The Dead Body That Claims It Isn’t: I’m not dead.
The Dead Collector: What?
Large Man with Dead Body: Nothing. There’s your ninepence.
The Dead Body That Claims It Isn’t: I’m not dead.
The Dead Collector: ‘Ere, he says he’s not dead.
Large Man with Dead Body: Yes he is.
The Dead Body That Claims It Isn’t: I’m not.
The Dead Collector: He isn’t.
Large Man with Dead Body: Well, he will be soon, he’s very ill.
The Dead Body That Claims It Isn’t: I’m getting better.
Large Man with Dead Body: No you’re not, you’ll be stone dead in a moment.

– Monty Python and the Holy Grail

So it goes between John Cleese, Eric Idle and John Young.

But there is a sea, or rather lake, that is not dead yet either, feels happy, and is going for a walk on Thursday. The Dead Sea, located in the Judean Desert, roughly divided between Jordan and Israel, has a salinity of 33% – more than eight times that of seawater (3.5%). No animals or plants can survive these conditions, and the lake does look dead to the casual observer. But in the late 1930s Benjamin Elazari Volcani discovered that the Dead Sea does, in fact, support several types of microorganisms. A bit of history: Volcani’s research into microbial life in the Dead Sea led to him being awarded the the first doctoral degree in microbiology by the Hebrew University of Jerusalem, 1943. In 1975, Mullakhanbhai and Larsen named Halobacterium volcanii, a halophilic isolate, after B.E. Volcani. It is now know as the archaean, not bacterium, Haloferax volcanii.

At 33% salinity we all float. When you're down here with us, you'll float too.

Several other archeael isolates were found, noting that the Dead Sea is not quite dead yet. In fact, the lake sports what might be an underreported biodiversity. In addition to archaea it also has fungi, bacteria, protozoa and mermaids. OK, maybe not mermaids.

Now the Dead Sea has been found to be more alive than ever. A groups of Israeli and German divers have found freshwater springs deep in the Dead Sea. The springs are about 30m deep, and lie in of large craters 30meters in diameter. Look at the video below, taken by the divers. Between 1:54 and 2:10 you can see the freshwater mixing with the saltwater. The stark differences in salinity makes for a surreal underwater smoke effect. And, the real kicker, at 2:26 you can see a thick microbial mat, like gunk all over the rocks near the spring.

It would be very interesting to find out who, exactly, comprises this mat. As far as I know, this analysis has not been published yet. But the initial results are reported in National Geographic:

Preliminary analyses of samples collected in the craters suggest that the springs’ bacterial communities are very diverse—akin to what you’d find living on rocks in a regular saltwater sea, he added.

The top of the springs’ rocks are covered with green biofilms, which use both sunlight and sulfide—naturally occurring chemicals from the springs—to survive. Exclusively sulfide-eating bacteria coat the bottoms of the rocks in a white biofilm.

Not only have the organisms evolved in such a harsh environment, Ionescu speculates that the bacteria can somehow cope with sudden fluxes in fresh water and saltwater that naturally occur as water currents shift around the springs.

All I can say is: wow. Microbial mats in the Dead Sea, which we only find about now. The  Dead Sea thriving with whole carpets of life. Who’d've thunk?

ELAZARI-VOLCANI, B. (1943). Bacteria in the Bottom Sediments of the Dead Sea Nature, 152 (3853), 274-275 DOI: 10.1038/152274c0

Mullakhanbhai, M., & Larsen, H. (1975). Halobacterium volcanii spec. nov., a Dead Sea halobacterium with a moderate salt requirement Archives of Microbiology, 104 (1), 207-214 DOI: 10.1007/BF00447326

Buchalo, A., Nevo, E., Wasser, S., Oren, A., & Molitoris, H. (1998). Fungal life in the extremely hypersaline water of the Dead Sea: first records Proceedings of the Royal Society B: Biological Sciences, 265 (1404), 1461-1465 DOI: 10.1098/rspb.1998.0458

“Let another man praise thee, and not thine own mouth; a stranger, and not thine own lips.” — Proverbs 27:2

“What-ever” –  Me

In PLoS Computational Biology this week, a trio of researchers provides a review of the challenges that metagenomics might ― and already do ― pose for bioinformaticians. The authors refer to metagenomic sequencing data as “noisy and partial.” Their review specifically addresses the computational requirements presented by metagenomics, rather than a comprehensive review of the current technologies. The review concludes with a “representative studies illustrating different facets of recent scientific discoveries made using metagenomics.”

