Jerry Coyne Doubts That Symbionts Cause Speciation. Let's Discuss.

Any new or unexpected concept/data will be confronted with criticisms and doubts. But over roughly the 20 years that I have been studying speciation by symbiosis (TREE 2012 review), I found that the most common criticism is the least formidable. It concerns the fact that symbionts have not been shown to be a "cause of speciation", and it has just been used again by evolutionary biologist Jerry Coyne. It is time to clear this up once and for all to generate some unity around speciation by genetics and symbiosis. I have been deeply influenced by Coyne's seminal work on speciation genetics. I admire his research, yet he has not engaged me in discussions on speciation by symbiosis despite my attempts to share/discuss our work with him. I welcome the opportunity to debate him on this issue.

From Quanta Magazine, "There are no studies as of yet that prove definitively that the microbiome causes speciation," Coyne states.

Note: I previously addressed this concern in a 2003 book chapter on Symbiosis And The Origin of Species.

The criticism, while true, fails to distinguish speciation by symbiosis from speciation by nuclear genes. Rarely do speciation workers know whether the particular isolating barrier that they are investigating is or was a cause of speciation. Speciation genes found in the nucleus make a big splash in evolutionary biology, and rightfully so, but often they are found in such old species pairs (i.e., Drosophila melanogaster and D. simulans diverged millions of years ago) that researchers can not claim they are a cause of speciation as well. Read that twice.

The concern by Coyne and others is a more general and practical problem to the study of speciation, as the formation of species takes a long time. Whether or not microbial symbionts prove to be a causative agent now is not necessarily an indicator of whether symbionts have played a role in speciation in the past or will play a role in the future. The same holds true for speciation genes in the nucleus. Most of the time, the best that biologists can do is discover the factors that cause reproductive isolation and thus the entities (genes or microbes) that can cause speciation, rather than cause speciation. 

Most reproductive isolation likely evolves in allopatry as an incidental byproduct of divergence. Simply demonstrating the genetic or microbial basis of speciation may be the closest we get to this issue. In the Quanta Magazine, I think Bradford Harris gets it right when it comes to why we see the inequality in judging speciation studies.

Do It Yourself Fecal Transplant?

YouTube is chalk full of videos like this one of fecal microbiota transplantations at home. Shocking at first, you quickly understand that the desperate nature of C. difficile infections and the patchy, but growing, distribution of clinics that offer fecal transplants has compelled a DIY treatment. I am in no way advocating for this method, just passing on the information since my post in 2012, Can a Fecal Transplant Cure…,  has attracted over 12,000 views as of May 25 this year. There are many resources listed in that post including web sites for locations that perform fecal transplants.

Here is another video of author Michael Hurst describing and acting out a DIY treatment. He used fecal transplants to treat his Ulcerative Colitis in 2011 and has been symptom free since.

Video: Bill Gates narrates "Defeating Dengue" with Wolbachia

This week Bill Gates appropriately labelled mosquitoes the most dangerous animals in the world in this blog post. The nearly two-minute long video below is narrated by Gates, who explains how Wolbachia researchers in the Eliminate Dengue project have been aggressively infecting mosquitoes with Wolbachia bacteria and releasing the mosquitoes into areas where dengue virus is a significant problem. "Wolbachia blocks the disease…It has a very good chance of success", Gates says.

I F***ing Love Science. I f***ing love Charles Darwin.

The viral video age demands that science have a video anthem. And here it is (uncensored). Lyrical shots go out to Charles Darwin, Carl Sagan, and Rosalind Franklin. Rumor has it that the epic Facebook page I F***ing Love Science (13 million people follow it) will officially have this song as its official theme song. I would be remiss not to share it here. Science needs so much more entertainment like it.

Flipping Discovery Based Research: An Interview With High School Students

For the past decade, the international outreach program Discover the Microbes Within! The Wolbachia Project has embraced a learning revolution in discovery-based research, inquiry, and collaborative bidirectional learning. I had the pleasure to capture some of these elements with this video below. Here is the YouTube link if you can't see it.

Recorded on April 22, 2014, three talented high school students from the School for Science and Math at Vanderbilt talk about their learning experiences in peer-to-peer learning. In the last five months, their goals were (i) to become experts in the international outreach program Discover the Microbes Within! The Wolbachia Project (ii) synthesize and retool the content to transmit it back to a metro Nashville high school classroom and (iii) find out what they learned about themselves and scientific literacy during the process. The latter is what this portion of the interview captures and is the "secret sauce" of peer-to-peer learning. Find out what they had to say.

