what is wrong is your skin – right? Well not really.  He will talk in a limited way about diet but he has no deep diet context. He will treat your skin mainly topically and if all fails, he will prescribe Accutane.  A drug that can have very serious side effects. Accutane is like chemo – it is a brutal treatment. But even through you may clear up – you are not cured. Your acne is in abeyance.

You are severely depressed. Your GP sends you to a Psychiatrist who no longer will talk through what has gone on but will prescribe one or more drugs that will interrupt the mechanism of your thoughts. For a while. Over time the risk is that you will get worse and even suicidal. He will raise the dose and add new drugs. You are on a treadmill.

You have cancer. Your GP sends you to the Surgeon who adds in the Oncologist and the Radiologist.

They remove the cancer cells that they can and then give you chemo and radiation. You look and feel like this. (My wife went through all of this and I dare not show you what she looked like)

You may be “cured”. My wife is still here after 9 years. But this is not a CURE. It – like Accutane or Antidepressants has knocked the disease back on its back foot.

So what then is the pattern here and how do we do better than this?

Note how all these stories start the same way. You notice something wrong and then you go to the gatekeeper the GP. There has been no work done before you are ill. For medicine has no answers to WHY you get ill.

You might know this. But what you don’t know maybe, is that NONE of these diseases effect in a major way populations that don’t eat the modern diet.

Note how each of these “specialists” deal with a silo of you and few or none expand this silo to includes the wider you of your entire bodily system – your social world – your ancestry – and how you inhabit your body and the physical world. They only know their bit. This is what I mean:

This is the ignition system of an engine in a car.

This is a broader context – we drive cars on roads with people in them in varying conditions. To understand CAR – you have to work back from this and not up from the ignition system. If all the context you have starts from the parts – you MUST get lost. So it is with medicine and cell biology. They fuss about the working parts and the direct linkages. Worse, because they focus on direct linkages, they miss the side effects.

For we are NOT MACHINES. We are complex systems nested in complex systems. Their basic metaphor is wrong.

This is why they miss WHY we get ill as we do. They miss the connection between their areas and all others. They miss the truth that there is one simple big idea as to why we get the diseases of modern civilization. And that is this -

We are designed to be naturally healthy – all living beings are – so long as we live our lives inside the parameters of how our nature has evolved. That means that if we eat what we are designed by our nature (How we have evolved) to eat AND if we live in social systems that suit our nature best (Think of how all our hunter gatherer ancestors lived) and if we inhabit our bodies and the natural world as we have evolved to do ( Be active and outside a lot) The we will be healthy.

This is true because of the systems aspect of our context. Get the optimal systems fit and our system will do fine. We are NOT machines with simple direct causes and effects.

Simple isn’t it? You and I can all use this simple and huge idea.

Just as 150 years ago, we also learned how to combat infection. Also behind that was a huge but simple idea. If we lived in large numbers in a concentrated space, we would set up the ideal systems conditions for infection. Once we learned how germs and vectors like mosquitoes and fleas worked, we could change the systems conditions. At a large scale such as in a big city and on a small scale such as in the OR.

All the mumbo jumbo of pre germ medicine was swept away. Only to pop up in how medicine works on chronic disease today.

They will tell you that only if your kid is vaccinated, will you be able to protect her from infection such as measles. But they have missed the history.

We defeated infection not by drugs and not by a speciality in a disease. But by smart use of the knowledge of the systems issues and clever public health.

All these infectious diseases are the product of the modern world. They arise from our living in close contact with animals and other humans. They are novel to all who have not lived a modern (defined as agricultural and urban life). So when they were introduced to people who did not share this life and who therefore had low immunity, they killed millions. Western man killed of most of the natives in the Americas.

All infectious disease is related. It takes hold inside the crucible of close contact between man – animal and man. The plague came from this and so does flu. The breakthrough is not a drug, for the germ or virus will adapt. It is to work in a systems way to break the cycle.

