I Got it From My Momma

Moms are great. They teach you to walk. They teach you to wash your hands so you won’t get sick. They teach you not to put cockroaches in your mouth so they won’t get sick. They teach you to never drink milk without smelling it first. And never drink it from the jug! We get a lot from our moms. Without them we’d pretty much be unable to function as humans. And without them, we’d be unable to function as ecosystems.

You probably know that you get half of your genes from your mom and half from your dad. You might know that you get all of your mitochondrial genes from your mom. But what you don’t know you get most of your bacterial genes from your mom as well. And this makes up the majority of the genes within your body. You have 10 bacterial cells for each human cell in your body but you have about 100 bacterial genes for every human gene.

Like most symbiotic science, we haven’t know this for long. We used to think the uterus was sterile and that the first dose of bacterial companions came with birth. The assumption kinda went, “Bacteria are bad. Baby is fragile. Womb is safe. No bacteria in womb, keep baby safe”. We used to think we got all our bacteria from the vaginal canal. A large number of the first colonizers for a newborn come from there. You can see this in a distinct difference in the levels of bacteria between deliveries via C-section and natural birth. This has made a case against C-sections, supported by a connection between this reduced level of bacteria and an increased likelihood of developing allergies.

(Check out this MinuteEarth video on pets, bacteria, and birth)

Think of it as a Fetal Microbiota Transplant. This transfer is ongoing, from conception to birth to infancy and childhood. We get bacteria through the placenta, through the vaginal canal, through breastfeeding and even through kissing. The connection between romantic kissing has been recently characterized as much larger than we originally thought. And the similarity in bacterial composition of romantic partners is incredible.

What’s interesting is that romantic kissing is thought to be a transposition of the mother-child kissing which has been present in our species much longer. And if kissing started that way, could it be that it had a benefit of microbial transmission? And do these benefits of donating bacteria apply to couples too?

(Check out this NPR article on the 80 million bacteria in a romantic kiss)

But you and your bacteria aren’t paired for life. Your microbiome changes drastically throughout life. You could have just as much difference between your microbiomes as a teenager and as an adult as between you and another person. And bacterial genetic diversity is huge across populations, ethnic groups, and diets. Shifts in diet can result in a very different composition of your gut bacteria within 24 hours.

This new understanding of what is passed on from generation to generation is incredible for us as organisms. Not only do we inherit traits like physical appearance and temperament, we inherit a relationship. The symbiosis our mother has with her bacterial cells is passed on to us. It’s as if we are given a puppy born of the trusty dog that our mother has had since the day she was born. And this puppy will develop and grow and change. If we treat it well it will grow strong and protect us just as we protect it. If we treat it poorly, and don’t feed it well or abuse it, it may turn around and bite us. And if we spoil it with too many treats and too little discipline it may become an overweight brat that can barely help us or help itself.

So as you celebrate thanksgiving this year, don’t forget to thank your mom for all she has done. You have more to thank her for than just those cute notes in your packed lunches, and the amazing turkey that she spent 10 hours on. You have your life to thank her for. And part of that life, is your symbiotic bacteria. Something you just can’t live without.

From Mumbai, with Love

A cockroach is crawling in a dark alley, looking for the night’s meal. He crawls over the human waste and rubbish, produced by the high concentration of over 12 million people in the city of Mumbai. It’s paradise for a pest like him. You couldn’t see him, but you might see the enemy that is about to strike. A metallic, blue-green speck, glinting softly in the yellow light coming out of the dirty glass of the apartments on either side. It’s a small, solitary wasp. This wasp doesn’t build nests to raise its larvae in. It doesn’t work together with other wasps. And it definitely answers to no queen.

The wasp isn’t looking for nectar tonight. She’s far from any flowers and has egg-laying on her tiny wasp brain. She is a jewel wasp. Jewel wasps are parasites that sting a cockroach and lay their eggs on a soft part of the roach’s leg so they can emerge and enter the roach’s body. But the craziest part of the whole murder mystery is that the roach remains alive after being stung and even after the larva hatches and begins to eat it from the inside out.

