Do Hosts Handpick Their Microbiome?

I found this microbiome talk from 2011 by John Rawls today and thought it would be good to share here. The work addresses the question of whether gut microbial communities are specific to their host species. Basically, he asks:

"DOES A HOST CARE ABOUT WHICH MICROBIOME IT GETS?" 

If you follow this blog, you'll know that we have discussed a series of studies that indicate microbiomes are uniquely qualified for their host species, sometimes in ways that the phylogeny of the animal yields the same relationships as the "phylosymbiosis" pattern (guest blog post) in the microbial community. These discoveries are important because they emerge out of an initial paradigm in which studies within species have shown variation in the microbiome upon changes in diet or disease. But comparative biologists who think in ecological/evolutionary ways have started to illuminate the rules of microbiome assembly across different species.

It's now safe to say that in the last few years, we have gained a clear understanding that under controlled laboratory studies, the crosstalk between microbiomes and host genomes is undoubtedly intimate, clear, and specific. The gut microbial community is strongly shaped by host selection, perhaps even independently of a phylosymbiosis pattern from 16S data (Oh et al 2010, ISME). If we understand the molecular signals between this conversation, then we can better understand superorganisms (our genes + microbial symbionts) in evolutionary and applied ways.

Human Microbiome Project - John F. Rawls, University of North Carolina at Chapel Hill from Kavli Frontiers of Science on Vimeo.

Microbiology Video: "We owe them our very lives!"

It is no secret that many readers of this blog are awestruck by the universality, diversity, and significance of microbes. Indeed, Earth is a “microbial planet” in the sense that the oldest (over 3.8 billion years ago) and most abundant forms of life are the ones too small to be seen by the unaided eye. Even more powerful is the quote in the video that "We owe them (bacteria) our very lives".

If you ever want to share those sentiments with friends, family, students, colleagues, or heck, politicians - then this new HD cinematic video is a perfectly simple introduction. Check it out….it is worth the four short minutes and then some.

Introduction to Bacteria from Frank Gregorio on Vimeo.

By NIAID_Flickr [CC-BY-2.0]
via Wikimedia Commons

Related blog posts:

The Gravity of Symbiosis (Nov. 3, 2013)

The Story Behind Mom Knows Best: The Universality of Maternal Microbial Transmission (Aug. 20, 2013)

Does the Federal Government Slow Innovation and Markets?

You think you know, but you have no idea.

This talk takes a sledge hammer to the idea that government funding of science and technology is a waste and slows innovation. At a time when everyone needs to heed the call that American science is broken, this talk single-handedly champions the idea that government IS the risk taker in the market, rather than the risk-fixer.

The internet, gps, Siri, touchscreen, etc - all stated below to be birthed with seed money from the Uncle Sam. Bottom line, if you like your cell phone, then you will like the next thing (federally-funded) scientists and engineers create too.

Stand up for congressional members and candidates that support science for they in turn will make funding decisions that will support future luxuries of a modern world, not to mention a growing stock market spurred by revolutionary products.

Blow Your Mind Podcast on Da Hologenome

Most Recent Episode:

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Into the Hologenome

1 day ago31 minutes

How can the bacterial fauna thriving inside our bodies influence evolution? Find out in this episode of Stuff to Blow Your Mind.

The Gravity of Symbiosis

This post is lifted from my blog at the International Symbiosis Society's website, which just started a blog series by members of the community to foster dialogue and debate. I thought that I would post it here as well because it continues a stream of posts here on the fusion of the microbiome and evolutionary sciences from the vantage point of our laboratory's work. I think the last paragraph is perhaps the most salient, so either skip ahead or follow through.

View From 32,000 Feet

Darwin and the 20th century pioneers of biology would have been astonished to see the countless roles that microbes play in shaping eukaryotic life. From the origins of eukaryotic cells to pharmaceutical products, Life as we know it would be unrecognizable without microbes. Integrating microbes into all facets of the life sciences today is a vision that is not only driven by exciting questions at the perimeters of the biological disciplines, but one that seems more achievable today than ever before, at least from a our vantage point within the symbiosis field.