So it is with chronic disease.

All are related. All stem at first from a mismatch in diet and then are amplified by a mismatch in our social and natural environments.

So if you have bad acne, depression and cancer – or arthritis – or IBS or crohns – or worry about alzheimers – or have heart disease – or have their marker and best pathway type 2 diabetes – then know that all are related.

On PEI, the average man becomes disabled by 65 and lives on in this state for 9.7 years. The main cause for this is Type 2 Diabetes.  It is estimated that by 2030 1/3 of the population will have it. So, as more people hit their 60’s and more suffer from Type 2 Diabetes, the need to respond rises exponentially. We live in a time of epidemic and medicine as it is practised today cannot help you.

Diabetes drives many other conditions including cardiovascular disease. PEI adults in 2006 with diabetes had to be hospitalized much more often than those without it. 16 times more often for lower limb amputations. 6 times more often with kidney disease. They had 5 times more heart attacks. 4 times more heart failure. 3 times more strokes. They stayed 3 times longer in hospital. Had 2 times more visits to physicians and 2 times more to specialists

Most diabetics don’t just take one medication, but several. A typical regimen for an adult diabetic after a couple of years of treatment and following the dietary advice of the American Diabetes Association includes Metformin, Januvia, and Actos, a triple-drug treatment that costs around $420 per month. Two forms of insulin (slow- and fast-acting), along with two or three oral medications, is not at all uncommon

You can help yourself by understanding the ideas on this site and on our sister site The Missing Human Manual

Now how you apply this knowledge is not simple. Changing your diet in a system that pushes the wrong choices on you is hard. You don’t just “Buck Up” when depressed. You don’t just get cured with cancer either.

But knowing what we do now – gives us the kind of start that we all had back in 1880 when the pioneers took on infection and rolled it back in a generation.

Michael and I are working to provide you and policy makers the best context so that you can make the best choices.

You get ill when you look like this – this is how I looked aged 59 – I weighed 205 lbs. How I look here has all the signs that you have not lived your life according to the rules.

This is how I looked aged 18 just as I was going out to celebrate my sister’s 16th birthday. I weighed 140 lbs. I was just about to go to South Africa to work as a diamond prospector.  I would walk 11 miles a day in the Kalahari desert and think nothing of it. I was at my peak of fitness.

This story is not all going to be about weight though. It is going to be about knowledge and hope.

This new fat and unfit me was also a new thing. For right up until my late 40′s I was relatively thin and still able to do a lot of things.

Then one day in my 50″s, it seemed as if a switch has been turned on. Each year, I put on a few pounds and became progressively weaker. Then about 58, this process started to accelerate. My knees also were hurting a lot and I was investigating knee replacement! But I thought that all of this was normal.

I thought aged 59, that putting on weight and feeling poorly was my destiny. After all we all get fat and ill as we age – don’t we?

I did try the conventional way – a bit. My wife Robin begged me to lose the tummy. The conventional wisdom meant that I had to take a lot more exercise and I had to eat less. I tried. I signed up and took more exercise but I injured myself and felt awkward and gave up. And I loved my food…. So like so many of us, I was resigned. The “Cure” that all talk about was too hard for me.

Anyway, I told myself that this was my destiny. I would be like all the other people and get ill as I got older. If I had not learned what I know now and if I had done nothing

What had happened to me is surely what has happened to millions – maybe to you too.

When did the “switch” turn on for you and you started to get fat and weak? Do you think that, like me, that this is the new “normal” for you? Do you think that that this is all that is going on?

For what I have learned that this is not all about the weight and the visible?

What is really going on is that inside of you and I is a progression of deterioration that will lead to the chronic diseases that plague us today.

So how and why do we get them? And why do they seem to turn up suddenly as if a switch is thrown? Why is medicine so bad at preventing us from getting them? Why does medicine do such a bad job of “curing” us – for once we get heart disease, we have it. Once we get depression, we have it. Once we get cancer, it can come back. Once we get Type 2 Diabetes, we always have it – NO MATTER what meds we take. The meds do not cure us. They enable us to stay alive in poor health.