–   http://www.genomeweb.com/blog/week-plos-75

I participated in writing this article for two reasons: first, Phil Bourne, the Editor in Chief of PLoS Computational Biology is a very persuasive fellow (in a good way). Second, one of the mandates of my position at the CAMERA project at the time was to develop new and innovative bioinformatics methods for metagenomics.  As I was immersed in the field and the latest professional literature anyway, writing a review seems like a good way to communicate the latest and greatest in the field, both to others but also to ourselves (John, Adam and I, all working in CAMERA). So we decided to write this up. While writing it, this article went through a few drastic alterations: Life Happened to me a couple of times, including changing jobs and a 3,500 km move, which caused a few months  of hiatus in the writing. Once we got back to writing, the field changed: new research and new software materialized and at least one software package we were writing about fell off the face of the Earth, so revisions and insertions were necessary. Second, the manuscript started to blow up uncontrollably: there is so much to touch upon in computational metagenomics! Obviously, the field is a moving target but anything we write, especially about software, will be outdated by the time it is published. We therefore decided against the laundry list approach, and focused more on general methods. We also culled a lot of interesting things (sequencing validation, eukaryotic metagenomics)  to keep the article relatively brief and flowing.

I hope you like the final result. There’s the comment section in PLoS, you are welcome to make good use of it.

Wooley, J., Godzik, A., & Friedberg, I. (2010). A Primer on Metagenomics PLoS Computational Biology, 6 (2) DOI: 10.1371/journal.pcbi.1000667

Blog Action Day focuses this year on climate change, which, like everything else on this planet, is also a microbial matter. Howzat? Methane (CH₄) is a greenhouse gas which has heat retention capability 23 times of that of CO₂.  Soil methanogens are the chief global producers of methane. There are an estimated 7.5x 10⁹ tons of methane trapped in a frozen peat bog in West Siberia which constitute 25% of the estimated methane trapped in soil and ice-age permafrost worldwide. Due to global warming, this permafrost is melting, releasing methane, which in turn contributes to global warming in a vicious cycle. The Nature paper, and an article in TerraNature.

Not only there, but trapped methane in the melting Arctic Ocean is also being released.  The ocean floor permafrost is melting,  clouds of gas bubbles are welling up in “methane chimneys”

These “methane chimneys” sometimes contained concentrations of the gas 100 times higher than background levels and were so large that clouds of gas bubbles were detected “rising up through the water column,” Orjan Gustafsson of the Department of Applied Environmental Science at Stockholm University and the co-leader of the expedition, said in an interview. There was no doubt, he said, that the methane was coming from sub-sea permafrost, indicating that the sea bottom might be melting and freeing up this potent greenhouse gas.

Susan Q. Stranahan, environment360

This may be the only permafrost we will have in a few years

The concern is that methane release might lead to a tipping point in global climate change: flipping a switch rather than turning a dial. At some point, global warming might turn into a runaway scenario when a critical concentration of atmospheric methane is reached. Martin Kennedy and colleagues at the University of California, Riverside claim that this is how Snowball Earth has ended 635 million years ago: a rapid warming period following a runaway positive feedback prompted by a methane pulse.

The effects of permafrost thaw in Dawson City, Canada

How big a problem is this? Big.  We have only recently begun to understand the magnitude of the role of methanogens in soil chemistry. It is very large.  Even in arctic climes, cold adapted methanogens are active at below 0C temperature, down to -20C. However, a study conducted by Dirk Wagner and colleagues shows that a 3 degree rise in soil temperature from -6C to -3C  would increase methane production dramatically. This means that not only trapped methane will be released due to soil thawing, but also that methane production itself will increase due to more favorable growth conditions for soil methanogens. So permafrost thawing hits the atmosphere with a double-whammy of methane release, supporting the concern about a runaway positive-feedback cycle that  will cause sudden climate change.

Dr. Permafrost may actually be the hero here, rather than the villain

Kennedy, M., Mrofka, D., & von der Borch, C. (2008). Snowball Earth termination by destabilization of equatorial permafrost methane clathrate Nature, 453 (7195), 642-645 DOI: 10.1038/nature06961

WAGNER, D., GATTINGER, A., EMBACHER, A., PFEIFFER, E., SCHLOTER, M., & LIPSKI, A. (2007). Methanogenic activity and biomass in Holocene permafrost deposits of the Lena Delta, Siberian Arctic and its implication for the global methane budget Global Change Biology, 13 (5), 1089-1099 DOI: 10.1111/j.1365-2486.2007.01331.x

Why we are islands

In the previous post we have seen how  our bacterial population affects  our weight  and that by changing our dietary habits we can change the species composition in our guts. Also, we saw how a metagenomic analysis can lead to verifiable hypotheses: using a metagenomic analysis, Gordon’s lab discovered that the microbiome in the guts of obese mice have a high level of bacteria from the Firmicutes division; they also found that they contain a high level of carbohydrate-active enzymes or CAzymes.  These CAzymes break down sugars in our foods more efficiently, extracting more calories that contributes to weight gain in a vicious cycle.