Let us briefly look backwards in order to look forwards. The fusion of evolutionary biology and Mendelian genetics spurred a modern synthesis in which the biologist sees the world through a refined set of filters: the genome is stably inherited, subject to natural selection, and defines who we are as individuals and how species arise from descent with genetic modification. Yet there is a transformation occurring today in our capacity to understand who we are beyond our nuclear genes.Indeed, biologists take the archetypal examples of mitochondria, chloroplasts, and endosymbionts for granted, but the science of the microbiome has emerged in the last decade to massively widen the recognition, if not scope, of Life's dependency on microbes. One luminary in our field lost to history, Prof. Ivan E. Wallin, remarked in 1927:

"It is a rather startling proposal that bacteria, the organisms which are popularly associated with disease, may represent the fundamental causative factor in the origin of species"

Below I will summarize our most recent foray into speciation by symbiosis. This post is far too small to give a full and fair treatment of the topic, and I apologize to my colleagues in advance for not citing their work.

From Many Genes and Microbes, One Species

Approaches to studying the gut microbiome in animals have largely been diet- and disease-centric. Relatively little is known about the comparative structure and evolution of bacterial communities among closely-related host species, but this knowledge gap is starting to change. For instance, as speciation events progress from incipient to complete stages, does divergence in the composition of the host-associated microbial communities parallel the divergence of the host's nuclear genes? (Brucker and Bordenstein 2012a link) We hypothesized that if host phylogenetic relationships, in part, structure gut microbial communities, then related species of animals reared on the same diet will not acquire the same microbiome, but instead host species-specific communities of microbes. We discovered that the gut microbiome was indeed different between closely related species of insects reared on the same diet, and the constituents and composition of the bacterial communities in each species changed in parallel with the genomic relationships of the host species (Brucker & Bordenstein 2012b, link) - a pattern we have since termed "phylosymbiosis" (Brucker and Bordenstein 2013 link, and Figure 1 below).The significance of phylosymbiosis is also evident in primates (Ochman et al. 2010, link) and hydra (Franzenburg et al. 2013, link).

Figure 1.Phylosymbiosis. Like phylogenomics, phylosymbiosis is a total microbiome metric that retains an ancestral signal of the host's evolution. (a) The central prediction is that divergence in host genes is positively correlated with differentiation of the microbiome. (b) Parallel dendrograms between the host phylogeny and the microbiome relationships is one test of phylosymbiosis (c) Schematic of a real data example from our model study system.

We recently tested the hypothesis that the gut microbiome assists animal speciation, even in the well-studied Nasonia genus where nuclear speciation QTLs were genetically mapped to chromosomes. First, we demonstrated that gut bacterial diversity in F2 hybrids goes markedly awry in comparison to that of pure species controls (Bordenstein and Brucker 2013, Science, link). Second, curing this altered gut microbiota eliminated hybrid lethality (Figure 2), the misexpression of immune genes associated with hybrid lethality, and marker ratio distortions away from Mendelian inheritance for speciation QTLs. Finally, we recapitulated hybrid lethality in germ-free hybrids by orally inoculating them with resident strains of the dominant bacteria within species. Thus, in a series of "gain" and "loss" microbiome experiments, we demonstrated that reproductive isolation in this genus is not dependent solely on genetic divergence, but also on the interactions between the host genome and gut microbiome. It is enticing to speculate that this phenomenon will be common in animals since they all have a gut microbiome that is increasingly seen to affect numerous aspects of fitness. Time and experimentation will tell. A simple experiment would be to test if hybrid inviability can be cured in diverse germ-free systems.

Speciation by symbiosis has been subject to healthy skepticism. For example, one interpretation of the data above is that the gut microbiome is just an environmentally conferred stress on the wasps’ fitness, and hybrids are hyper-susceptible to this stress. So the presumed stress of microbiome colonization on hybrid wasps can be compared to a predator eating hybrids more than the vigorous parentals that escape predator detection. However, in this argument, the microbiome is seen as purely extrinsic to the host. Like all metazoans, Nasonia's gut microbiome is inevitable and plays a large beneficial role in host fitness - survival and reproduction. Thus, removal or suppression of the microbiome in Nasonia is quite maladaptive, causing a ~15% decrease in survival from egg to pupal stages (Brucker and Bordenstein, 2012, link) and delayed development into adulthood by two to three days. Thus, in contrast to an extrinsic predator, the narrative here is that microbiome is essential for within-species fitness. Similar to a beneficial set of genes, the microbiome is also causal to reproductive isolation in hybrids, much like the way a classical geneticist studies speciation genes that are adaptive within species but break down in hybrids.

Figure 2. Hybrid lethality in Nasonia. Top: Non-hybrid 3rd instar larva. Bottom: Hybrid 3rd instar larva that is melanized and dead.