Let’s find the answer simply by going back and looking at infection. When we see the model here, we can see the answers to the questions above about chronic disease.

Cholera is always around. But for humans to get it, Cholera has to have an ideal environment to propagate and to spread. Cholera is not spread through the air but through direct contact with human feces. So, if you put a lot of people together and you have no proper sewage disposal system and you allow the sewage to contaminate the water supply, you have the ideal conditions for an epidemic.

Now you can develop a “cure” – (now we know how to treat Cholera – heavy hydration with pure water). But the real cure is to take away the environment that gives cholera the edge. For instance, Cholera is always a threat today when a natural disaster such as an earthquake or hurricane damage sewage or water systems as happened in Haiti. You cannot contain the epidemic by vaccination or treatment. You have to work upstream and fix the sewage system and supply clean water asap.

This chart tells the story. See how most of the scourges of infection were beaten back BEFORE the advent of drugs.

Even TB!

All were “cured” by work on the upstream issue of environment. All these diseases were the product of changes to our social and physical environment caused by Industrialization. It was when millions of us left the small communities that fitted our own nature better. We arrived in the cities knowing nothing of the consequences of overcrowding. We found ourselves in the same predicament as say these animals now!

All these animals will die if they live like this. To prevent this they are given antibiotics as a routine. This is not sustainable and is dangerous as we are breeding super bugs as a result.

The only way that is sustainable is the change the environment. That is what we did for ourselves.

It was John Snow, a Dr, who discovered that Cholera was water born. He was never accepted by the establishment and died before his discovery was accepted. It was Joseph Bazalgette who built the sewers that made it possible for 8 million people to live in London.

We think that medicine “cured” infection. Medical knowledge about the environment for infection was the cure not any vaccine or drug.  But of course Big Pharma and the Medical Profession take the credit and today tell us that the ONLY way to be healthy is to use drugs.

All of this story about how we really conquered infection is true for the Chronic Diseases of our time. They all stem from environmental causes. Which in turn arise because we have not known the consequences of changes we have made to our diet, our work culture and how we live and work.

For just as we can never adapt to living in concentrations of millions without a good sewage system and a secure water supply, we also can never adapt to:

• Eating a diet that is mainly composed of grains and sugars and other foods such as dairy and legumes
• Living and working in a culture where we have little or no control or say
• Losing touch with what our bodies really need in terms of activity, sleep and exposure to the natural world

My getting fat and pre diabetic was all related to not knowing any of this too. I too had no context. I bought the Kool Aid about the fact that I should eat MORE grains and dairy. I had no idea that how much control I had in my life was a key factor in my health. My only thought about my body was that I should “Take more exercise” which is only a fragment of the larger truth and a part of my life where I would have to find the time and pay someone else and do – for me – silly things not connected to what I did every hour of the day.

I also did not know this.

Every animal has evolved to be healthy throughout its life. Evolution would not support a population that had to “carry” a large segment who could not cope.

We humans are no exception. In fact, in all societies where people live according to our design, we remain fit until we die. People who do not eat the modern diet, who have a culture that is more personal and who are active and spend a lot of time outdoors live long and healthy lives. Like this man.

He is from Kitava and he is my age. I hope I can be like him! Don’t you?

Our challenge is time. If you get cholera, you can be well this morning and dead by supper. The impact of Infection is obvious and quick.

But the diseases that we get today are slow building and hidden.

This is the “Switch” I was talking about. You seem fine – and then you have a heart attack. You are thin and in 10 years you are obese. You are fit and then crippled with arthritis. You go off to your routine breast exam and find you have stage 3 cancer.

This moment is different for us also depending on our ancestry. If your ancestry is longer adapted to the modern diet, the switch may not go on until your 50′s. If you are a First Nations person, it may go on right away from birth.