This is not a horror film from a parallel universe of sentient cockroaches that have nightmares of emerald enemies. You can find the jewel wasp in South Asia, tropical Africa and the Pacific Islands. It delivers two separate stings to the cockroach when it attacks. One penetrates the roach between its front legs and paralyzes it temporarily. This makes it stop struggling and allows the wasp to perform the next, more delicate procedure. The second sting goes directly into the brain of the roach. The wasp actually has special mechanoreceptors on its stinger that sense when it is touching the soft tissue in the brain, helping the wasp’s accuracy and preventing it from misfiring somewhere else within the roach’s head.

The venom from the sting puts the roach into a zombie-like state. It will walk and even swim when given the stimuli of being pulled or being placed in water, but it won’t move anywhere of its own accord. The wasp goes and finds a burrow to safely keep its roach minion and then pulls it by the antennae like a toddler leading a well-trained Great Dane through the park on a leash.

Not for the faint of heart, this video shows the jewel wasp in action.

The jewel wasp is a special type of parasite, called a parasitoid. This means it uses the host to raise its offspring and the host is killed in return. And parasitism is symbiosis. These species are so intimately connected. You can’t have two separate species live much closer together than beginning life inside one another. But it is definitely one-sided in benefits. It’s a closeness that definitely goes beyond clingy. The jewel wasp needs the roach to survive. All the roach gets is an oblivious zombie-like state followed by being completely eaten from within.

So how has evolution not provided cockroaches with a better defense against these wasps than just kicking and squirming? Why don’t they run away upon first sight of a jewel wasp? This is in part explained by something called the rare predator effect.

The rare predator effect is any advantage given to a predator based solely on the fact that it is not a huge threat to a population as a whole. Individual roaches are very susceptible to the jewel wasp. But there aren’t enough jewel wasps to make the cockroach’s ability to survive a concern of evolution. There isn’t the selective pressure there that would make it adapt to try and overcome the wasp. Roaches are so good at what they do, and humans are so good at making life easy for them, that it really isn’t a concern of the greater cockroach species whether a few of their kin become baby wasp nurseries.

Humans take advantage of the rare predator effect all the time, although maybe not in such a gruesome fashion. One interesting and relatively unknown habit is called worm grunting. You get a thick wooden stake, beat it into the ground with a flat iron rod. Then you grate the rod back and forth across the top of the stake to send loud vibrations into the ground. Shortly after, if you do it in moist, fertile soil during the cool morning before dawn, hundreds of earthworms come wriggling out of the soil and onto the surface. So are they sensitive to the sound coming through the soil? Does it hurt their little wormy ears?

Not quite. Researchers have discovered that this response will also occur when a mole is on their trail. The mole is a natural predator of worms and they have developed this escape route whenever they think they hear one digging through the soil nearby. The mole tracks them by scent and won’t follow their scent up to the surface. So 9 times out of 10, due to the high number of moles trying to eat worms, fleeing to the surface would be a great move. But that 1 time it is a human doing a weird worm grunting thing, the worm is going to die on the end of a fish hook, inside some trout’s mouth.

Symbiosis is so interesting in its complexities. With the rare predator effect we see how the interactions of two species are not only dependent upon those two species, but on the entire community. The actions of a cockroach-murderer in the alleys of Mumbai depend on the broader community of 12 million humans and who-knows-how-many successful roaches. The worm-grunter getting fish bait by the bucket in the boondocks depends on the success of the mole that has been hunting worms for many, many millennia.

And I love it.

Check out these super weird humans being rare predators. The biologist in that video who studied the phenomena of worm grunting is Dr. Ken Catania of Vanderbilt University.

Goodbye Antibiotics, Hello Lysins

The year is 2034. 20 years have hurtled by since the world’s worst Ebola epidemic. After travel and trade restrictions were placed on all of western Africa out of fear, the virus was contained. This stifled the aid coming from Europe and North America and containment came at the cost of 10,000 more lives in year 2 of the outbreak. Liberia continued to suffer the worst and the strain would dissipate and then flare up every few months. The worst would come in the dry season. No rain to wash away the sewage of the suffering . No water to clean the hands of those who tried to help.