The Gravity of Symbiosis

The term "holobiont" is used to define the host and its collection of beneficial symbionts. It does not differentiate intracellular or extracellular symbionts as it is a lens to view the individual as an engineered collection of organisms. Therefore, the term "hologenome" naturally follows as a definition of the total genetic material of the holobiont. The hologenome emphasizes that the animal’s genome, mitochondria and beneficial microbiome are an aggregate of genes that together form a unit of natural selection (Zilber-Rosenberg and Rosenberg, 2008, link). To be historically accurate, the term hologenome was originally and independently proposed in 1994 by Richard Jefferson in a seminar on PCR technology (YouTube link). The evidence motivating these terms spans the essential roles of the microbiome in eukaryotic fitness (McFall-Ngai et al, 2013, link), including digestion, immunity, olfaction, organ and neuronal development, etc.

However, the hologenome concept is controversial, perhaps more so than the holobiont. These terms are gaining attention but are still rather new to biology and should be subject to questions. Some view the individual solely through the refined filter of the nuclear genome. In this case, the microbiome is purely extrinsic to the host animal and therefore unable to co-evolve sensu stricto with the host genome. In order for the microbiome to change in parallel with the host genome, stability of the two genomic units by vertical transmission or host selectivity in microbiome community structure is required. Current evidence specifies multiple paths for stability that we must delve much further into.  For example, maternal microbial transmission may be universal in animals for some fraction of the microbiome (Funkhouser and Bordenstein, 2013, link) and specificity provided by the host immune system can further cement the essential foundation for host-microbiome stability and co-cladogenesis (as evident in phylosymbiosis).

In Nasonia, the phylosymbiotic associations of parental host genes and microbes are both required for fitness within species, but are in negative epistasis in hybrids undefined comparable to nuclear-nuclear and cytonuclear gene interactions that function normally within species but cause hybrid incompatibilities.  In this light, the discovery of the phylosymbiotic gut microbiome can be understood as part of a co-adapted unit, which functions normally within species, but breaks down in hybrids between species.

Of particular relevance is that the vital fitness traits conferred by the gut microbiome within species blurs the lines between what biologists conventionally define as the environment or the organism. And perhaps this point is the most salient. Intrinsic and extrinsic views of the microbiome are largely semantic filters placed on our definition of the individual. Nature may not care about this linguistic argument. What matters is stability of the associations, no matter if we define them as intrinsic genome-by-genome or extrinsic gene-by-environment interactions. Today, it is convention that mitochondria represent anciently acquired bacteria that have a fully integrated partnership with the animal genome. The continuum of symbiosis stretches from these obligate relationships of endosymbionts to the host farming the microbiome.

I extend my thanks to the ISS board for asking me to write this blog post and for you reading it. I look forward to reading your future posts and extending this social medium to the symbiosis community.

Warmest regards,

Seth

In Defense of the Hologenome

In a perspective article published in Zoology, we recently wrote:

"The hologenome concept of evolution specifies that the animal's genome, mitochondria and microbiome are an aggregate of genes that together form a unit of natural selection (Zilber-Rosenberg and Rosenberg, 2008). The evidence motivating this concept spans the essential roles of the microbiome in eukaryotic fitness (McFall-Ngai et al., 2013), including digestion, immunity, olfaction, organ and neuronal development, etc. However, the hologenome concept is controversial because many biologists view the microbiome as extrinsic to the host animal and therefore unable to co-evolve sensu stricto with the host genome."

As an illustration of the controversy, I am posting an email dialogue that we recently had with a prominent expert in evolutionary biology and a postdoc on our paper on the hologenomic basis of speciation. The discourse below is meant to highlight the points and counter-points of the dialogue and perhaps convert a few skeptics.  I am blogging it because I believe it will be a far more effective way of advancing this discourse into the community, rather than just keeping it between a few scientists with limited benefit. 