I think this delay and difference has hidden the danger from us all. Not helped by a vast industry – Food and Medicine – that makes a fortune from this and who have captured the media and so public opinion with their message – “Eat more grains and take a pill”.

So in my next post we will explore why we cannot adapt to this any more than we can adapt to drinking water contaminated by feces.

They are not – and you should not dismiss them.

They are in fact the early signs of a new revolution in human society, economy and culture. A revolution where we return to working with nature and where we accept that we too are part of nature.

Where we accept that trying to dominate nature and so each other is an idea that is taking us and much of life on the planet to doom.

For we can only abuse the rules of Nature so far and we can only abuse our own nature so far and Nature will push back. And when she does, we lose. The Natural world and our own Nature is not infinitely plastic.

Nature can take a lot of damage but a Tipping Point will arrive when we go too far. We can only take so many fish out of the sea, clog up the atmosphere with only so much CO2, lose only so much topsoil, use more water than we have.

The same is true for us as part of Nature. We can eat junk food, live in crazy circumstances and in crazy social and political systems – for a time. But when we do, nature will push back at us too.

For the planet is a closed natural system with key rules. And so are we. The closer the planet is to its interacting norms, the more it can support life. And the same is true for us.

Millions of years of evolution have set up an ideal set of environments, food, social, physical in which we are designed to be at peak health and happiness. The closer we live our lives to this set of ideal environments, the healthier and happier we will be, (Thesis #2). Conversely, the further away we live our lives from these ideals, the worse our health and our happiness.

We live today at a time when most of us live as far away from Nature and our Nature that is possible. She is pushing back harder and harder. As more of us get sick and as change to climate makes life hell for millions. we see her as the enemy but in fact, she has always rewarded those that work with her.

Our only chance as a species is to “Go Home”. To go home to working with her.

The beauty of this impending revolution is that we know how to be in this new relationship with nature and each other – for we are hardwired to do this. We have just been distracted by 10,000 years of a phase of development. Maybe we have been like teens – all about me? Maybe this is our time to be young parents and be a true member of the community of life again?

Ideally we are designed for this new/old relationship with nature and our nature – the life of a Hunter Gatherer.

Does this mean we have to go home to the caves and wear skins? No – no more than at the time of the Renaissance, we went back to wearing Togas. No it’s all about ideas and principles and mindset.

Men and women in the 15th century applied ideas that had been forgotten and even prohibited to how they lived their lives and so created the modern world. A world based on observation rather than dogma.

What I think could happen now is the same. We can and should use the PRINCIPLES of the Hunter Gatherer World to design the Post Industrial and Post Agricultural Society that will have to evolve to help us get though Peak Oil and Climate Change.

This series will explore how this is taking place – without any “Plan” or leader. The new world is naturally emerging as it should be! But what I think we can do is accelerate the process of transformation by seeing it more clearly.

For to “Get There” all we have to do is to accept that we are there – all Dorothy had to do to go home was to say “I want to go home”.

For “Home” is deep inside us. It waits only for us to say yes. All we need to know to do well in this New/Old World is hard wired inside us. All it has to be is remembered.

You and I can immigrate to this New World today.

Then the “New World” was a place.

Today the New New World is a State of Mind. We don’t have to get on a boat. We just have to see ourselves in a new light. The moment we do, we have arrived at the pier. Life will still be hard, it always is for immigrants. But few who got off at the pier ever wanted to go back to the old country.

So in this series I hope to paint you a picture of what this new country will be like. You might see that you are almost there. I doubt that many of you will be surprised. The ideas are not new they are older than us. But we have forgotten them.

So I offer you not a new book but a mirror. And at the heart of it all is the heart and love and the acceptance of our true place. We will, as Paul hoped for, have grown up.

