Fungi are pretty. And the ones in your home are (hopefully) smaller than this.
I’m very excited to be going to this meeting in June that focuses on the microbiome (i.e., all the living microbes) of our built environment – our homes, work places, sewers, etc. I’m used to thinking about the genetics of much larger living things – like chipmunks – where large non-living things – like rivers – create barriers between populations within a species which allows the populations to evolve independently. It’s been surprisingly difficult for me to apply my background “macro” knowledge to my new “micro” interests. How do different microbial species arise? What is a microbial species, anyway? Specifically restricting my many questions to our homes – what barriers could cause divergence between seemingly connected individuals?
Bacteria abound on our skin and when we come in contact with items in our home, our bacteria are directly transmitted to the surface (think door knobs). Additionally, we shed skin cells – and their bacteria – in our homes resulting in a near constant snow of human-associated (and pet!) bacteria. These facts lead to human occupancy being a source of our indoor microbiome. But bacteria are not the only miniscule things sharing our living spaces. What about other microbes? And now for the question of the day: where does the fungi in your house comes from?
Often I think we as scientist do a really good job of convincing ourselves that our work is important. However, our research rarely makes a big enough splash that a study is widely accepted by everyone as awesome. Trust me, I have recently tried to excitedly explain to a non scientist at a party why finding the recessive mutation behind disliking cilantro was sooooo cool. It didn’t work…
But this study is so cool that it has already blown up the blogosphere. So much so that I was considering posting on an awesome new review by two of my favorite researchers out of the UK (if you haven’t read this yet you should. Also check out Britt Koskella’s blog… it’s pretty awesome). But being a roller derby skater myself (Rolling Hills Derby Dames), I decided I couldn’t let such an awesome study go by without posting about it.
At the moment, the field of microbial ecology is going from big to huge. This is partially due to the inexpensive availability of genome data making it possible to asses the frequency and species of microbes within all sorts of environments. It could also be due to the immediate applicability to human health, as the composition of the microbiome has been linked to obesity, bacterial vaginosis and potentially irritable bowel syndrome.
These communities vary across different parts of the body and individuals, and change over time. And although we know quite a bit about how pathogens can be passed from person to person due to contact, not much is known about the effect contact has on the microbiome.
Lots of contact.
Photo Credits to Scott Butner
Historically, medical research has focused on pathogenic bacteria when trying to understand the relationship between human health and microorganisms. This makes intuitive sense – since pathogens make us sick – but our bodies host way more nonpathogenic bacteria than pathogens and they function in keeping us healthy. Our gastrointestinal tract has trillions of bacteria in it and much recent work has been trying to understand these complex communities. Mice are a common model for understanding human gut microbes and health. Enter Obie, the obese mouse (Figure 1, left) and Lenny, the lean mouse (right).
Figure 1: Obie and Lenny
Obie and Lenny are genetically different at a locus in their genomes that codes for leptin – a hormone that inhibits appetite. Mice that can’t make this hormone become very hungry and morbidly obese. These two mice also differ in the composition of their gut microbiota – obese individuals (both mice and human) have different amounts of the main bacterial phyla in their gut and as a result, are able to more efficiently extract calories from food. In other words, if you give both of them the exact same amount of food, Obie is going to get more calories from it than Lenny, contributing to Obie’s weight problem. In humans, where the status of our “leptin locus” is not normally known and probably not as straightforward as the case of Obie and Lenny– it’s been hard to tell whether this shift in gut microbiota is the CAUSE of obesity or the EFFECT of obesity. That brings me to today’s paper: a short communication in The ISME Journal (that’s open access!) by Fei and Zhao that addresses this exact problem.
Colostrum |cuh-laas-trum| (noun): the first secretion from the mammary glands after giving birth, rich in antibodies
The amount of research happening right now on microbes and human health is enormous. Think multi-hundred-million dollar, international-collaboration enormous. I’m sure the interest has been building for a long time, but the game changer I’m aware of is Ley et al. (2005), which showed that bacterial communities in obese mice were statistically similar to those from other obese mice and statistically different from normal-weight mice. Turnbaugh et al. (2006) showed that the shift that occurs from normal to obese* microbial communities favors microbes that are more efficient at extracting energy from a given amount of food. I’ll repeat that part: obese individuals extract more calories from a given piece of food than normal-weight individuals extract. The obese individuals have lower bacterial diversity, a trait that has also been linked to allergies. The childhood obesity epidemic is of particular concern to us all – up to a third of American children are obese and the detrimental health effects of this disease are well documented. Having a well-functioning gut microbiota may be a key to healthy weight.