At the same time, other studies have shown that there is a large diversity of species in the human gut, at a finer resolution than the broad divisions of Firmicutes and Bacteroidetes. But how really diverse are our gut bacteria? And how is this diversity affected by our own genetic makeup, what we eat, and how fat we are? Some answers  were published in last week’s  Nature. Gordon’s group compared the microbial content of the feces of adult twins, both fraternal and identical. The goal was to try and assess the contribution of the genetic makeup and contrast it with the environmental contribution. Since the twins were adults, most of them (70%) were not living together, thus exposed to somewhat different environments. In addition, stool samples were taken from the twins’ mothers (where available), and controls were taken from pairs of unrelated individuals. Also, each participant in the study contributed stool samples in different time periods, for self-comparisons. All this data was analyzed to receive a better picture of how different factors affect our gut microbiome.  The factors that were analyzed were genetic makeup (genotype), environment and, of course, body weight. The differences that were analyzed were the bacterial species inhabiting twins (identical and fraternal) twins and mothers and pairs of unrelated people; all individuals were also tagged as obese and lean.  The other set of differences that were analyzed were functional differences: how different were the frequencies of CAzy genes between the pairs of twins and non-twins, obese and non-obese  in this study.

What they found was that identical twins were no more alike than fraternal twins, or unrelated individuals when the differences between bacterial species that constitute their respective microbiomes were analyzed.  In other words, you cannot really say if two different samples, or even population of samples come from siblings (identical twins or otherwise), related family members, or just unrelated individuals. Furthermore, there was not a single common bacterial species that was found to be common in an abundant frequency in the guts of all 154 people in this study. This is where the title of this two-part post finally becomes clear: every man is an island, populated by a unique set of bacteria. We are quite different in the population of  species of bacteria that inhabit our guts. Furthermore, our gut bacteria species are quite different today than they were two months ago, according to this study. So not only our we islands, but we have a serious population turnover as well.

Still, our gut microbiome can be regarded as a “tissue” same as our liver, or lungs. Our bacteria take up certain foods in our digestive tract and break it down to make it available to us.  Different bacterial species maybe, but they end up doing almost the same things, as was revealed in the second part of this study.  This part of the study shows that, in contrast with species distribution, there is an identifiable core set of bacterial metabolic pathways in our guts. Furthermore, certain core pathways were identified between obese individuals, but not between obese and lean individuals.

One memorable scene in Monty Python’s Life of Brian is when Brian, the unwilling faux messiah tells the crowd of worshipers he is trying to rid himself of :  “You are all individuals”. To which the huge crowd replies, in unison: “Yes! We are all individuals!” He continues saying “You are all different!” and they answer in one voice “Yes! We are all different!” (The first minute of this clip is relevant).

Somehow, this is similar to what is going on in our individual microbiomes. We are all different: we have quite different bacteria. But in terms of what they do, they do pretty much the same things. The functional differences between individuals are much less than the species differences. OK, yes, we are comparing different metrics: differences between the lump sum of functions are measured differently than differences between the lump sum of species. I won’t get into that here, there is a link to the paper at the end of this post for those wishing to delve into the methods used.

All that being said, obese individuals had less  species diversity than lean individuals, but whether two obese individuals were related or not was almost irrelevant. The cause and effect fro this observation were not dealt with here: are people fat because of their more uniform and better sugar harvesting microbiome, or does their diet cause that? In a previous study of humans, it was shown that dieting humans do change their bacterial flora, so free will may have hope. Like any good scientific study, this one answers a few questions, but raises more: how do bacterial populations assemble themselves in our gut to perform the same functions in all human beings? Could an ecological misassembly be at least partially responsible for obesity? We are still not sure how much of our own genomic makeup contributes to this, although it may seem that the contribution is not large.

I would like to finally do some justice to John Donne, whom I have quoted partially and out of context. When saying “No man is an island”, Mr. Donne was not talking about our microbial world; he was talking about our spiritual one, and about one of the most fundamental aspects of it, our perception of human mortality. Here is the paragraph from Meditation XVII. I linked the title to the full text of Meditation.