And for more information, I posted the video from a google+ hangout on the hologenome below that was comprised of several evolutionary biologists and microbial ecologists (link to blog post). After we got the kinks worked out for the video chat, we had a productive one hour chat. 

~~~~~~~~~~~~~~~~~~~~~~~

Dear XXX and YYY,

Thanks again for getting in touch with your commentary.  We  appreciate the opportunity to address your concerns, and we pledge to make this process productive so that we can all learn something in the discourse. You’ve listed a number of issues in this short commentary, but we think that we can demarcate them into four discrete areas to discuss. Do correct us if there’s anything critical that you feel that we’ve missed. 

Rob and I can start by saying that a short Science paper doesn’t do much justice for convincing the community in one shot. Thus, we expect  and welcome this discussion;  we have encouraged such in our preceding blog posts, google hangout discussions with other scientists (skeptics and supporters alike), and our Zoology article.  And there are more experiments to be published, of course. We also think that posting this discourse on our blogs (either anonymously or not) would be helpful so that the broader community can see the pros and cons of the arguments.

1. " The claim that coadapted gut bacteria cause hybrid lethality and speciation in Nasonia requires that bacterial gut assemblages of Nasonia recapitulate their hosts’ phylogeny, are species-specific, and are coadapted to their hosts in the sense that “foreign” microbiota lead to lower fitness."

There are three issues that you question in the above statements. First, the Nasonia gut microbiome recapitulates the hosts’ phylogeny. We demonstrated this pattern in our Evolution paper, this article, and a third set of experiments that we are currently working on.  So we think your commentary here stems from a misinterpretation of what phylosymbiosis is, rather than its lack of evidence. Here’s how we view it operationally. Phylosymbiosis is simply the reconstruction of the host’s phylogeny with a UniFrac inference method used to compare microbial community relationships. Like phylogenies, UniFrac trees are statistical inferences based on the weighted (Fig 2B) and unweighted abundances (Fig 2C) of OTUs. Remarkably, both the weighted and unweighted Unifrac trees are in complete agreement with a phylosymbiotic microbiome.  We suspect you are laser focused on the pie charts, which create the illusion that G and V have very similar communities based on the single, dominant Providencia genus. The individual OTUs are collapsed and simplified in the pie charts into a broader genus category. If we were to reconstruct the tree based on one OTU, like Providencia, you might be correct; however, these widely-accepted UniFrac trees developed by the microbiome field are reconstructed based on all OTUs in the microbial communities. Take for example the simple comparison that the younger species, G and L, share 41% of the OTUs in their communities while the more divergent species, G and V, share  24% of the OTUs in their communities. 

Your second claim is that the Nasonia gut microbiome is not species-specific.  In the same light as above, any one OTU can be present in all of the species but the metric that we use here is the total microbial community. It is species-specific because (i) there are a number of OTUs (besides Providencia) that are specific to each Nasonia species and (ii) the divergent Nasonia genomes select upon the microbiome diversity that can inhabit them. Because we have placed all of the Nasonia in our studies under identical environmental conditions, the variation we see in species’ microbiomes is explainable by gene-microbe interactions. 

Finally, the third claim that foreign bacteria should cause hybrid lethality is not a requirement at all. In fact “foreign” is an unusual term to describe this process. What matters is the ability of the host genome to recognize and thus epistatically interact with the microbiome. So, an OTU could be foreign in one generation, but still be part of the recognizable microbiota in subsequent generations. Perhaps a simple way of looking at this is from a genetic perspective. Like a beneficial gene within species that breaks down in hybrids, we expect that beneficial bacteria or those closely related to the native microbiome in Nasonia should cause lethality. In contrast, an unrecognizable “foreign” bacteria should not cause lethality because it is not part of the of  recognizable microbial community and thus epistasis within species that breaks down in hybrids. Ongoing experiments in our lab currently support these predictions. 

In conclusion, we urge caution because the claim that "none of these are established" or later that "these data...do not meet these criteria" (and throughout the top paragraph of page 3) dismisses widely accepted means of analysis and interpretation for microbial communities. 

2. "“Phylosymbiosis” connotes relative stability of the gut bacterial communities within species."....Brucker and Bordenstein (1) provide no evidence that the gut bacteria of Nasonia are sufficiently constant and species-specific to contribute to speciation."

Some clarification of the phylosymbiosis model is required in our response here because it seems to us that you have extended the term to something that we do not adhere to. As defined in the Science paper, it is “a term...to denote the microbial community relationships that recapitulate the phylogeny of their host”. Phylosymbiosis is a pattern that is not necessarily derived from a continuous process of stable OTUs each generation. Instead, phylosymbiosis derives from the host genome interacting with the environmental microbiome to collect an assemblage of (similar) microbes whose community relationships parallel the evolution of the host genome each time they are measured. We come to this conclusion because the null hypothesis for a totally random or diet-centric collection of microbes in a host is that phylosymbiosis would not be evident in the microbiome data.