Rescue finally came from within. A small lab in Freetown, Sierra Leone found a cure. They had been seeking grants to speed up the research at the time of the international embargo. No cure would have come from the west anyway, since cures don’t produce as high a profit as treatment does. The lab discovered a curious little virus that produced a molecule which antagonistically blocked the Ebola virus. They found it in bats where it had coevolved in competition with Ebola. When isolated and concentrated it provided the weapon needed to finally stop the epidemic.

If only this discovery had com earlier. If only all those deaths could have been prevented. If only the senate hadn’t been lost to the Republicans in the midterm elections.

My fictitious ramblings aside, this option isn’t far from the realm of possibilities. We’ve been fighting microorganisms with other microorganisms since 1942 and known about the potential for it since the 20s. Antibiotics are in fact any compound produced by microorganisms to fight other microorganisms (like pathogenic bacteria). Penicillin comes from the Penicillium mold that uses it for defense. We isolate it and use it for our own defense.

Antibiotics have become wildly successful over the last 50 years. The only problem is that their success has led to overuse and excessive prescriptions. Especially with our new understanding of the human microbiome. When you realize you have bacteria you need and commensal bacteria that help keep out pathogenic ones, wiping your slate clean isn’t the best idea. Wide spectrum antibiotics are just too good at killing. Antibiotic treatments have also led to resistant strains of bacteria which make the medicine less effective.

But there is an alternative that doesn’t originate in a mold, but in a virus. Bacteriophages are viruses that infect bacterial cells. They reproduce themselves many times and then burst out of the cell. One component of their bursting mechanism is a group of enzymes called lysins. Lysins are each very specific to the kinds of bacteria that the bacteriophage preys on. And we can isolate them and potentially use them to treat pathogenic infections without wiping out the diversity of microbes in our body.

Imagine lysins are keys and the peptidoglycans in the cell wall that they bind to are locks. Viruses use these keys to unlock the cell wall and burst out of the cell. Since the viruses are exiting, they put the key in the lock from the inside. In some bacteria (Gram-negative) the keyhole is blocked on the outside by another layer, made of lipids. That means viral lysins work, but artificially isolated lysins don’t. In Gram-positive bacteria, it isn’t blocked. So isolated lysins can break open and kill the cells without being inside.

One reason lysins might be the next big thing in medicine is the fact that it is a lot harder for bacteria to become resistant to them. Rapid evolution helps bacteria to develop into strains that antibiotics can’t kill. But viruses have been coevolving with their specific prey for much longer than we’ve been around. And the peptidoglycan keyhole they unlock is such an integral part of the cell’s structure that it is very hard to change. It’s like you’ve lost the spare key to your safe but can’t change the lock without destroying the safe.

In reality, antibiotics won’t be replaced completely anytime soon. Partly because right now there is no way to make lysins work on Gram-negative bacteria. But another reason is the fact that lysins make antibiotics work better. Research has shown that the two treatments work synergistically. Lysins can even re-sensitize bacteria that have grown resistant to antibiotics. Although it stops the science from being an outright revolution, it does improve their chance of gaining prevalence. If lysins are first proposed as a supplement for antibiotics and not a replacement, it helps them get a strong foot in the door. Everyone who has had even a small interaction with modern medicine knows antibiotics and that gives them a medical rapport that lysins don’t have yet.

Human studies are set to begin soon, so that means lysins are definitely something to keep an eye on in the next few years. We won’t have to wait until 2034 to see how this new understanding in the symbiotic field will change the world. The future is now.

If you want to get down to the real scholarly research behind Lysins and how they work and what’s next, check out this review paper. On a cautionary note, 3 out of 4 of the authors of the paper are employees and shareholders of the ContraFect Corporation. This doesn’t make the paper suspect, per se. It just makes the authors more likely to be very optimistic about the future of the science. Since they have a strong interest in its success.

Read this article, “All the World’s a Phage” for more on bacteriophages.

