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.

Bacteria, Circumcision and HIV. Oh my!

Basically every place on our bodies is loaded with bacteria. All of these communities are important (I’ve written about some of the ways before) and more and more research seems to be finding that our microbes play an active role in fighting (or causing) disease.

So maybe it’s obvious that microbes in our swimsuit areas could be involved in sexually transmitted disease. OK, maybe not “obvious” but it may be the case with HIV and the penis microbiota. Did you know that circumcision reduces the rate of HIV transmission to men by 50 – 60%? That’s a pretty significant reduction (no pun intended). There are two major (and non-mutually exclusive) hypotheses as to how circumcision accomplishes this – morphological and bacterial. [SIDENOTE: if you are unfamiliar with the technical aspects of circumcision, I suggest Wikipedia – which has a lot of information but contains an image or two that may not be safe for work – or this Mayo Clinic site.]   

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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.

Hey. Where’d you get that fungus?

Fungi are pretty. And the ones in your home are (hopefully) smaller than this.

I’m very excited to be going to this meeting in June that focuses on the microbiome (i.e., all the living microbes) of our built environment – our homes, work places, sewers, etc. I’m used to thinking about the genetics of much larger living things – like chipmunks – where large non-living things – like rivers – create barriers between populations within a species which allows the populations to evolve independently. It’s been surprisingly difficult for me to apply my background “macro” knowledge to my new “micro” interests. How do different microbial species arise? What is a microbial species, anyway? Specifically restricting my many questions to our homes – what barriers could cause divergence between seemingly connected individuals?

Bacteria abound on our skin and when we come in contact with items in our home, our bacteria are directly transmitted to the surface (think door knobs). Additionally, we shed skin cells – and their bacteria – in our homes resulting in a near constant snow of human-associated (and pet!) bacteria. These facts lead to human occupancy being a source of our indoor microbiome. But bacteria are not the only miniscule things sharing our living spaces. What about other microbes? And now for the question of the day: where does the fungi in your house comes from?

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Roller derby is like giant hug with every girl on the track: swapping microbes due to contact

Often I think we as scientist do a really good job of convincing ourselves that our work is important. However, our research rarely makes a big enough splash that a study is widely accepted by everyone as awesome. Trust me, I have recently tried to excitedly explain to a non scientist at a party why finding the recessive mutation behind disliking cilantro was sooooo cool. It didn’t work…

But this study is so cool that it has already blown up the blogosphere. So much so that I was considering posting on an awesome new review by two of my favorite researchers out of the UK (if you haven’t read this yet you should. Also check out Britt Koskella’s blog… it’s pretty awesome). But being a roller derby skater myself (Rolling Hills Derby Dames), I decided I couldn’t let such an awesome study go by without posting about it.

At the moment, the field of microbial ecology is going from big to huge. This is partially due to the inexpensive availability of genome data making it possible to asses the frequency and species of microbes within all sorts of environments. It could also be due to the immediate applicability to human health, as the composition of the microbiome has been linked to obesity, bacterial vaginosis and potentially irritable bowel syndrome.

These communities vary across different parts of the body and individuals, and change over time. And although we know quite a bit about how pathogens can be passed from person to person due to contact, not much is known about the effect contact has on the microbiome.

Lots of contact. Photo Credits to Scott Butner

Lots of contact.
Photo Credits to Scott Butner

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Which came first: The obese chicken or its obese microbiota?

Historically, medical research has focused on pathogenic bacteria when trying to understand the relationship between human health and microorganisms. This makes intuitive sense – since pathogens make us sick – but our bodies host way more nonpathogenic bacteria than pathogens and they function in keeping us healthy. Our gastrointestinal tract has trillions of bacteria in it and much recent work has been trying to understand these complex communities. Mice are a common model for understanding human gut microbes and health. Enter Obie, the obese mouse (Figure 1, left) and Lenny, the lean mouse (right).

Figure 1: Obie and Lenny

Obie and Lenny are genetically different at a locus in their genomes that codes for leptin – a hormone that inhibits appetite. Mice that can’t make this hormone become very hungry and morbidly obese. These two mice also differ in the composition of their gut microbiota – obese individuals (both mice and human) have different amounts of the main bacterial phyla in their gut and as a result, are able to more efficiently extract calories from food. In other words, if you give both of them the exact same amount of food, Obie is going to get more calories from it than Lenny, contributing to Obie’s weight problem. In humans, where the status of our “leptin locus” is not normally known and probably not as straightforward as the case of Obie and Lenny– it’s been hard to tell whether this shift in gut microbiota is the CAUSE of obesity or the EFFECT of obesity. That brings me to today’s paper: a short communication in The ISME Journal (that’s open access!) by Fei and Zhao that addresses this exact problem.