Like phylogenomics, phylosymbiosis is the total microbiome metric of the host’s evolutionary        relationships. As we outlined in our 2012 TREE article, phylosymbiosis is a pattern that emerges under controlled conditions and will be subject to change with environmental dynamics.  Surely, bacterial OTUs can vary with environmental conditions and that variation is in fact one route to speciation by symbiosis that we raised in our TREE article in 2012. Different diets can unquestionably drive different microbiomes. The variation in microbiomes that were observed in our publications and ongoing research stems from variations in fly host microbes that the Nasonia are reared upon and the method of observing the microbiome (Evolution paper was cloning and sequencing, Science paper was Next-Gen). Furthermore, when we observe the bacterial sequences across our laboratory experiments and even in published genome sequences of Nasonia, we observe a conserved set of OTUs within the microbiome that spans nearly a decade of lab rearing; specifically Proteus, Providencia, and Acinetobacter.

In this current work and that of our 2012 Evolution paper, we independently demonstrate that when wasps are raised under the same environmental conditions, phylosymbiosis emerges.  But the phylosymbiotic microbiome itself does not have to be identical between environments, just as gene expression or epigenetics does not have to be identical between generations or environments. The remarkable thing in Nasonia is precisely that the UniFrac tree analysis finds phylosymbiosis independently in two published studies at different times and one more unpublished study in our lab. Thus, the phylosymbiosis pattern itself is stable, but the specific OTUs present in Nasonia do not have to be. We see this clarification not as a problem  but as a reflection of the natural way by which the host genome interacts within the microbiome.

We also are the first to admit that like any laboratory study of speciation, the processes observed in the laboratory are isolated observations whose importance is not whether they occur in nature, but that nature has the potential to operate and drive speciation events with them.

3. "Under their hypothesis, restoring the hybrid community to that of the parents (both of which have similar gut bacteria) should reduce lethality.  However, when the authors perform this experiment, they do not find significantly increased hybrid viability (Figure S1B; crosses g/v and v/g)"

We understand your position here. It would seemingly make sense that the resident microbial community from one of the parents could rescue hybrid inviability because they now have a normal microbiome.  But let's look at the data and the reasoning behind the experiments. First, Providencia is only one of the many species that naturally occur in Nasonia parentals as well as conventionally-reared hybrids. Thus, the mono-inoculation experiment here is not testing the specific prediction that a full, multi-faceted microbiome can rescue the hybrids. We previously tried this experiment by enriching for bacterial communities from parentals, but ran into several confounding problems of host material being present with the enriched microbial communities.  

Second, we're now skeptical that this prediction will actually hold water. Consider the gene-gene analogy from a speciation genetic perspective. You can only rescue hybrid mortality when you knock-out the epistatic genes, which is what we analagously did with the microbiome. But placing the "correct" gene in a hybrid background would only reinstate the epistasis that underscores the hybrid incompatibility. Thus placing the correct microbe, either specifically or a close relative, should recapitulate the epistatic interaction and mortality. Under this reasoning, your claim that a normal microbiome should rescue lethality is not supported either in our hologenomic view or a nuclear-centric view of hybrid incompatibilities 

4. " When the authors perform this experiment, they do not find a significant difference between Nasonia inoculated with their normal bacterial community (Providencia) or with a completely novel bacteria (Enterococcus)"

Some background on these two bacteria might be helpful here. Enterococcus is actually present in both hybrids and non-hybrids (we state that in the third page of the main text, also see our supplemental tables) and thus we expected it to kill because the host genome would recognize it. Ongoing experiments with very distantly related bacterial species that Nasonia may not be able to recognize do not seem to kill the hybrids, which is what we would predict. Thus, we assert that your reasoning here is backwards.

In summary, a major part of our effort is to convince evolutionary biologists that the microbiome arises from an element of host control and under host control they are part of an extended phenotype with genomes themselves. Microbial ecologists have weighed this evidence to be quite self-evident in the past few years, though not every study bears out an element of host control. Oddly enough, both fields accept the intimate interactions between the host genome and ancient endosymbionts / organelles; but clearly they emerged from predecessors that were more free-living and “farmed” from the environment until they became obligate and germline transmitted. What we are seeing here is a continuum of symbiotic interactions.

Guest Blog Post On The Story Behind A New Phylosymbiosis Paper