Meditation XVII

No man is an island, entire of itself; every man is a piece of the
continent, a part of the main. If a clod be washed away by the sea,
Europe is the less, as well as if a promontory were, as well as if a
manor of thy friend's or of thine own were: any man's death diminishes
me, because I am involved in mankind, and therefore never send to know
for whom the bell tolls; it tolls for thee.

Peter J. Turnbaugh, Micah Hamady, Tanya Yatsunenko, Brandi L. Cantarel, Alexis Duncan, Ruth E. Ley, Mitchell L. Sogin, William J. Jones, Bruce A. Roe, Jason P. Affourtit, Michael Egholm, Bernard Henrissat, Andrew C. Heath, Rob Knight, Jeffrey I. Gordon (2008). A core gut microbiome in obese and lean twins Nature, 457 (7228), 480-484 DOI: 10.1038/nature07540

If this discussion piqued your interest, and you would like to learn more about humans, microbes and their relationships, I recommend this book.  Clarification: I have nothing to do with the author, the publisher, or Amazon.com to which I link from simple convenience. I read this book, and I liked it, that’s all.

Good Germs, Bad Germs: Health and Survival in a Bacterial World

]]> http://bytesizebio.net/index.php/2009/01/26/every-man-an-island-pt-2/feed/ 3 http://bytesizebio.net/index.php/2009/01/25/every-man-an-island-pt-1/ http://bytesizebio.net/index.php/2009/01/25/every-man-an-island-pt-1/#comments Mon, 26 Jan 2009 01:15:43 +0000 Iddo http://bytesizebio.net/?p=199

No man is an island, entire of itself

— John Donne, Meditation XVII

Scanning electron microscope images of B. thetaiotaomicron, a prominent human gut bacterium, and the intestine. From: Human Gut Hosts a Dynamically Evolving Microbial Ecosystem Gross L PLoS Biology Vol. 5, No. 7, e199 doi:10.1371/journal.pbio.0050199

Only one out of ten cells in our body is human

In a certain sense, every man is an island; this interesting finding comes from Jeffrey Gordon’s lab in Washington University. To understand why that is so, we need to understand something about the make up of our bodies. Adult human bodies are comprised of 10¹³ cells. These cells are broadly divided into different types that compose the tissues and organs that make us function the way we do. However, those are not all the cells that are in the human body. In addition to our own cells, we have 10¹⁴ bacterial cells that reside in and on us. Think about it: only one out of ten cells in our bodies contain the DNA inherited from our parents. The other nine cells are not human.

Most of the bacterial cells in our body  are located in our gut, about 1.5 kg of bacteria. All along our gastrointestinal tract really, from our mouth to our anus. The others are on our skin, our respiratory system (lungs, trachea, nose) and ears. These bacteria too, are roughly divided into different types that perform different functions, some of them actually beneficial to us. Skin bacteria, mostly benign, actually prevent the colonization of our skin by disease causing bacteria. Our  mouth is a slightly different story: the bacteria sitting on our teeth form plaque, a rough surface which accelerated the colonization by by other bacteria that metabolise sugar into acid. This acid eats through the tooth enamel and causes dental caries. That is why we wage a constant battle with toothbrush and toothpaste against bacteria. Other interesting stories are associated with our respiratory tract, our ears, and the upper GI tract.

But today we will talk about our gut, the bacteria that live there and some surprising findings on how they affect, and are affected by, our body weight.  Oh yes, and why every man is an island.

“It’s not your fault, it’s your gut microflora”

Two years ago, Gordon’s group published two papers that made quite a splash both in the scientific world and in the popular media.  They have shown that there is a difference in the bacterial taxonomic composition between obese and non-obese humans. They have shown that obese mice and people harbour in their guts a dominant population from the bacterial division Firmicutes. At the same time, lean  people (or even those on a weight-loss diet) and lean mice,  have less bacteria from the Firmicutes division and more from the Bacteroidetes division.  To try and understand why that is, they performed a comparative metagenomic functional analysis of mouse gut bacteria. They compared a sample of  DNA sequences extracted from the population of bacteria in the guts on lean mice,  to DNA sequences from bacteria in obese mice. They found that in obese mice the gut bacterial population contained more enzymes that broke up complex carbohydrates, like starch.  Other experiments showed that indeed, the population of bacteria in obese  mice break up  complex sugars more efficiently; that is, the bacterial populations of obese mice provide their hosts with smaller sugar molecules that are readily absorbed through the gut, creating a vicious feed-forward cycle:  if you are a fat mouse, you will get more calories from the same piece of chow than if you are a lean mouse. Their conclusion was that the human gut bacterial population is intimately connected with what we eat. High poly-carbohydrate  foods eventually enrich their consumers’ guts with carbohydrate loving bacteria; and those, in turn, “reward” their hosts with the back-handed compliment of making more simple and easily absorbable carbohydrates available to them, making them fatter.

