Pssst. Your holobiont is showing.

Here’s a sad story: Species A mates with Species B. They succeed in making a Hybrid Baby but their Hybrid Baby dies before it can fully develop. (I warned you it was sad.) Why did that happen? Sure, sometimes two genomes are just too different to successfully coexist – both the stars and the chromosomes must align to make a baby. Other times, as recently reported by Brucker and Bordenstein, the Hybrid Baby’s microbiota is the problem.

I think (or rather Google thinks) this is a Nasonia wasp.

In Nasonia wasps, there are three closely related species that all diverged less than one million years ago: Nasonia vitripennis (who I’m going to refer to as the V wasp), N. giraulti (the G wasp) and N. longicornis (the L wasp). When L and G mate and their LG offspring are mated to other LG offspring, 8% of the males die. When V and G mate and their VG offspring are mated to other VG offspring, 90% of the males die.

The phylogeny of the three Nasonia wasps (left) and the crosses that result in hybrid male lethality.

The phylogeny of the three Nasonia wasps (left) and the crosses that result in hybrid male lethality.

Brucker and Bordenstein hypothesized that microbes were responsible for the hybrid lethality of the the VG hybrids. Through DNA sequencing, they found that the gut microbes of the VGxVG wasps were unlike either parental type (in abundance or diversity), whereas the LGxLG wasps were. So, when a hybrid’s gut microbiota is like one of the parental species, the hybrid males live. When the gut microbiota is unlike a parent, the hybrid males die. They further found this could be boiled down to a change in the single dominant species: whereas a Providencia bacterium was most abundant in both V and G parents, a Proteus bacterium was most abundant in VGxVG wasps.

But that doesn’t conclusively show that microbes are responsible for the hybrid lethality. Brucker and Bordenstein then compare germ-free hyrbids to conventional hybrids – in other words, if we remove the germs (the microbiota, that is), do the hybrids still die? The short answer is no. Under normal conditions, about 80% of the pure Vs and pure Gs survive, whereas only 10% of the VGxVGs survive. Under the germ-free conditions, about 70% of the pure Vs and pure Gs survive and 60% of the VGxVGs survive. That’s a pretty significant increase in living hybrids! And to strengthen the case even more – when the germ-free wasps were fed a mixture of Providencia and Proteus bacteria, the hybrid survival rates went down to about 30%.

The authors perform other experiments for this study that include analysis of wasp genomic loci that were previously linked to hybrid lethality and a transcriptomic analysis, where they find immune genes to be a significant player. However, I’m going to switch gears a little bit and talk about the context the authors frame their discoveries in: the HOLOGENOME concept.

Most evolutionary biologists probably consider the individual as the fundamental unit of natural selection. We think about the genes of one mother or one father being passed on to one descendant. But is this view too constrained? The “hologenome” is all the genomes that belong to the “holobiont” – an organism and all its microbes. The Hologenome Theory of Evolution posits that the holobiont is the fundamental unit of natural selection, not just “the big organism”. Generally speaking, this makes a lot of intuitive sense, I think: we macros are pretty dependent on micros to get our genes to the next generation. But is the reverse true? To be THE fundamental unit of selection, the holobiont must pass its hologenome to its offspring – and I’m not sure this assumption universally holds. Certainly some macro-organisms always pass specific micro-organisms to their offspring (coprophagy in mammals might be a good example). But in most cases, where our microorganisms come from is a mix of vertical transmission (from our parents) and horizontal transmission (from the environment). I just can’t make this distinction make sense with what I think I know about heredity and selection. Natural selection depends on traits that make an organism more fit being passed on to its offspring and if some – or most? – of our microbiota is randomly acquired from the environment, natural selection can’t act on it. On the other hand, it’s very possible reality doesn’t abide by our definitions: perhaps only a few microbial taxa need to be passed directly from parent to offspring and these “founders” get microbial communities off on the right track and the rest of the communities fall into place from the environment.

Regardless – Brucker and Bordenstein pretty conclusively turned that sad story into a science story by showing that in Nasonia wasps, gut microbes play an integral role in hybrid survival. And if the Hologenome Theory of Evolution applies anywhere, I’d say it does here!

A healthy viable Nasonia holobiont (top) and an unhealthy, inviable Nasonia holobiont (bottom). From Brucker and Bordenstein (2013), figure 1B.

The sad story told in pictures: A healthy, viable Nasonia holobiont (top) and an unhealthy, inviable Nasonia holobiont (bottom). From Brucker and Bordenstein (2013), figure 1B.

Brucker, R. M. & Bordenstein, S. R. 2013. The hologenomic basis of speciation: gut bacteria cause hybrid lethality in the genus Nasonia. Science 341: 667-669.

When the going gets tough, mutualism gets going

C. alliodora III

Cordia alliodora. Photo by Karen Blix.

Evolution by natural selection is not usually considered very peaceful—the “survival of the fittest” is usually assumed to come at the expense of competitors for food or shelter or other resources. But the “fittest” can also be those who recruit assistance from other individuals, or other species—and who provide assistance in return.