That brings me to today’s topic: human breast milk (which I’ll refer to as HBM for the rest of the post). Cabrera-Rubio et al. (2012) analyzed the bacterial composition of HBM from 18 women at three time points over 6 months. The mothers in the study varied in weight and delivery method. The researchers were basically exploring what factors influence the microbial composition in breast milk, with an emphasis on weight of the mother. They used next-generation sequencing to produce a library of sequences that were analyzed for what specific bacteria were found in each sample and how the samples relate to one another as whole communities.
I couldn’t bring myself to Google image search “human breast milk” so instead I searched “babies”. Note1: there were over a billion hits (click the image to see the little text above it). Note2: the third “Related Searches” term was “black babies” which made me think – why ARE all the Google babies the same color? Curious.
Sometimes my job requires me to manually remove the contents of a dead bird’s intestines. I call this skill “hand-pooping”. And at rare and beautiful times, my job requires me to go someplace awesome. Last week was one of those rare times and I went to Switzerland.
I have attended several scientific conferences over the years, but last week I had the privilege to attend my first “workshop”: Ecology and Evolution of Host-Associated Microbiota. A workshop differs from a conference in one basic and important way: the number of people speaking at a given time. At a workshop, there’s only one person speaking at all times, whereas at a conference, where everyone is encouraged to give a talk, there can be 10+ people talking at once and the attendee must choose which talk to go to. These both have positives and negatives but I had no idea how wonderful one concurrent session could be! There was no agonizing over the schedule and no running around – just one person to see and, for better or worse, no other option.
This workshop had a lot of pleasant logistical aspects. There were ~150 people attending, which was a really nice size. It was small enough to be able to speak to almost everyone there but large enough that a great cross section of the discipline was represented and it was never boring. Although the main conference organizer, Dr. Dieter Ebert said it wasn’t super intentional, there was nearly a 50-50 ratio of male to female speakers, a feature I noticed after the second woman spoke. It’s not rare to see a nearly equal male to female ratio at meetings, but when it comes to invited speakers (aka “big wigs”), the ratio is usually y-chromosome biased.
This post is a guest contribution by Dr. Levi Morran, NIH postdoctoral fellow at Indiana University. Levi studies the role that both coevolutionary relationships and mating systems play in shaping evolutionary trajectories. His research using experimental coevolution to test the Red Queen hypothesis recently appeared in Science and was featured on NPR and the BBC.
The 40 Year-Old Virgin
In the movie, The 40 Year Old Virgin, Steve Carell’s character (the title character) asks a sex education instructor, “Is it true that if you don’t use it, you lose it?” Given the context, I’ll allow you to put the pieces together and figure out just what he was referencing with the question. But, the phrase “use it or lose it” is quite catchy isn’t it?
Surprisingly, the phrase is thought to have some relevance in the field of evolutionary genetics, particularly regarding bacterial genomes. You see, widespread gene loss and genome reduction has been observed in some strains of bacteria, particularly those that specialize in certain environments (Cramer et al. 2011; Ernst et al. 2003; Smith et al. 2006). But, how and why do bacteria “lose it”, and do they lose it because they don’t use it?
It is a truth universally acknowledged in evolutionary biology, that one species interacting with another species, must be having some effect on that other species’ evolution.
Actually, that’s not really true. Biologists generally agree that predators, prey, parasites, and competitors can exert natural selection on the other species they encounter, but we’re still not sure how much those interactions matter over millions of years of evolutionary history.
On the one hand, groups of species that are engaged in tight coevolutionary relationships are also very diverse, which could mean that coevolution causes diversity. But it could be that the other way around: diversity could create coevolutionary specificity, if larger groups of closely-related species are forced into narower interactions to avoid competing with each other.
Part of the problem is that it’s hard to study a species evolving over time without interacting with any other species—how can we identify the effect of coevolution if we can’t see what happens in its absence? If only we could force some critters to evolve with and without other critters, and compare the results after many generations …
Oh, wait. That is totally possible. And the results have just been published.