Website for the Discover the Microbes Within discovery-based research program: http://discover.mbl.edu

We're hiring

POSTDOCOTRAL FELLOW IN METAGENOMICS AND MICROBIAL ECOLOGY

Seth Bordenstein (http://bordensteinlab.vanderbilt.edu) is seeking a postdoctoral fellow in metagenomics, microbial ecology, or systems biology.  The ideal candidate will pursue innovative research that compliments ongoing work in the lab on evolution, genome-microbiome interactions, and phylosymbiosis. We particularly encourage applications in the following areas:

·      Host-associated microbiomes (including but not limited to 16S rRNA gene sequencing, metagenomics, metatranscriptomics, metabolomics, and bioinformatic analyses using animal, plant or microbial systems)

·      Systems Biology (including but not limited to novel approaches in the genesis and processing of multi-omic data and models to integrate these data)

·      Quantitative and Computational Biology (including but not limited to bioinformatics, comparative functional genomics, and population genetics of large data sets)

We welcome cross-disciplinary approaches to understand how animals develop, function, interact and evolve. All candidates must have demonstrated excellence and creativity in applying next-generation sequence data to quantitative community, evolutionary, or ecological themes.

To apply or ask questions, please send information to Seth Bordenstein (s.bordenstein@vanderbilt.edu). Please submit a CV and 1-2 page research statement describing your research interests, background and your goals for your career and postdoc. Please also include the names and contact information for at least 3 references. Applications will be reviewed immediately until a suitable candidate is identified.

Is Natural Selection Not the Right Brand for Evolution?

FROM THE MARCH 2014 ISSUE

Mutation, Not Natural Selection, Drives Evolution

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I just read the above article in Discover (link: March 16, 2014) that captured my curiosity. Famed population geneticist Masatoshi Nei claims that evolutionary biology has overly relied on "natural selection" as the brand name for evolution, and he makes a fair argument. He suggests an alternative - mutation driven evolution - that can seem subtle in comparison to natural selection at first glance, but it is not subtle. Why would biologists revise their heavy use of natural selection in favor of evolution by mutation?

• First, mutations come before natural selection. Without genetic variation, there can be no change in an organism that is directed by natural selection. Nei states:

Mutation means a change in DNA through, for example, substitution or insertion [of nucleotides]. First you have to have change, and then natural selection may operate or may not operate. I say mutation is the most important, driving force of evolution. Natural selection occurs sometimes, of course, because some types of variations are better than others, but mutation created the different types. Natural selection is secondary.

• Second, evolution by natural selection ignores that some variation arises by neutral mutations (that have no effect on the organisms' function) and population size crashes can cause those mutations to spread. So why would biology want a universal brand name like Natural Selection that misses the "neutral" side of evolution?

• Third, it is Nei's opinion that natural selection is a deterministic force that simply replaces the hand of God as that deterministic force. Herein lies something important to consider.

If you say evolution occurs by natural selection, it looks scientific compared with saying God created everything. Now they say natural selection created everything, but they don’t explain how. If it’s science, you have to explain every step. That’s why I was unhappy. Just a replacement of God with natural selection doesn’t change very much. You have to explain how.

Part of the crux of the theory of evolution is that random mutations arise in a manner that is inconsistent with a deterministic hand. Changes are not orchestrated by want of a higher power but by random genetic processes that cause errors in the DNA code. It's equivalent to the randomness of the universe. 

My favorite Nei quote is at the end. It is a message for all students of science:

But any time a scientific theory is treated like dogma, you have to question it. The dogma of natural selection has existed a long time. Most people have not questioned it. Most textbooks still state this is so. Most students are educated with these books. 

You have to question dogma. Use common sense. You have to think for yourself, without preconceptions. That is what’s important in science.

Al Gore on the Microbiome and Darwin

When former Vice President Al Gore preaches the MICROBIOME, it may be time to switch fields as the bubble of exponential growth has officially burst. Sorry folks, but tis true. He does give a shocking and swift shout out to Darwin though. In all seriousness, I applaud the former VP for preaching fairly accurate science. Every drop of science education counts in the U.S.A. 

President Obama to introduce Fox's 'Cosmos' series on March 9

"We are made of star (microbe) stuff. We are the way for the (micro)COSMOS to know itself." - Carl Sagan (modified)

Tomorrow night, Science comes back to mainstream TV to reclaim its rightful entertainment and knowledge value. Join the journey and share the excitement about the new COSMOS show hosted by Neil Degrasse Tyson - the heir apparent to  Carl Sagan - who is serving the public's appetite for science and wonder. The mission of this TV show and what we all do as scientists are aligned in advancing science education and the beauty of discovery. 