“When I was a child, I spake as a child, I understood as a child, I thought as a child: but when I became a man, I put away childish things. For now we see through a glass, darkly; but then face to face: now I know in part; but then shall I know even as also I am known. And now abideth faith, hope, charity, these three; but the greatest of these is charity.”

Here then is the structure of the series:

1. In the next post “The Emergent New Hunter Gatherer Society”: we will see how the new Unemployed, the Under Employed and the Freelancers are not failures or misfits but are New Immigrants who are in engaged in a massive new project – to redesign our economy and food system using these principles. We are creating this new world for ourselves and for our children because we don’t fit the existing system and worse it works against our real needs.

2. “The Principles of HG Life as they are practised today”: We will extract the principles from the emergent patterns and see how they can be used as our guide for making our own choices and how they put meaning on our lives. What can each of us do to disconnect us from the old system and connect us to the new?

3. “The Principles of Real Revolution”: The full power of the old system is lined up and is already pushing back at the new. “THEY” know we have their number and they know we are death to them and they will fight tooth and nail to defeat us. So it is important for us to know how to deal with this and people like Gandhi and Havel show us the way.

4. “The Heart of the Matter – Food”: There are several factors that shape human culture. Our primary energy source, climate, our primary communication tools. So Peak Oil, Climate Change and the Web will rock the old system and make the birth of the new essential. For the old system cannot cope with these changes. But the real deal is the food system. How we get our food is THE most powerful factor is shaping human society, culture and so power. What will it be about the new food model that is the Game CHanger? Why will it set you free? Why will it change everything – where and how you live and who has power and who does not.

You and I can go home – all we have to do is to change our mind about who we are and where we are.

Here is a piece that make me cry every time I read it out loud – it says it all for me.

There will come a time when humanity will choose to go against nature, to exploit her bounteous gifts, causing a sickness across the planet. People will forget the ecstasies of communion, and life will become drab and colorless.

In these coming dark ages, though, a deep sense of loss will cause the beginnings of a Great Return. They will look at the landscape and the old temples, built to withstand the cataclysms of millennia and understand once again the sacred laws of Existence.

When this day comes, humanity will have come of age. It will consciously acknowledge its role in the creative impulse that comes from the Sun, fertilizes the Earth, and calls forth the flame in the hearts of men and women to worship Life and the miraculous forces behind Creation.

Miller, Hamish & Broadhurst, Paul. The Sun and the Serpent: An Investigation into Earth Energie

Lack of power and control and low social status is a major factor in making us ill.

So if we cannot change the system, how can we get more power, control and social status?

This week we will look at how we might do this.

These posts will all be about each of us as individuals. For the revolution starts with each one of us and not out there. On Monday we will look at the most extreme example - how Viktor Frankl kept his power in the death camps. For he could not change his world he could only control how he reacted to it.

“I did not know whether my wife was alive, and I had no means of finding out (during all my prison life there was no outgoing or incoming mail); but at that moment it ceased to matter. There was no need for me to know; nothing could touch the strength of my love, my thoughts, and the image of my beloved. Had I known then that my wife was dead, I think that I would still have given myself, undisturbed by that knowledge, to the contemplation of her image, and that my mental conversation with her would have been just as vivid and just as satisfying. ’Set me like a seal upon thy heart, love is as strong as death.’” pp. 56-58.

We today are also confronted by a culture that can overwhelm us and is bad for us. It has taken us away for being human. For the centre of the Industrial Culture is “Work” and “Industry”. We ask each other – “What do you do? We tend to answer by giving our work role – “I’m an engineer” or “I work for Bell”. We almost never say “I like to garden” or I am a dad. The Question “How are you?” is usually answered with “I’m so busy!”

Work not life is what our culture is all about.

From our earliest years we are taught that paid work is the centre of life. We have to work hard at school so that we can get paid work. We have to focus at school – because we have to give the right answers to the set questions. If we do get paid work, we have to focus all the time. For it is focus on the expected results that is the way – isn’t it? We have to try and balance work and family and usually work wins. if we dont have good work and pay, we are also doomed as failures. So we cannot win.