Read “Phage Renaissance” for more on the use of whole-phage therapy and lysins in a variety of medical treatments.

This Sucks

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Ebola Sucks

Ebola. It’s inundated the news and we’re all sitting on the edges of our sanitized seats waiting to hear about the next stateside case and the reports of how those affected stupidly went bowling or bought Chinese food out in public and endangered the entire American people. We become crazed consumers of news at a time like this. We look for any reports and sift through sources and refresh everything twice.

One contributor to the craze is the sheer scale of the outbreak. This is uncharted territory for us. Since March, there have been over 10,000 cases and over 4,000 deaths. (I think that’s over 4,000 too many deaths for hazmat suit Halloween costumes, right?) How abnormal the Ebola Virus is also grabs our attention. It’s a gruesome virus, averaging at a 50% kill rate, transmittable only through body fluids. We don’t know when it will stop. But we do know it feels like we’re living in a sci-fi novel as it unfolds.

And such devastating viruses like Ebola belong in science fiction– The Hot Zone, anyone? When you look at the ecology of viral diseases, we see a difficult balance they have to find to be successful. Viruses can’t reproduce on their own. They need the cellular machinery of a host. They hijack this machinery and use it to pump out copies of themselves. Eventually this kills the cell when too many copies are made. The cell will burst open and release the viral molecules to infect other cells. But when the cell bursts, that means there is one less cell to use for reproduction.

A virus will often exhaust the system and cause it to crash by reproducing too quickly or it will be stamped out by the immune system by not reproducing aggressively enough. Successful viruses are found somewhere in between – aggressive enough to reproduce quickly and vigorously but passive enough to let the host live and pass it on to a new host. They have to navigate the symbiotic schematic in order to coexist without killing their host completely. Ebola is at the top of this spectrum. It kills a lot, but sticks around long enough to be passed on given the right conditions. Luckily this is what will stop its conquest. It kills too much to be contagious enough to take over the world. So it will wind down. Eventually.

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We Suck

Think about us as Ebola. In many ways we are viruses of a much bigger world. We inhabit the earth and couldn’t reproduce without it. We are parasites that have so far harmed other inhabitants and our host more than helped anyone but ourselves. We’ve changed our atmosphere and our ocean. We’re in the process of depleting most natural resources. We’re in the fast lane for killing our host. And we don’t really have the option of jumping ship when it starts to take on water.

Luckily, we have brains. So unlike viruses we can usually think ahead and see what the future might bring. This means thinking about the balance we need to find in order to keep our host alive. A lot of the damage we’re doing – climate change, the limited nature of non-renewable resources – goes beyond the scope of this blog. And you can find it in high volume elsewhere. But many issues of our virulent symbiosis with the earth come down to sheer numbers. We have grown too big, too fast. And this overpopulation drives many diseases that could be promoted if we didn’t produce so much waste and provide breeding grounds for so many parasites.

The good news for the human parasite is that one group of these diseases has the potential to be wiped out if we master the help of two other parasites: a bacterium called Wolbachia and a pest called Mosquito.

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Mosquitoes Suck

Mosquitoes are parasites. Pests. Annoying. They sustain themselves on the blood of mammals like us. More than annoying, they can be deadly. They transmit smaller parasites like the Dengue Virus. A parasite that carries a parasite. Wolbachia is yet another parasite that infects mosquitoes. It is an “obligate intracellular parasite”. That means it is a parasite that lives inside the cells of another organism and it can’t live anywhere else. And it is really good at what it does. Wolbachia infects about 40% of all arthropod species.

The cool thing about Wolbachia is that it has been found to block the Dengue Virus when present in mosquitoes. That means that any mosquito infected with Wolbachia can’t get infected with Dengue. So it acts as a parasite, infecting a parasite, to block another parasite. Talk about an Inception of symbiosis. But we can use it to cut down Dengue Fever incidence, and it is already being done. Does it sound like a pipe dream within a pipe dream?