Here is Neil Degrasse Tyson speaking at his usual best on scientific literacy.

Guest Blog Post on Helicobacter pylori: Friend or Foe?

We're not too far into 2014 and we already have a contender for "favorite paper of the year". This treat is the story behind that paper - one that remarkably interconnects phylosymbiosis with human health. 

Human and Helicobacter pylori coevolution shapes the risk of gastric disease 

Kodaman et al, PNAS 2014 

Contributed by Carrie L. Shaffer, PhD

Twitter @CLShafferPhD

Electron micrograph of H. pylori (Source)

Global dissemination of Helicobacter by modern humans

One of the most successful human pathogens in recorded history is Helicobacter pylori, a Gram-negative bacterium that has colonized the gastric niche of modern humans since our migration out of Africa approximately 60,000 years ago.  Since leaving Africa, H. pylori has diversified in parallel with its human host.  Because of the predominantly vertical transmission of H. pylori within family units and the chronic carriage of H. pylori for nearly the entire lifetime of an individual, we have the remarkable ability to trace human migrations by analyzing H. pylori genetic signatures.  Recent evidence suggests that H. pylori has colonized humans for at least 100,000 years, and points to a second exodus out of Africa 52,000 years ago that resulted in generation of a hybrid European lineage of H. pylori strains (Moodley et al.).

Today, H. pylori colonizes the gastric mucosa of at least 3 billion people worldwide. Gastric colonization by H. pylori results in the development of asymptomatic chronic non-atrophic gastritis in all cases.  However, in a small percentage of cases, severe gastric disease can manifest, including emergence of peptic ulcers and gastric adenocarcinoma, which is currently the second leading cause of all cancer-related deaths worldwide. In contrast to the United States, where the prevalence of gastric cancer is low, the incidence of gastric adenocarcinoma varies globally with the highest rates occurring in Japan, China, South America, and Eastern European nations.

Because of its diverse and segregated geographic and ethnic landscape, the South American country of Colombia serves as an ideal natural laboratory for the study of H. pylori-related disease and its association with gastric adenocarcinoma. Separated by only 200 kilometers, the Colombian towns of Tuquerres and Tumaco have sharply contrasting rates of gastric cancer.  Tuquerres, located in the altitude of the Andes Mountains, has one of the highest rates of gastric cancer in the world (approximately 150 cases/100,000 people), whereas the coastal town of Tumaco has a gastric cancer rate of just 6 cases per 100,000 people, despite a nearly universal rate of H. pylori colonization throughout Colombia.  

Health outcomes echoing a continued legacy of European colonization

A rich history of settlement by native Amerindians coupled with both colonization and conquest by Spanish invaders and the introduction of African slave trades led to racial and ethnic segregation within Colombia.  People residing in modern day Tuquerres are mainly of mestizo (Spanish and Amerindian) descent, while the residents of Tumaco are primarily of mulatto (African and Spanish) descent.  These observations led us to the central question of our recently published paper in PNAS (Kodaman et al.): Are the rates of gastric cancer in Colombia governed by human or Helicobacter ancestry? We reasoned that a 25-fold difference in the rate of stomach cancer between the two populations could be attributed to differences in the host genetic composition; differences in host immune responses to chronic infection; phylogeographic origin and/or virulence factors harbored by H. pylori; environmental factors such as diet and smoking status; or a combination thereof. 

Our previous work (de Sablet et al.) demonstrated that European H. pylori ancestry is strongly predictive of increased premalignant lesions and epithelial DNA damage in both Colombian populations, while African H. pylori phylogeographic origin is associated with reduced severity in histologic disease parameters.  These findings are significant because we were able to show that in this region, the genetic ancestry of H. pylori is both a risk factor for development of gastric disease and a determinant of gastric disease severity, irrespective of the presence of the major virulence factors CagA (an oncoprotein present in some strains of H. pylori) and VacA (a secreted toxin present in all strains of H. pylori).  However, this study was constrained to a small subset of our larger cohort, and thus, we wanted to further investigate how Helicobacter phylogeographic origin contributes to development of gastric cancer.