Our industrial culture means that every other part of life than work and industry is secondary. By giving up the rest of ourselves and our world to this meme we have to get stressed because we know we are missing out on important parts of ourselves. We have next to no power or control.

So how do we get our power back?

Do we have to take to the streets? Maybe. But even then we have no power or control.

The irony is that power and control and social status does not come from outside but inside. Like Dorothy in Wizard of Oz – the way home is always in our control – all we have to do is to ask.

Here then is a simple tool that asks you the right questions – it’s a great start:

Though there are a variety of ways in which evolutionary biologists can usefully study aging, there is one that is central.  That is the use of experimental evolution to produce extensive differentiation in patterns of aging, with respect to both rates of decline in age-specific mortality or fecundity as well as the cessation of such declines.  Experimental evolution of aging has been achieved with many populations from the genus Drosophila, as well as on a lesser scale in other species, including the laboratory mouse.

The reason why this particular experimental paradigm is so important is that it can be used to generate well-replicated material to which the full armamentarium of biological research can be applied.  Here is what has been accomplished with Drosophila populations with experimentally evolved differences in aging:  (i) extensive tests of the basic Hamiltonian theory for aging; (ii) tests of the alternative evolutionary genetic mechanisms that might underlie the Hamiltonian evolution of aging; (iii) extensive characterization of the aggregate physiology of slowed aging; (iv) initial characterization of the physiological transitions involved in the cessation of aging; (v) genetic and whole-genome characterization of the molecular genetic foundations for aging.  Some, but by no means all, of this work is summarized in the book Methuselah Flies.

Much more work of this kind could be done with experimentally evolved populations of Drosophila, but of greater interest would be a comparably extensive project using a small mammal.  This is because we are mammals.  If we are to acquire extensive and detailed information about the functional genomic foundations of our aging, a readily bred and housed mammal would be the best system with which to do so.  I spent fifteen years arguing for such work, from 1984 to 1999.  Over the last decade, I took a break from this mission to focus on the demographic and genomic extension of my work with fruit flies.  But now that we know how effectively genomics can be applied to products of experimental evolution with very different rates of aging, I am all the more convinced of the salience of pursuing similar research with mice or some other readily maintained laboratory mammal.  Naturally, this work should be conducted with all due care where potential artifacts and problems are concerned, such as inbreeding and the use of overly novel environments.  But it has been relatively easy to apply experimental evolution to the problem using fruit flies; properly designed and replicated mouse studies could yield results of much greater medical significance, even if they are unlikely to be of comparable scientific value given they cannot be carried out on the same scale as the Drosophila work.

But while we are waiting for the results of such a necessarily protracted mouse evolution project on aging, the question remains what evolutionary thinking can offer us as a means of ameliorating our aging immediately.  The remainder of the 55 turns to this challenging question.

in fact it is generation time that governs rates of evolution. human beings, who tend to have several children over the course of a multi-decadal life, have relatively slow generation times. it can take millions of years for noticeable evolutionary shifts to occur in a population that grows and reproduces slowly, simply because the genetic mutations that lead to evolution are very rare, and advantageous mutations take a long time to become established in a population.

it has long been known that microbial evolution occurs rapidly- noticeable genetic shifts can be observed in a manner of days or weeks. the evolution of pathogen resistance to pesticides or medicine occurs through natural selection for a rare genetic mutation that allows survival. because microbial populations often grow exponentially and generation time can be as short as twenty minutes, rare genetic mutations can sweep through a population and become ubiquitous rapidly. this is evolution in action!

historically, experiments in microbial genetics have focused on determining the function of an existing gene. this is generally accomplished by creating a strain with a defective, mutant version of the gene of interest, and observing how its function differs from the normal gene. studying defective mutants, however, does not provide insight into how gene pools can be improved.