Wolbachia is transmitted maternally and helps its arthropod hosts spread and dominate populations. If a male mosquito carrying Wolbachia mates with a female that doesn’t have it, none of the offspring would carry Wolbachia. Cytoplasmic Incompatibility causes this mating to fail. We aren’t quite sure how it works molecularly, but it results in decreased egg-laying by the females. This gives mosquitoes with Wolbachia an advantage over mosquitoes without it.

And there are several projects that have already been carried out in the field where Wolbachia infected female mosquitoes are released and soon take over the population. Eliminate Dengue project is one group and Mosquito Mate is another (where male Wolbachia-positive mosquitoes are released and actually reduce the entire population).

In the end, this is what learning about symbiosis (and any other scientific field) is really about. Yes, we pursue knowledge for knowledge’s sake. But a better understanding of ourselves and the world we live in helps us to better live in symbiosis with the creatures around us. We can adapt and advance and knowingly fix the problems we have created unknowingly.

So here’s to hoping we get it right.
And here’s to hoping that the Hazmat Halloween costume wasn’t the most viral of the year.

Check out this video for more on the mosquito-wolbachia project Eliminate Dengue.

The Good, The Bad, & The Cancerous

More on our flawed perception of bacteria, and the cancer-causing kind (yeah, that kind sucks.)

In 2009 I got an award at 9th grade prize-giving for my performance in visual arts class. I wasn’t even in visual arts class. And for good reason. It probably showed just how good I was at getting teachers to like me. My reputation as an artist definitely didn’t do it. And it couldn’t have been that I was mixed up with someone else – I would have been the only white boy in the class.

In 1975 three American scientists won the Nobel Prize (a little harder to win without earning) for Physiology or Medicine. They had been working on the “interaction between tumor viruses and the genetic material of the cell”. That same year, Bandaru S. Reddy, a cancer researcher, co-authored a paper that illustrated a link between bacteria and cancers. He used a carcinogen (DMH) – that is, a cancer-causing chemical – to try and induce colonic tumors in rats. 93% of normal rats and 20% of germ-free rats showed tumors. This was a minor note in his paper, but it set the stage for more research into how bacteria are connected to cancer.

Reddy passed away in 2009, which seemed to be a big year for undeserved art awards and undeserved death. But his paper is still out there, coming all the way from 1975, which was a big year for the microbiome and developing our understanding of it.

Today, research has gone beyond finding a link between the microbiome and tumors to actually understanding how it works. At least a little bit. As you could probably guess from the germ-free rat research, the bacteria aren’t what cause cancer to develop. Not on their own. But we now know they can inflame tumors, or trigger immune responses that accidentally develop tumors. That’s why when they aren’t present, the carcinogen doesn’t work as well.

You’re probably thinking “Just wait a minute, Paul. Last week you told me the nice little bacteria in my poop can save lives… now you’re telling me it is bad and can influence cancer”. Not quite. Here we need to pause and recognize two errors in our casual understanding of bacteria.

  1. Lumping all of bacteria together in one group. There are up to 1 billion different species of bacteria. Billion. With a ‘b’. To help you with that idea of how huge a billion is: 1 million seconds is 12 days, but 1 billion seconds is 31 years. They all have different genomes and do different things and hang out at different tables in the cafeteria.
  1. Thinking of bacteria as “bad” or “good”. They can have negative or positive or neutral effects, but “bad” and “good” are inaccurate.

When it comes down to it, every organism is selfish. We’re all looking out for the good of ourselves or of our own species. That applies to microorganisms too. Anything they do, whether inside us, or on us, or in a hydrothermal vent in the pacific, is for their own benefit. So a bacteria that hurts us when it profits is no more bad than a cheetah that profits from the body of a gazelle. The words don’t fit in a moral sense and they don’t fit in a value sense. Our relationship with all of these microorganisms is too complex for that, and probably more complex than we understand right now.

So with other organisms, unlike with teachers, it isn’t really about getting them to like us or accidentally pissing them off and causing them to make you stand in the corner even though you’re an 11th grader and should know better. You shouldn’t be trying to be a good student or a bad student so they’ll like you, but you should be trying to do what is best in your long term interest. And that’s more of what we need to understand – how do our long term interests coalesce with those of our tiny residents and neighbors?