In our follow-up study, we expanded the number of patients analyzed to 242 (122 from Tumaco and 120 from Tuquerres), and focused our efforts on analyzing human ancestry in parallel with the phylogeographic origin of the H. pylori cultured from patient-matched gastric biopsies.  Using Immunochip analysis to genotype nearly 200,000 SNPs in each patient’s blood sample, we determined that human ancestry closely followed expected patterns based on historical events: the people of coastal Tumaco trace the majority of their ancestry to Africa (58%), while the mountain population of Tuquerres are largely of Amerindian (67%) and European (31%) descent. We used multilocus sequence typing (MLST) to determine the matched H. pylori phylogeographic origin from each patient, and classified each isolate into an ancestral haplotype based on analysis of housekeeping gene sequences using STRUCTURE.  Helicobacter phylogeography recapitulated our previous report indicating that the bacteria derived from ancestral European, African, and East Asian (Amerindian) lineages.  The matched human and Helicobacter ancestries were then correlated to histopathology scores from gastric biopsies taken from each patient in order to determine if either human or H. pylori genetic ancestry was associated with disease severity.

The answer surprised us: we found that perturbation of human-Helicobacter phylosymbiosis can shift a benign infection to a potentially catastrophic relationship that results in disease progression to gastric cancer.  Rather than either the human or the bacterial ancestry acting alone, the contribution of bacterial-host genetic interplay was found to be the most significant factor for predicting disease outcome.  This result was even more captivating when we analyzed the influence of the major carcinogenic virulence factor CagA on the progression of advanced gastric disease within this cohort – human-microbe incompatibility had a greater effect on the risk for developing severe disease than the bona fide Helicobacter oncoprotein.  We went on to show that disruption of human-Helicobacter phylosymbiosis accounts almost entirely for the differences we observe in stomach cancer risk between Tumaco and Tuquerres.  To our knowledge, this study was the first report of matched genetic analysis of the host and pathogen with subsequent correlation of human-microbe phylosymbiosis to clinical outcome.

Reflections of a distant past

So what do our results mean? One theory is that invasion of Colombia by the Spanish conquistadors introduced ancestral European H. pylori to the Amerindian populations, and these bacteria replaced the East Asian H. pylori strains naturally harbored by the Tuquerres population.  It is thought that H. pylori of European ancestral origin may be more virulent than some other lineages, including H. pylori of ancestral African and Amerindian haplogroups. Since many people are often co-infected by multiple H. pylori strains, it is reasonable to hypothesize that H. pylori of European lineage could have outcompeted strains of Amerindian lineage in native Colombians. Alternatively, co-infection with multiple H. pylori strains and the natural competence of the bacterium leads to a propensity of H. pylori to uptake DNA for recombination, resulting in generation of new strains that are entirely unique at the DNA level. Another possibility is that differences in virulence factors between H. pylori phylogenetic lineages could provide a competitive advantage during co-infection. In fact, analysis of the cag pathogenicity island (which encodes components of a molecular machine used by H. pylori to inject CagA into gastric epithelial cells) in several Amerindian H. pylori isolates revealed numerous changes, including gene rearrangements, indels of approximately 11.2 kb (one quarter the size of the entire pathogenicity island), and gene inversions (Olbermann et al.).  Despite these dramatic variations in macrodiversity, the Amerindian isolates retained functional secretion system machinery, suggesting that the changes are non-deleterious to pathogenicity island function, and are likely under neutral or positive selection.  Strikingly, our study reveled that patients with a high proportion of Amerindian ancestry who are infected with H. pylori strains that have a substantial percentage of African lineage (>20%) develop the most severe gastric lesions. Perhaps the frequent differences in macrodiversity found in Amerindian H. pylori isolates are essential for maintenance of host-microbe phylosymbiosis in the native Colombian population.

The results of our study provide insight into an ongoing debate in the field regarding classification of H. pylori as a pathogen rather than a commensal.  While it is true that H. pylori colonization is associated with a significantly increased risk for development of gastric disease, H. pylori may provide some benefits to its host.  For example, it has been suggested that H. pylori colonization is protective against development of esophageal reflux, cancer of the upper stomach, and cancer of the esophagus.  H. pylori may help to prevent Mycobacterium tuberculosis infection from progressing to active tuberculosis, and may play a role in providing protection from development of asthma and other allergic diseases.  The protective advantages of this fascinating microbe are intriguing, but nonetheless, additional investigation will be required to determine the mechanisms by which H. pylori provides such advantages to its host.  Our study points towards co-analysis of host and microbe genomic variation to identify those at highest gastric cancer risk so that we can selectively target H. pylori eradication.

Finally, our study brings new perspective to the so-called ‘African Enigma,’ a theory that describes the discordant prevalence of H. pylori infection and H. pylori-related disease in continental Africa.  Our findings suggest that maintenance of a harmonious host-microbe phylosymbiotic relationship can account for the low incidence of gastric disease throughout Africa in spite of H. pylori colonization rates estimated at greater than 90%.  In future investigations, it will be important to recapitulate our findings in cohorts from diverse sites including Africa, East Asia, and additional locations within Central and South America in order to determine the extent to which human-Helicobacter phylosymbiosis dictates disease outcome in global populations.