This was the perspective of Peter Kropotkin, a Russian prince and political anarchist who studied the wildlife of Siberia while working as an agent of the Czar’s government. In the harsh conditions of the Siberian winter, Kropotkin reported finding not a bitter struggle over scarce resources, but what he called “Mutual Aid” among species, as well as in the human settlements that managed to eke out a living.

Something like what Kropotkin described is documented in a new paper by Elizabeth Pringle and colleagues. Examining a protection mutualism between ants and the tropical Central American tree Cordia alliodora, Pringle et al. found that drier, more stressful environments supported more investment in the mutualism.

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Your dinner or your life: What determines the sprint speed of gazelles, zebras, giraffes … and ostriches?

2010 076 Masai Mara b 24

Thomson gazelle, on the run. Photo by ngari.norway

In the evolutionary history of big herbivores and the carnivores that prey upon them, the phrase “arms race” is only technically a metaphor. Antelope and zebras are literally born to run, and many of the things that chase them, like wild dogs or cheetahs, are either masters of endurance or champion sprinters. The evolutionary story almost writes itself: over millions of years of chasing, and being chased, whenever the predators evolved to become faster, the prey were selected to run even faster—until a cat evolves that can go from 0 to 60 faster than my Volkswagen Rabbit.

Except of course there’s more to life than running for your life. An antelope’s frame is under more demands than evading cheetahs—it also needs to travel long distances to follow food availability with the shifting rainy season. In fact, the North American fossil record suggests that big herbivores on that continent evolved long legs for distance running millions of years before there were predators able to chase after them. And then again, not all predators run their prey down; lions, for instance, prefer to pounce from ambush.

In a paper recently released online ahead of print in the journal Evolution, Jakob Bro-Jørgensen sets out to disentangle exactly these competing explanations.

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Who are the people in your neighborhood, Baba Brinkman?

Baba Brinkman’s latest salvo in his quest for a fact-based justification for his proposal to select meanness out of the human race by not sleeping with it really boils down to a question most members of my generation will likely remember from a childhood saturated in “Sesame Street”: Who are the people in your neighborhood?

We’ve come to this question because Brinkman has finally discovered that there is, in fact, data that might suggest genetic variation contributes to variation in “meanness”—even if he couldn’t be bothered to cite it in connection with the campaign up to now:

In his new post, Yoder’s argument is not that male violence isn’t an adaptation; rather, he argues that our violent tendencies have been so completely drilled into us by natural selection that they show insufficient genetic variation for selection to act on …

He’s right that a complete lack of individual genetic differences in proneness-to-violence would be a death-blow for my campaign, but luckily for me and all the other peaceniks who support the DSWMP credo, Yoder simply didn’t bother to look up any of the evidence.

You have to love how, after implicitly conceding the factual point—that in his first attempt to shore up the scientific basis of DSWMP, he cited data that has nothing to do with the question at hand—Brinkman chides me for not doing my homework. In fact I’ve acknowledged at every step of our little back-and-forth that there is a body of research which suggests there’s some genetic contribution to variation in what we might call “meanness.” My argument isn’t that this genetic contribution doesn’t exist—it’s that this genetic contribution is pretty much meaningless from the perspective of an individual person’s dating life.

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Baba Brinkman says he wants my money

But he doesn’t want it badly enough to actually address the substance of any of my criticisms of his scheme to rid the world of meanness via “an entirely defensible ‘bottom up’ form of eugenics.”

Oh, and I see he’s speculating about my sex life. Real charmer, this guy.

In his non-response response, Brinkman doubles down on his fixation with the fact that, across human populations, males become more likely to be involved in violent crime right around the time we hit puberty:

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@NothingInBio at #Evol2013: What we’re presenting

Cecret Lake - Alta Utah

The Evolution 2013 meetings are nearly upon us, and most of the team here at Nothing in Biology Makes Sense! are going to be in Snowbird, Utah for the joint annual meeting of the American Society of Naturalists, the Society of Systematic Biologists, and the Society for the Study of Evolution. Rather than make you hunt through the online program, here’s where we’ll be, and what we’re presenting:

  • Amy will present “The population genetics of rapidly evolving reproductive genes: How much variation should we expect to find?” on Sunday at 9:30, as part of the Evolutionary Genetics and/or Genomics section in Cotton D/Snowbird Center. [program link]
  • Look for some of CJ’s work in a lightning talk by her dissertation advisor, Mark Dybdahl, titled “Identifying the molecular basis of coevolution: merging models and mechanisms” on Monday at 11:45, in Superior B/Cliff Lodge. [program link]
  • Noah will present “What can we learn from sequence-based species discovery? An example using sky island fly communities” on Tuesday at 9:30, as part of the Community Ecology and Evolution section in Peruvian A/Snowbird Center. [program link]
  • Sarah will present “Nature, nurture and the gut microbiota in the brood parasitic Brown-headed Cowbird” on Tuesday at 10:30, as part of the Community Ecology and Evolution section in Peruvian A/Snowbird Center. [program link]
  • Jeremy will present “Evidence for recent adaptation in genome regions associated with ecological traits in Medicago truncatula” on Tuesday at 2:45, as part of the Genetics of Adaptation section in Rendezvous A/Snowbird Center. [program link]

Looks like we’re in for a busy Tuesday! But this year, you won’t have to choose between us.