Symbiosis is when the path to what we want and the path to what they want get wrapped up together. Sometimes it means they get in our way, like these tumor inflaming bacteria. But a lot of the time, our paths line up and we need each other. And so we have to put up with all of them somehow. The good, the bad, and even the cancerous.

Check out this article for more on the inflammation of tumors by microbes:

http://www.sciencedirect.com/science/article/pii/S0092867414002967

Check out this article for some interesting work on the connection between phylosymbiosis and gastric disease:

http://symbionticism.blogspot.com/2014/02/guest-blog-post-on-helicobacter-pylori.html

Jeepers (micro) Creepers

A blender, a pair of rubber gloves a turkey baster, a healthy friend free of any diseases, a steady hand and some lube. My name is Steve-O and welcome to Jackass!

Right now you’re either scared, disgusted or both. Or just confused. If you’re confused, let me explain the laundry list above. It’s the basics of what you need for a rough and dirty DIY FMT. That stands for Do-It-Yourself Fecal Microbiota Transplant.

If you’re disgusted, that’s pretty normal. Fecal means poop and poop is gross. And taking someone else’s and putting it up your butt? That’s just weird. You’re thinking, did this start out as some sick fetish before people realized it was good for your health?

And scared makes sense right now, but after reading this post, that will change. I have a suitemate this year that got a bacterial infection on his face. It developed sores. He went to student health right away and got an ointment with antibiotics and it cleared up pretty fast. But the fear lingered. The rest of us guys (5 of us) freaked out for a week or two after he was fine. We were so scared of getting it. Scared of touching him. Scared of touching something he touched. We all washed our hands all the time and washed our sheets and pillowcases at least twice that month. We’re scared of bacteria. In any form. And killing it is usually our best move right?

This fear isn’t exactly incorrect. Bacteria cause conditions ranging from sore throat to Lyme disease to pink eye to anthrax. But the idea that leads to the fear is incomplete. And you can figure that out by taking a look at all the bacteria inside us.

Bacterial cells outnumber human cells 10 to 1 in our own bodies. This group of cells is called the human microbiome. And it acts like any other ecosystem – except we are the environment. These bacteria compete for resources and space and many of them provide useful functions for us. Like any other ecosystem, this one is most stable when balanced and any species that gains dominance will prove harmful. Clostridium difficile is a bacteria that lives in our gut normally but causes watery diarrhea and abdominal cramps when it becomes too prevalent (called a C. diff infection).

Antibiotics are usually the cause of this infection. They are used to try and kill some other bacteria that is causing us harm elsewhere and accidentally kill many of C. diff’s competitors. All it takes is a little bit of antibiotic resistance and a bacteria can rise to be king of the intestinal jungle.

Treating C. Diff can be problematic too because the usual prescription is more antibiotics – which sometimes work but usually just level the competition even more. One treatment that started out as fringe-medicine and quack-doctoring is the FMT. Just think of it as a blood transfusion – except with poop.

Poop transplants (FMT) are a simple solution to a complex problem. The idea is that when your internal ecosystem becomes unbalanced, you can replace it with a sample from a well-balanced ecosystem which can then grow and replenish the diversity of your intestines. It’s like fighting fire with fire. The best weapon against a rogue bacterial infection is a group of healthy bacteria that crowd them out. In fact, the expression “fighting fire with fire” comes from a technique to deal with forest fires called backfiring. Firefighters start their own, controlled fire and burn a swath of forest ahead of the wildfire. This takes up the space and resources the wildfire would use and essentially crowds it out.

(Look at this video where one of my favorite channels, MinuteEarth, explains FMT succinctly, with funny poop cartoons. )

Bacteria and poop are similar in a few ways. A clump of bacteria probably smells bad. You’d never want to put bacteria in your mouth. And we generally can’t imagine any good purpose for either. It’s just a gross fact of life we live with. But maybe that isn’t the whole story. It’s not incorrect – poop is indeed nasty and can transmit many diseases, like Cholera and Ebola – it’s just incomplete. Poop, and especially the bacteria inside it, aren’t things we have to be afraid of after all. They’re both part of the story of symbiosis. Healthy, diverse poop is something we need. And all those bacteria need a place to live. We need each other.