now scientists are growing microbial cultures whose entire genetic makeup is known, and performing experiments that test evolutionary theory. any number of questions are being asked- how do the bugs evolve in response to an environmental change? a new food source? the introduction of a genetically different strain? for example, if a microbial population that requires oxygen to breathe is suddenly placed in a low oxygen environment, will genetic shifts occur that allow the microbes to use oxygen more efficiently? this certainly seems to be the case with humans- human populations that have existed for centuries at high altitudes, where oxygen is scarce, exhibit slight alterations in genes that encode hemoglobin, the protein that binds oxygen and transports it throughout the body. controlled evolution experiments allow replication, which means that scientists can now ask how frequently a positive evolutionary outcome, such as increased oxygen efficiency, occurs.

though such experiments may only provide a simplistic illustration of evolution, the mechanisms leading to genetic changes in microbial populations are remarkably similar to the basic mechanisms governing genetic change in higher organisms, including humans. insights developed from these experiments may be a first step towards unraveling the complex chain of events that has created the extraordinary diversity of adaptive traits across all types of life.

Behe has provided a useful survey of mutations that cause adaptation in short-term lab experiments on microbes (note that at least one of these—Rich Lenski’s study— extends over several decades). But his conclusions may be misleading when you extend them to bacterial or viral evolution in nature, and are certainly misleading if you extend them to eukaryotes (organisms with complex cells), for several reasons:

Go to Professor Coyne’s site for the whole review.

It’s all fair enough and no one is really up in arms about Behe’s paper itself. But isn’t it interesting how quickly the creationist intelligent design crowd started distorting the facts?

Over at the intelligent-design site Uncommon Descent, the ever befuddled Denyse O’Leary has already glommed onto the review I wrote yesterday of Michael Behe’s new paper. And, exactly as I predicted, she distorts Behe’s conclusions:

So, not only must the long, slow process of Darwinian evolution create every exotic form of life in the blink of a geological eye, but it must do so by losing or modifying what a life form already has.

In other words, she’s extended Behe’s conclusions, based on viral and bacterial evolution in the lab, to evolution of “every exotic form of life” on the planet. This is exactly what one cannot do with Behe’s conclusions.

It really isn’t a surprise that this happened; Creationists are always distorting scientific papers – and specifically so they can prop up their religious beliefs. I’m just impressed with the utter accuracy of Professor Coyne’s prediction.

This distortion is hardly news, of course—I’m completely confident that Behe not only expected it, but approves of it—but I feel compelled to highlight it once again. Luskin’s three distortions, which correspond to the three caveats attached to Behe’s results:

1. Luskin doesn’t mention that Behe’s analysis concentrated only on short-term laboratory studies of adaptation in bacteria and viruses.

2. Luskin also doesn’t mention that these experiments deliberately excluded an important way that bacteria and viruses gain new genetic elements in nature: through horizontal uptake of DNA from other organisms. This kind of uptake was prohibited by the design of the experiments.

3. Luskin implies that Behe’s conclusions extend to all species, including eukaryotes, even though we know that members of this group (and even some bacteria) can gain new genetic elements and information via gene duplication and divergence. And we know that this has happened repeatedly and pervasively in the course of evolution.

About an hour ago I finished up my last assignment for this semester, and man, it’s always a relief when that special moment arrives. But after reading this creationist intelligent design proponent garbage, I’m already getting antsy to go back and continue with my legitimate education.

At a recent evolution and ecology discussion group (EEDG) meeting, we discussed a recent paper on bet-hedging (Beaumont et al., 2009). Bet-hedging is, technically, a “strategy that reduces the temporal variance in fitness at the expense of a lowered arithmetic mean fitness” (Ripa et al. 2009) (Thanks JR for the ref).

Bet-hedging is an interesting idea, evolutionarily speaking, because *by definition* it involves the evolution of a strategy that has “lowered arithmetic mean fitness.” Of course, what isn’t considered very often, is that evolution does not (or only incidentally) maximize arithmetic mean fitness; rather it maximizes geometric mean fitness. Arithmetic and geometric mean fitnesses are expected to diverge if there is any environmental variation in fitness.