The beef I have with The Paleo Diet

I’ve heard a lot about “The Paleo Diet” lately and every time a popular news source (say NPR or ABC or Fox News or New York Times) does a piece, I cringe a little bit. For those of you who have never heard of the Paleo Diet (from Wikipedia):

The paleolithic diet…is a modern nutritional plan based on the presumed ancient diet of wild plants and animals that various hominid species habitually consumed during the Paleolithic era—a period of about 2.5 million years duration that ended around 10,000 years ago with the development of agriculture.

So that’s the basic idea – people restricting their diet to things that we ate before modern agriculture. I don’t really have a problem with the diet, per se – removing highly processed foods and increasing your activity level is a good idea for almost anyone. But the rationale that always accompanies the diet – that’s where the cringe comes in.
The rationale goes like this (again from Wikipedia):

Paleolithic nutrition is based on the premise that modern humans are genetically adapted to the diet of their Paleolithic ancestors and that human genetics have scarcely changed since the dawn of agriculture, and therefore that an ideal diet for human health and well-being is one that resembles this ancestral diet.

I can break this rationale down into three assumptions/statements:
1. Evolution acts to optimize health.
2. Evolution adapted us to eat a specific diet.
3. Therefore, today, we should eat that diet to optimize our health.

As an evolutionary biologist, I think there are logical and scientific flaws to each of these statements.

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Is corn the new milk? Evolutionarily speaking, that is.

Cross-posted from Denim and Tweed.

ResearchBlogging.orgIt is a widespread misconception that, as we developed the technology to reshape our environment to our preferences, human beings neutralized the power of natural selection. Quite the opposite is true: some of the best-known examples of recent evolutionary change in humans are attributable to technology. People who colonized high-altitude environments were selected for tolerance of low-oxygen conditions in the high Himalayas and Andes; populations that have historically raised cattle for milk evolved the ability to digest milk sugars as adults.

A recent study of population genetics in Native American groups suggests that another example is ripening in the experimental fields just a few blocks away from my office at the University of Minnesota: Corn, or maize, may have exerted natural selection on the human populations that first cultivated it.

The target of this new study is an allele called 230Cys, a variant of a gene involved in transporting cholesterol. 230Cys is known only in Native American populations, and it’s associated with abnormally low production of HDL cholesterol (that’s the “good” kind of cholesterol) and thereby increased risk for obesity, diabetes, and heart disease. In Native American populations, the genetic code near 230Cys shows the reduced diversity associated with a selective sweep, which suggests that, although it’s not particuarly helpful now, this variant may have been favored by selection in the past.

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#Evol2012: Puffin poop and predation pressures


A final few propitious presentations from the Evolution meetings in Ottawa:

Kirsten Bowser is running puffin faeces through next-generation sequencing to identify what the adorable seabirds eat—and she’s already found some prey species that wouldn’t be easily identified just by watching what puffins bring back to their nests.

Brian Counterman showed that hybridization between subspecies of the South American butterlfy Heliconius erato with different wing patterns can transfer wing patterning between subspecies—mostly by transferring a single chunk of DNA that doesn’t code for any protein, but performs a regulatory function. What’s more, the same region is being moved between multiple pairs of hybridizing H. erato subspecies.

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Evolving invaders

This post is a guest contribution by Kathryn Turner, a PhD student at the University of British Columbia, who studies the evolution of invasive thistles. Kathryn writes about her scientific interests at the slyly named site Alien Plantation and tweets under the handle @KTInvasion.

ResearchBlogging.orgInvasive species are a big problem. A real big problem. In the US alone, invasive species cost nearly $120 billion in damages per year (Pimentel 2005). 42% of species on the Threatened and Endangered list are there primarily because of invasive species.

Which leaves us with two questions. First, most obviously, how is it that a species is able to come into a new environment that it is not adapted to, surrounded by new environmental conditions and foreign biological interactions, and thrive? Thrive so exaggeratedly, that it can out-compete and displace species which have been there for millennia, adapting precisely to those environmental conditions and biological interactions? How can an individual survive to propagate a population? How can any species accomplish this? Second, less obviously: why can’t more species do it? Humans transport animals and seeds (and spores and larvae, etc, etc) around all the time, but only 10% establish self-sustaining populations, and only 1% spread to new habitats, becoming potentially invasive; this is known as the ‘tens rule’ (Williamson 1993) – a funny ‘rule of thumb’ for which I could never quite figure out the math.

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