Which makes this a love story and not a horror film after all.

(But if you don’t want to feel like you’re in neither film and actually on an episode of jackass, don’t do it at home. There are many clinics around the US that do FMTs and lots of doctors and hospitals will now do consulting for the procedure. It’s a real procedure. It’s gaining respect and acceptance. And one day it might be a standard option.)

Check out the post that Dr. Seth Bordenstein (Associate Professor of Biological Sciences and Pathology, Microbiology, and Immunology at Vanderbilt University) wrote on the treatment here for more info.

And how could you not go to a website named thepowerofpoop.com?

In The Beginning

“In the beginning God created the heavens and the earth. Now the earth was formless and empty, darkness was over the surface of the deep, and the Spirit of God was hovering over the waters. And God said, “Let there be light,” and there was light.”

That’s Genesis 1, the beginning of the universe as told by the Bible. And it’s a common start for curiosity to strain against the unknown. Despite the poetic satisfaction it gives, and the awe it inspires, it tends to be unsatisfying for me. Whether you believe it or not, there just isn’t a lot to go on there. It’s not a scientific document. It has no detailed description of how the world was made. It gives no depth of understanding. And some people are okay with that.

I’m not.

The beginning of the universe is not something I’d endeavor to explain in this blog (at least not yet). But I would take a shot at the beginning of one of the three domains of the living universe: Eukaryota. Eukaryotes (You-carry-oats) include plants, animals, fungi and a few other groups. You are a eukaryote (that’s how I’d remember the difference between it and prokaryotes which they arose from somewhere around ). Estimates of when eukaryotes arose go as far back as 3.5 billion years, but we’re still not so sure. It’s hard to be confident in setting a date on the first eukaryotic life, partly because single cells are much harder to find and work with (don’t forget they’re really tiny) and because such ancient fossils are harder to come by (don’t forget that they’re really old – I said billion. i.e. 3,500,000,000 years).

But the cool thing about us eukaryotes and what makes them relevant to this blog is their origin. For many people, it’s hard to believe we came from single-celled organisms. But there’s even more. We came from single-celled organisms that had other single-celled organisms living inside them. Free-living bacteria became incorporated into primitive eukaryotic cells and eventually lost the ability to live outside of them. Mitochondria and chloroplasts are the organelles which once lived on their own. What connects them to free-living bacteria is their size, their double-membranes, their ability to divide on their own (akin to binary fission) and the presence of their own circular DNA, which is about the same size as bacterial chromosomes.

This means that the earliest known case of symbiosis is the reason our entire domain of life exists. Without it, there would be no dogs to be had as pets, and no bread to be made from wheat. There would be no cows to rear as food and no grass to feed them. There would be no alcohol made through yeast fermentation, and no human to drink it. Based on this fact alone, symbiosis is incredibly significant. And seeing how close this symbiotic interaction can be (where participants are no longer separable or even distinguishable) means it is something we have to pay attention to. That is why symbiosis matters in every field of biology and every area of our life. Without it there would be no life as we know it.

When I first learned about this symbiotic origin of life, I was in high school. I had a great biology teacher named Mr. Hall. He was tall, with broad shoulders, and had a personality to match. He naturally took over any room he was in. And when he taught, you better take his word as gospel. Despite my budding love for Biology, I often made his job more difficult. In 10th grade I would get in trouble for talking too much and he would send me to stand by the door. In 11th grade I made him disappointed when I knew places in Jamaica like Guts River and Treasure Beach that he was trying to use as illustrations for different habitats – disappointed because the “real Jamaicans” in the class didn’t know them. But 12th grade brought the worst frustrations – I asked too many questions. I remember always being intrigued, always wanting to go deeper, always asking why. And whenever Mr. Hall didn’t know why or just needed to move on in the syllabus he’d say “Because God made it that way.”