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C is for colostrum; C is for cool

Colostrum |cuh-laas-trum| (noun): the first secretion from the mammary glands after giving birth, rich in antibodies 

The amount of research happening right now on microbes and human health is enormous. Think multi-hundred-million dollar, international-collaboration enormous. I’m sure the interest has been building for a long time, but the game changer I’m aware of is Ley et al. (2005), which showed that bacterial communities in obese mice were statistically similar to those from other obese mice and statistically different from normal-weight mice. Turnbaugh et al. (2006) showed that the shift that occurs from normal to obese* microbial communities favors microbes that are more efficient at extracting energy from a given amount of food. I’ll repeat that part: obese individuals extract more calories from a given piece of food than normal-weight individuals extract. The obese individuals have lower bacterial diversity, a trait that has also been linked to allergies. The childhood obesity epidemic is of particular concern to us all – up to a third of American children are obese and the detrimental health effects of this disease are well documented. Having a well-functioning gut microbiota may be a key to healthy weight.

That brings me to today’s topic: human breast milk (which I’ll refer to as HBM for the rest of the post). Cabrera-Rubio et al. (2012) analyzed the bacterial composition of HBM from 18 women at three time points over 6 months. The mothers in the study varied in weight and delivery method. The researchers were basically exploring what factors influence the microbial composition in breast milk, with an emphasis on weight of the mother. They used next-generation sequencing to produce a library of sequences that were analyzed for what specific bacteria were found in each sample and how the samples relate to one another as whole communities.

I couldn’t bring myself to Google image search “human breast milk” so instead I searched “babies”. Note1: there were over a billion hits (click the image to see the little text above it). Note2: the third “Related Searches” term was “black babies” which made me think – why ARE all the Google babies the same color? Curious.

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Scientific workshops are great!

Sometimes my job requires me to manually remove the contents of a dead bird’s intestines. I call this skill “hand-pooping”. And at rare and beautiful times, my job requires me to go someplace awesome. Last week was one of those rare times and I went to Switzerland.

I have attended several scientific conferences over the years, but last week I had the privilege to attend my first “workshop”:  Ecology and Evolution of Host-Associated Microbiota. A workshop differs from a conference in one basic and important way: the number of people speaking at a given time. At a workshop, there’s only one person speaking at all times, whereas at a conference, where everyone is encouraged to give a talk, there can be 10+ people talking at once and the attendee must choose which talk to go to. These both have positives and negatives but I had no idea how wonderful one concurrent session could be! There was no agonizing over the schedule and no running around – just one person to see and, for better or worse, no other option.

This workshop had a lot of pleasant logistical aspects. There were ~150 people attending, which was a really nice size. It was small enough to be able to speak to almost everyone there but large enough that a great cross section of the discipline was represented and it was never boring. Although the main conference organizer, Dr. Dieter Ebert said it wasn’t super intentional, there was nearly a 50-50 ratio of male to female speakers, a feature I noticed after the second woman spoke. It’s not rare to see a nearly equal male to female ratio at meetings, but when it comes to invited speakers (aka “big wigs”), the ratio is usually y-chromosome biased.

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Use it or lose it?

This post is a guest contribution by Dr. Levi Morran, NIH postdoctoral fellow at Indiana University. Levi studies the role that both coevolutionary relationships and mating systems play in shaping evolutionary trajectories. His research using experimental coevolution to test the Red Queen hypothesis recently appeared in Science and was featured on NPR and the BBC.

The 40 Year-Old Virgin movie poster

The 40 Year-Old Virgin

In the movie, The 40 Year Old Virgin, Steve Carell’s character (the title character) asks a sex education instructor, “Is it true that if you don’t use it, you lose it?” Given the context, I’ll allow you to put the pieces together and figure out just what he was referencing with the question. But, the phrase “use it or lose it” is quite catchy isn’t it?

Surprisingly, the phrase is thought to have some relevance in the field of evolutionary genetics, particularly regarding bacterial genomes. You see, widespread gene loss and genome reduction has been observed in some strains of bacteria, particularly those that specialize in certain environments (Cramer et al. 2011; Ernst et al. 2003; Smith et al. 2006). But, how and why do bacteria “lose it”, and do they lose it because they don’t use it?

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Ecological complexity breeds evolutionary complication


ResearchBlogging.orgIt is a truth universally acknowledged in evolutionary biology, that one species interacting with another species, must be having some effect on that other species’ evolution.

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.

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