The hoatzin is an amazing bird. Look at it:
It’s awesome. The hoatzin is the only bird in the family Opisthocomidae and its taxonomic position amongst other birds is unresolved. It’s a weak flier and it smells bad (think cow manure) and both of these traits are due to the awesomest thing about the hoatzin: it’s a foregut fermenter.
The hoatzin has an enlarged crop for the purpose of fermentation (see figure below). A “crop” is an anatomical structure in throat of some animals (including most birds) that primarily stores food. In the hoatzin, however, it does much, much more. Foregut fermentation is a digestive strategy where microbes living in or before the stomach break down vegetation for their host. Microbes are required by foregut fermenters because only the microbes are capable of breaking down the cell wall of plants, a barrier that confines most of the nutrients found in plant cells. The hoatzin is the only bird to use foregut fermentation and is the smallest known foregut fermenter. It’s a weak flier because of the anatomical accommodations the enlarged crop requires. And it stinks because fermentation is an odoriferous process. (The bright side to being the Stinkbird is that the hoatzin is not eaten by humans and this probably contributes to the fact it is NOT endangered!)
Figure 1 from Godoy-Vitorino (2008); "Bacterial community in the crop of the Hoatzin, a Neotropical folivorous flying bird"
And this brings us to today’s paper. Previous work from the Dominguez-Bello research group has characterized the crop microbiota (and by that I mean, sequenced the DNA of and taxonomically identified the bacterial species present). The goal of the current study was to compare the microbiota at a population level. Godoy-Vitorino et al. (2012) sampled three birds at two populations in Venezuela roughly 500km apart (6 birds total). At each site, they performed vegetation surveys (to identify potential food sources) and recorded about 30 hours of hoatzin foraging behavior. To compare the microbial communities, Godoy-Vitorino et al. used a PhyloChip – a microarray specifically for identifying bacterial species in a complex sample.
Some of the biggest questions in evolutionary biology deal with the origin of life. For example, if I go back one generation, I find my parents. Two generations, my grandparents. Ten generations are human beings who may or may not have looked like me. Five hundred thousand are, oh, I don’t know. Maybe a bipedal hominid? Anyway, if we continue going backward like this, we inevitably get to time zero and encounter some big-time questions that can really cause a brain to cramp up.
One of these major questions that can cause someone to drool on their shirt in amazement of evolution is the transition of life from unicellular, sovereign entities to cooperative multicellular organisms. A recent paper by Ratcliff et al. (2012) from the University of Minnesota posits that the first step towards multicellular organisms is cellular clustering; they then proceed to evolve clustering in unicellular yeast and ask questions about the clusters.
RECIPE FOR EVOLVING MULTICELLULAR CLUSTERS FROM UNICELLULAR YEAST
Premise: Bigger things settle in solution faster than smaller things.
(Oversimplified) Materials: Unicellular yeast (Saccharomyces cerevisiae), test tubes, solution that the yeast can eat, time
Step 1: Suspend unicellular yeast in solution in a test tube.
Step 2: Wait 45 minutes.
Step 3: Transfer the cells at the bottom of the tube to a new tube with fresh solution.
Step 4: Return to Step 2 60 times.
Step 5: Look in microscope. Continue reading
Our bodies are teeming with bacteria: for every one human cell in your body, there are at least 10 microbial cells. That’s about 100,000,000,000,000 microbes – what are they all doing?
The communities of microorganisms that live on or in a particular host are called the microbiota, and are responsible for a lot of physiological and biochemical functions. It’s probably no surprise that the gut microbiota digest complex molecules we’ve eaten and they keep pathogens from colonizing our bodies (most of the time). They synthesize vitamins and amino acids that we can’t make ourselves. Recent studies have shown that variation in gut microbiota are associated with obesity, diabetes, normal brain development and insulin signaling (which has a downstream affects on body size and developmental rate). But there’s one effect that variation in microbiota can have on their host that is particularly fascinating to me: they can influence host mate choice.
In 1989, Diane Dodd reared fruit flies (Drosophila pseudoobscura) from a common stock on two different food sources: starch and maltose. She found that after multiple generations of isolation on their separate substrates, starch-flies preferred to mate with starch-flies and maltose-flies preferred to mate with maltose-flies. The result was robust and repeatable, but the reason why and its mechanism were unknown.