I now understand that these questions sit at the heart of what research is. It is the act of standing at some dead-end cliff of human knowledge and mustering the courage to look down. Curiosity straining against the unknown and the simple answers others give us that just don’t satisfy. Genesis 1 doesn’t satisfy. But I don’t think it is supposed to. We are meant to explore the universe. We are meant to question the world around us and I will continue to do so.

“In the beginning Paul created this symbiotic blog. Now the blog was formless and empty, a lack of interest was over the surface of the deep, and the cursor of Paul’s mac was hovering over the blog. And Paul clicked and said, “Now, let me write” and he wrote.”

And that was just the beginning.

Prelude

The big question:

“What do you want to be when you grow up?”

The answer I gave in Ninth Grade:

“Happy.”

The question is thrown around in every stage of childhood in some shape or form. As we got older it became more concrete: “What career do you want?”. Before graduating it became a little more specific, but no less daunting: “What do you want to study in college?”. I never knew what I wanted to do, but I did know a few things I liked. In high school I knew I loved biology. I spent the least amount of time on it when studying because it came so easily. I was the most engaged in class for it because it was the most interesting. And I always asked the most questions. I often went beyond the scope of our classes and made classmates angry because they saw it as time wasted if the content wasn’t going to be on the exam. My favorite moments were when in exasperation my biology teacher would resort to the answer, “Because God made it that way”. He was nominally Christian, as all Jamaicans tend to be, and knew that I was a the son of missionaries there. But that wasn’t ever good enough for me.

If the part where I just name dropped a little nation in the Caribbean threw you off, don’t worry. I’m used to it. In fact, I expect it. I’m often disappointed when people react calmly to finding out that this white, 6’4”, American-sounding guy who enjoys a good salad is from the island known for its smooth-sounding reggae and greens of a different kind. Growing up in the minority, influenced by my parents’ culture and by my local Jamaican neighbours and friends have given me a complicated identity. It’s all part of being a TCK, which I first really began to understand this past year when I applied for an internship to work with younger missionary kids(MKs) in Thailand. But more about that will come later. But first let me formally introduce myself.

I’m Paul. I’m studying Biology and English at Vanderbilt University. I lived in Jamaica for 18 years and now I live here in Nashville. I’ll be 21 in January. I’ll graduate in the spring of 2016. When I grow up, I want to be a science journalist. Or maybe a missionary. Or maybe an environmental biologist. Or maybe just happy. I guess that question still isn’t very easy for me. But I think if I knew exactly what I wanted to be, the rest of life wouldn’t be so interesting. One of the only things I’ve ever really known is that I love animals. I love watching them and learning about them. That’s why I’m studying Biology. Another thing I know is that I love to tell stories. That’s why I’m studying English. So stick around and let me tell you some stories.

Here is my first. One irony in my life is that I often forget how large my love for biology is. Like how you might forget how large your carpet is when it is covered in furniture. Even though it’s always underfoot, you never really think about it. But there are certain moments of clarity that bring it back to my mind. Like if you move your huge dresser and realize how bright and clean the carpet looks underneath. This summer, while on that mission trip in Thailand, I had a rediscovery of passion when I was supposed to give a talk on the importance of doing ministry at home. The most enjoyable part for me was when I showed a video of a grey kangaroo giving birth and how the barely-developed newborn, lacking hind legs and weighing as much as a sugar cube, would climb up the mother’s belly and into its pouch. THAT is what made me really animated and gave me energy and excitement while communicating my message to them. And my energy made me remember why I wanted to ask more hard questions and seek more elusive answers. And it made me remember that not everyone watches David Attenborough documentaries about marsupials in their free time.

So that is really the core of what this blog will be – the things that excite me. The ideas and areas of life that make me thrilled to tell stories and want to share them with the world. It will range from biology and science fiction, to race and culture and my Jamaican home. I’ll tell you about my family of fellow Jamericans and all my friends at Vandy who sometimes don’t believe where I come from. I’ll share the lab work I do with Drosophila and Wolbachia bacteria, and the readings I do of Chaucer. I can’t promise that you’ll enjoy it, but I can assure you that I will.