So here is another another way in which bacteria affect our well-being: our gut flora controls our caloric intake.  Consider a slice of whole wheat bread, about 100 calories.* This means that the actual caloric intake from a slice of bread will differ between individuals. Unfortunately, it is the fatter person who will, quite probably, receive more calories from eating the same slice of bread, because his gut bacteria will deliver more available calories to him.

This is not the first time such an observation was made. In 2004 the Gordon lab published a paper in PNAS, where they showed that Bateroidetes theta suppresses the formation of FIAF: Fasting-induced Adipocyte Factor. FIAF normally prevents the creation of fat, but high level of B. theta, associated with stress in humans, induce both a higher intake of carbohydrates, and the formation of fat from that intake.  Here is a case of bacteria exerting a hormonal influence on our bodies affecting our energy balance and our weight.

So we have an incredibly intimate association with the bacteria in our bodies, at times as strong as that we have with our own.. actually, it’s getting hard to distinguish where we end and where our microflora begins. Well, not really: a eukaryotic cell with the DNA we got from mom and dad in a double package of 23 chromosomes is probably more ours than a prokaryotic cell with a single or double chromosome. The point is that the bacterial population is as important to our well being as some of our “human-cell” tissues.

But do all obese people have the same microflora? How much of  our own genetic makeup influences our bacterial gut population and thus our body weight? And  what about the headline “Every Man an Island”, what does that have to do with anything?   Well, I’m pretty much getting to the end of this post, so please be patient, part 2 is coming up with some more interesting insights; and an explanation of the headline.

Peter J. Turnbaugh, Ruth E. Ley, Michael A. Mahowald, Vincent Magrini, Elaine R. Mardis, Jeffrey I. Gordon (2006). An obesity-associated gut microbiome with increased capacity for energy harvest Nature, 444 (7122), 1027-131 DOI: 10.1038/nature05414

Further reading:

• Fat Factors
• The gut microbiota as an environmental factor that regulates fat storage
• Microbial ecology: Human gut microbes associated with obesity
• An obesity-associated gut microbiome with increased capacity for energy harvest

To be Continued…

On a positive side, microbes also constitute the largest methane sink: those would be methanotrophs, “methane eaters” (see my previous post about Tom Schmidt lab’s work).  If we understand how these operate, perhaps we can halt the vicious cycle of methane release -> warming that leads to more methane release.

Bioinformatics is a critical component in all this. Environmental genomics is the research tool that is used to help diagnose these problem and document the flux in bacterial population.
I was delighted to see how many new algorithms and tools were emerging from those studies, some of that software being developed in the wet labs, rather than in “speciality” dry labs. Bioinformatics is becoming a lab skill, and that is a good thing.  What was even more encouraging is that the software was being developed with a forethought towards software sustainability and community use. Regarding software sustainability, one of the gripes people had (yeah, me too) is that there is a strong bias in Federal funding towards funding the development of new tools, as opposed to sustaining existing ones. Well, Lita Proctor and Ann-Lichens Park were actually very informative on the places we can apply to for software maintenace. We’ll see.  JAFA, one of my pet projects, is in a severe state of disrepair, and I plan on applying for funding for that soon enough.

Regarding software community use, thought was taken in proper licensing of some of the software mentioned. Being “license mindful”, and understanding the need for correct licensing is no longer the realm of Stalman-and-Torvalds-quoting nerds.

The Schmidt Lab is interested in upland soils are the Earth’s largest methane sink. In agricultural soil this capacity decreases: less methanotrophs. They estimate it takes 75 years for a microbial community to recover once agricultural soil stops being tended.They have shown a clear decrease in methanotrophs in agricultural soil, but it is not clear why the decrease occur.

Another interesting find in his lab was a technological one; they found an artifact in 454 sequencing: artificially replicated sequences. He estimated that about 10-30% of sequence replications found in his 454 runs are due to this artifact. The Schmidt lab actually wrote software to correct this, and they made it publicly usable via a web site.