In Beaumont et al., the experiment involves bacteria (Pseudomonas) growing clonally in a static microcosm. Thus, growth rate could be considered the “main context.” Every three days, however, the researchers plate out the population on agar plates and survey the population for variation in colony morphology. If there is no colony morphology variation, the researchers transfer a sample of the population into fresh media and continue the evolution in the same environment.

However, if the researchers detect colony morphology variation, they select a rare colony morph (randomly), and use it to initiate a new population under a new circumstance (a well-shaken microcosm). Beaumont et al. call this a Rare Type Exclusion Rule + Bottleneck. Whenever a rare colony morph is detected, the researchers alternate between static and shaken microcosms.

This leads to the first of several confusions that our discussion group encountered. What is confusing is that bet-hedging often considers different environments. And here, Beaumont et al. have two different environments, that is, static and well-shaken. However, I don’t think these environments have anything to do with the evolution of bet-hedging! That is, Beaumont et al. could have simply used their Rare Type Exclusion Rule + Bottleneck into the same environment (i.e., another static microcosm) and they could have still made an argument for the evolution of bet-hedging. They may not have obtained the same results, however the alteration between static and well-mixed was not, in my opinion, helpful in distinguishing what was exactly the bet-hedging strategy. This is because, what is being hedged, is growth-rate within a transfer cycle and the ability to generate a novel colony morph. The origin of the bet-hedging strategy does not have anything to do with the static vs. well-shaken environments.

I think I understand why the researchers used an alternating environment: so that the newly initiated population would be off its adaptive peak (i.e., having just adapted to a static microcosm, the genotype that is used to initiate the population in a shaken microcosm must now adapt to the shaking conditions. This, perhaps, spurs on adaptive evolution… more on this later.)

Back to the paper…

Now there are (at least) two evolutionary outcomes considered by Beaumont et al. First, is what I call adaptive tracking, whereby mutants arise and fix (or, at least, are “selected” by the researcher) during the sequence of variable environments (first static, then shaken, then static, etc.). As such, this would result in a population evolving new colony morphology forms de novo with each environment cycle. Presumably this occurred in ten of 12 replicates (we’ll probably get to read about these ten populations in Nature or Science in the next six months). In this paper, the authors report on the second evolutionary outcome: bet-hedging.

Rather than adaptive tracking, Beaumont et al. identify a strategy that evolved in two of 12 replicate lines. This bet-hedging strategy involves the evolution of a genotype that can produce variable phenotypes. Here, colony morphology evolves from being a fixed (genetically determined) trait to becoming a trait with stochastic expression. This bet-hedger must grow fast enough that it can persist within a transfer cycle, and it happens to produce novel colony morphs stochastically. If (and when) it a colony is selected by the researcher, and used to initiate a new population, the genotype is able to generate novel colony morphs immediately. This is the winning, bet-hedging strategy that is the focus of this paper.

This leads me to the second confusion encountered by our discussion group. And that is, the conflation of a stochastic switching strategy (producing stochastic colony morphs) with bet-hedging. Bet-hedging may involve a stochastic switching strategy, but does not have to. In general, any strategy that has reduced variance in fitness could be a bet-hedger, even if it has increased variance in phenotypic traits (i.e., colony morphology). I do not blame the authors for this confusion. However, I think an explicit statement about how the bet-hedgers here have both a reduced variance in fitness that was accomplished via a strategy that increased the variance in phenotypic expression would have helped.

to be continued…

(Why) were the first eight mutants wrinkly spreader (WS) mutants?
-Once a WS, always a WS?

References

Beaumont et al. (2009) Experimental evolution of bet-hedging. Nature 462: 90-93.

Ripa et al (2009) What is bet-hedging, really? Proc Roy Soc, B