Below is a guest blog post by Soeren Franzenburg (Twitter: @naturfokussiert) who recently migrated from Kiel/Germany to do a postdoc at Cornell University on animal-microbe symbioses in Angela Douglas' laboratory. When Soeren's paper came out, my jaw dropped to the table. Without hesitation, it is one of the best papers that I've read all year. It is a major contribution to an emerging theme in biology that the host genome, and specifically the immune system, "farm" the microbiome from the environment in specific ways. Hat tip to Greg Hurst @TheLadybirdman for the analogy of hosts farming the microbes from the heterogenous environment into their bodies.

If you're interested in microbial ecology, microbiomes, evolution, immunity, the hologenome concept, speciation, phylosymbiosis and more, this story is one you want to keep up on.  I have also gotten to know one of the senior authors on the paper, Thomas Bosch, over the last few months. It seems that conferences in evolutionary biology, the microbiome, or symbiosis might want to capture this emerging theme with a symposia on the genome-microbiome interface.

Finally, if anyone wants to write a guest blog post on the story behind their recent publication, do not hesitate to get in touch and we'll set it up.

The story behind: “Distinct antimicrobial peptide expression determines host species-specific bacterial associations”

Seth asked me, if I would like to write a guest blog post about my paper “Distinct antimicrobial peptide expression determines host species-specific bacterial associations” which was recently published in PNAS. Since the job of a scientist should not only be to perform research, but also to communicate science to a broader audience, I gladly accepted this challenge.

Picture of Hydra (Source: Wikipedia)

In this publication, we investigated the mechanisms underlying the assembly of bacterial communities associated with seven closely related species of the freshwater cnidarian Hydra.

It became increasingly evident in the past years that bacterial associates are essential for the host’s health, as supported by severe fitness disadvantages in axenic or certain gnotobiotic animals. As a consequence it would be advantageous for a host to actively select for suitable bacterial associates and maintain a defined host-bacterial homeostasis. This ability should be genetically fixed in the host’s genome. If the host’s genotype matters for microbiota composition, closer related host species should be colonized by more similar bacterial communities compared to distantly related species. This recapitulation of host phylogeny by microbiota compositions was recently termed a phylosymbiotic relationship.

However, besides host phylogeny, diet was shown to be one major determinants of microbiota composition in the wild and distantly related species with similar lifestyles can show convergence in their microbial communities. That is why observing phylosymbiotic host-microbe relationships and investigating the underlying host-mechanisms relies on studies with closely-related host-organisms and very well controlled environmental conditions, including diet. These issues were also discussed recently in a scientific Google⁺ Hangout, organized by Seth.

In our recent paper, we were able to show phylosymbiotic host-microbe relationships in seven species of the freshwater cnidarian Hydra. The studied species were separately reared in simple, water containing plastic-dished for up to 30 years under identical environmental conditions, including standardized diet. Nevertheless, their microbial composition differed substantially and revealed a highly phylosymbiotic pattern. Impressively, after three decades of identical cultivation, each species still maintained its specific, bacterial fingerprint.

Subsequently, we were able to pinpoint a group of species-specific antimicrobial peptides, called arminins, as critical determinants of the microbiota assembly. When axenic Hydra polyps were inoculated with bacterial communities characteristic for different Hydra species, the recipient host selected for bacterial taxa resembling its native microbiota, just like in an elegant reciprocal microbiota transfer experiments between zebrafish and mice conducted by Rawls et al. (2006). However, arminin loss-of-function polyps significantly lost this selective potential and ended up with untypical bacterial communities. When inoculated with their native bacterial colonizers, control- and arminin deficient Hydra were colonized equally, indicating that the species-specific microbiota is partially resistant to the antimicrobial peptides expressed by its host. Thus, the host’s immune system indeed plays a major role in selecting the bacterial associates. Since Hydra is a phylogenetically old organism, these observations are likely to be valid for more complex animals as well.

The paper ends with a short perspective on the role of symbiosis in speciation. Several studies have shown that the microbiota can act as a “metabolic organ”, allowing the host to feed on otherwise insufficient diet. For example, the symbiotic bacterium Buchnera provides its aphid host with essential amino acids, allowing the utilization of nutrient poor phloem sap as food source. Generally, changing the microbial partners can confer new traits to the host much faster than evolution of the host genome alone. These traits might open a new ecological niche and thus accelerate sympatric speciation.

The crucial question is: How do animals change their microbial partners? Our publication indicates that changes in fast evolving antimicrobial peptides are sufficient to drastically alter host-associated bacterial communities. Coupling fast evolving genes with the adaptive potential of changed bacterial partners could be a potential promoter for speciation.

Congrats to Soren et al for such a wonderful piece of symbiosis work.

Related blog posts:

1. The science of the superorganism: Host-microbiota specificity (November 28, 2012)

2. The large immune effect - vlog 2 (December 18, 2012)

3. Is the microbiota species specific? Cell paper weighs in (July 23, 2012)