Shannon Williamson from JCVI talked about marine viruses. Her group isolated bacteriophages (viruses that infect bacteria) using a combined filtering and bacteriocidal approach. When they analyzed the resulting  viral metagenome, they found genes that are homologous to known bacterial genes, yet cluster together in a “viral” branch of the tree. The most interesting explanation would be that some of these genes have been appropriated by the viruses to maintain the host while viral replication takes place. It is hard to rule out simple horizontal gene transfer though, since those viral genes were not compared with bacterial metagenomes from where the original samples were taken, but with known genomes only. Then again, how do you get a “bacterial only” metagenomic samples with no viral contaminants (including lysogenic phages)?

Eric Allen from the Scripps Institute of Oceanography talked about the metagenomics of extreme halophiles taken from Lake Tyler in Australia. Extreme halophiles live in very saline waters,. An interesting argument he made was for the tractability of such a system, due to the small number of species. He showed a cool slide of  a stick-figure standing at the bottom of a staircase, with the stairs themselves getting progressively higher, representing different microbial habitats ordered by their complexity.  The bottom stair was very low, and that was the acid mine drainage system. Acid mine drainage kills almost everything, and there are less than 10 microbial species that have been identified in this habitat. The next stair, slightly higher, was that of extreme halophiles, more complex than acid mine drainage, yet still species-poor. The top stair, twice as high as the stick figure itself was soil metagenomics: >10,000 species and quite insurmountable! One cool thing about extreme haliophiles is their shapes: many have regular geometric shapes: diamond shaped, or squares.

Square microbe! from Bolhuis et al. BMC Genomics 2006 7:169 doi:10.1186/1471-2164-7-169

The second day was opened by James Collins,  assistant director for directorate of biological sciences at the NSF. He talked about  NSF’s need to keep its finger on the pulse of biology: the field is in flux both due to new technologies that open up new questions, and changes in the biosphere itself due to global climate change: we are going through the largest mass extinction since the KT (dinosaur) one.

One cool figure that he had illustrated “trans-disciplinary” versus “interdisciplinary” vs. “multidisciplinary” vs. “separate disciplines”; reproduced here from memory. I guess that taking such complex human activities and interactions and placing them into Venn diagrams holds an appeal to my need to simplify and categorize.

Cross-talk between scientific disciplines.

Then the floor was opened for discussion.  Seemed like almost everyone agreed that the more genomes the better, and they would like to see more genomes and metagenomes coming up. A heated discussion then opened as to how funds should be allocated within this rather nebulous goal. To me it is clear that all levels of genomic annotation are currently insufficient. Some estimate gene calling error rate in whole genomes to be > 30%! I won’t even try to think about how high the error rate might be in metagenomes.  Computational Function Prediction is problematic too (I should know, I have been organizing a function prediction meeting for the past 4 years).  Perhaps we need more money for developing high throughput experimental methods as we continue with the bioinformatics. As much as I hate to say it, the curve that represents advances in bioinformatics annotation methods seems to be not as steep as it was five years ago.

The last talk I attended was by Nancy Moran from Arizona University. Nancy is a co-author of a paper I really like in PLoS Biology that talks about insect symbionts.The Glassy Winged Sharpshooter is an insect that feeds on tree sap. It harbors two bacterial symbionts: one supplies the vitamins to the host, whereas the other produces the essential amino acids. their genomes are very much in accord with those functions, each actually lacking the pathways the other provides, and feeding off each other’s products as well as feeding the host.

Another cool insect symbiont is the aptly named Hamiltonella defensa. This microbe protects pea aphids from parasitic wasp larva. The wasp lays its  eggs in the live aphid, and in an aphid that does not have H. defensa that larva would hatch and eat the aphid alive from the inside-out. But good-ol’ defensa kills the larva when it hatches in the aphid. (Or bad-ol’ defensa if you view aphids as a pest).  H. defensa is transmitted between insects (horizontally) as well to the next generations (vertically). Interestingly enough, some of these toxins are not encoded by the genome of H. defensa, but by a phage, APSE, that infects the bacteria. Aphids that carry the bacteria survive better than aphids that don’t, and those that carry the bacteria which, in turn, carry the virus survive even better.

I will let Jonathan Swift finish this one for me:

"So nat'ralists observe, a flea
Hath smaller fleas that on him prey,
And these have smaller fleas that bite 'em,
And so proceed ad infinitum."

Now excuse me while I shampoo my kids for head lice and boil wash all their clothes & beddings.