Announcement: Gordon Research Conference on Animal-Microbe Symbiosis | 2015

Very excited to see a 2015 Gordon Research Conference on animal-microbe symbiosis, in addition to the keystone meeting happening now (follow on twitter at #KSinvertebrate). These meetings indicate that the study of animal complexity is driving forward…that zoology requires microbiology.

Animal-Microbe Symbioses Identifying the Common Language of Host-Microbe Associations June 21-26, 2015 Waterville Valley Resort Waterville Valley, NH Chair: Nicole Dubilier Vice Chair: Edward G. Ruby

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Application Deadline

Applications for this meeting must be submitted by May 24, 2015. Please apply early, as some meetings become oversubscribed (full) before this deadline. If the meeting is oversubscribed, it will be stated here. Note: Applications for oversubscribed meetings will only be considered by the Conference Chair if more seats become available due to cancellations.

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Animals are intimately associated with a complex community of mutualistic microbes that are essential for their development, nutrition, and health. Research on animal ­microbe symbioses (we use the general term here to denote beneficial associations) has recently become highly active, after decades at the margins of mainstream biology. This renaissance has come from major advances in methods for studying uncultivable organisms such as molecular biological techniques (e.g., the ‘omics’) and imaging methods that can combine information about identity and function at the single-cell level. These and other new approaches are providing novel and unexpected insights into the biology, ecology, and evolution of mutualistic associations between animals and their microbiota. Correspondingly, there is considerable interest in and excitement about the animal microbiome, as visible in numerous papers in high-ranking journals and articles in the popular press. Remarkably, however, there is no regular meeting that focuses on the biology, ecology and evolution of animal - microbe symbioses.

The new Gordon Research Conference on Animal-Microbe Symbioses will provide a stimulating and international platform for understanding the current state of knowledge in this rapidly evolving and vibrant field. By bringing together scientists that work on symbiotic associations from a wide range of host and microbial groups, and are at the forefront of their fields, we will create a diverse and multidisciplinary forum for discussing the newest research directions, debating key questions, and identifying unresolved issues. We will invite researchers from other disciplines such as plant symbioses and pathogenic associations to expand our knowledge and discuss the commonalities and differences among host -microbe associations. Student and postdoctoral attendance will be encouraged by emphasizing the collegial nature of the conference, and the many opportunities for discussion during formal and informal meetings and the poster sessions. The meeting will not only contribute to a better understanding of basic biological research questions such as how prokaryotes and eukaryotes have evolved through mutualistic interactions, but will also be valuable for applied research. For example, pharmaceutical and biotechnological companies are investigating bioactive compounds produced by invertebrate symbionts as valuable, novel, antimicrobial and chemotherapeutic agents, and symbiotic microbes such as Wolbachia may help prevent the spread of human viral diseases such as dengue fever through insect hosts. We are thus confident that a diverse and multidisciplinary community of speakers, discussion leaders and attendees will provide the stimulus for a unique conference in the field of animal-microbe symbioses.

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Preliminary Program

A list of preliminary session topics and speakers is currently being developed by the Conference Chair and will be available by December 1, 2014. Please check back for updates.

The Hologenome Facebook Page - Discover Your Symbiotic Complexity

https://www.facebook.com/hologenome

I'm happy to announce a sister site on Facebook dedicated to understanding who we are as animal-microbe chimeras - who we are beyond the skin we're covered in. Come join us as we track the history and future of the science of the Hologenome - an "eyes up" view of the symbiotic complexity of organisms. The page starts with a 20 year old video on the topic.

A recent publication in PNAS by 26 luminaries in the life sciences echoes the inspiration for the site: 

"These new data are demanding a reexamination of the very concepts of what constitutes a genome, a population, an environment, and an organism. Similarly, features once considered exceptional, such as symbiosis, are now recognized as likely the rule, and novel models for research are emerging across biology. As a consequence, the New Synthesis of the 1930s and beyond must be reconsidered in terms of three areas in which it has proven weakest: symbiosis, development, and microbiology (115). One of these areas, microbiology, presents particular challenges both to the species concept, as formulated by Ernst Mayr in 1942, and to the concept that vertical transmission of genetic information is the only motor of selectable evolutionary change"

Where we go from here is up to us. This community site is one additional means to an end to see where the hologenome takes us. Looking forward to seeing you there.

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:

inShare

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.