Nothing in Biology Makes Sense: Making sense of the relationship between gut microbes and obesity

Obese mouse, non-obese mouse. Photo via Nothing in Biology Makes Sense.

Over at Nothing in Biology Makes Sense, Sarah Hird discusses an attempt to suss out whether your gut microbes change when you’re overweight, or your gut microbes can make you overweight.

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).

The new study demonstrates that bacteria cultured from the gut of an obese mouse cause normal-weight mice to gain weight when they’re fed a high-fat diet—and that the genetically similar mice without the bacteria can eat the same diet without becoming obese. You should definitely go read the whole thing.◼

Nothing in Biology Makes Sense: Making sense of gene tree conflict across an entire genome

The only illustration in The Origin of Species. Image via Wikimedia Commons.

This week at Nothing in Biology Makes Sense, I discuss my latest research paper, which has just been published online ahead of print in Systematic Biology. In it, my coauthors and I use a genome-wide data set to reconstruct relationships among a couple dozen species in the genus Medicago—a data set that proved to be kind of a challenge.

Using that data, we identified some 87,000 individual DNA bases that varied among the sampled species—single-nucleotide polymorphisms, or SNPs. That’s not a lot in terms of actual sequence data—but considering that every one of those 87,000 SNPs is a variable character, and that most of them were probably spread far enough across the genome to have independent evolutionary histories, it contains many more independent “gene trees” than most DNA data sets used to estimate phylogenies.

To learn how we tackled all those gene trees, and what we found when we did, go read the whole thing.◼

The Molecular Ecologist: If genes aren’t independent “beans,” speciation is easier

Three-spined stickleback profile Threespine sticklebacks are a classic case of speciation caused by natural selection. Photo by wolfpix.

This week at The Molecular Ecologist, my friend and collaborator Chris Smith writes, with two coauthors, about a new study simulating adaptive speciation in the face of gene flow, and the effects of linkage among genes involved in the adaptive divergence:

Models of speciation that involve ongoing gene flow remain controversial because gene flow is expected to homogenize differences between populations. However, genome-level effects may facilitate speciation with gene flow. For example, selection against immigrants may have the effect of reducing realized gene flow, even at loci that are not under divergent selection (Rundle & Nosil 2005). This global reduction in gene flow and increased divergence across the genome due to divergent selection is termed ‘Genome Hitchhiking’ (Feder et al. 2012). Genome hitchhiking may be enhanced by fitness epistasis – multiple loci interacting synergistically to cause reductions in fitness that are greater than selection acting on any one locus.

It turns out that speciation is more probable in models that don’t treat genes like independently evolving beans in a beanbag, bearing out a classic criticism of simple speciation models made most prominently by Ernst Mayr. However, true linkage among the selected genes isn’t necessary, either. All in all, this is an exciting new development for those of us who think natural selection might be important in forming new species, so you should definitely go read the whole thing.◼

Fire ants, foolish flies, and phylogenomics

DSC_9777.jpg Fire ants. Photo by hankplank.

I’m out of town at a conference this week (more on that at a later date), but it’s been a busy one for both blogging and academics. At the Molecular Ecologist, I’ve got a Q&A with Yannick Wurm, the lead author on a cool study that uses high-throughput sequencing data to demonstrate that one species of fire ants has a “social chromosome” which determines how many queens a single colony can support.

In particular this has been extensively studied in the red Solenopsis invicta fire ant: some colonies have up to hundreds of wingless queens, but other colonies contain strictly one single wingless queen. And this is stable: any additional queen you try to add to a single-queen colony is executed by the workers.

Then, at Nothing in Biology Makes Sense! I discuss a new study of local adaptation by a South African daisy, which fools bee flies into mating with its petals, the better to pick up and transport pollen.

What makes G. diffusa more interesting, to an evolutionary biologist, is that not all populations of the daisy practice this deception. The pattern of G. diffusa‘s petals varies across its range—and not all petal patterns prompt the pollinators to hump the flower.

And finally, the first paper from my postdoctoral work in the Tiffin lab is officially online at Systematic Biology. It’s a project in using a very large genetic dataset—tens of thousands of markers—to reconstruct the evolutionary history of the genus Medicago, which includes my current favorite plant. It’s attached to my very first Dryad data package, which provides all the original data underlying the paper. I’ll be writing about this work in more detail in the near future.◼

Herd immunity, unfalsifiable hypotheses, and the search for the missing heritability

Image created with Pulp-O-Mizer.

It’s been a busy week at the other blogs with which I’m variously affiliated. So busy that I’m going to run down what’s up at Nothing in Biology Makes Sense! and The Molecular Ecologist in a single omnibus post.

First up, Nothing in Biology Makes Sense!: My younger brother Jon (@Bonovox1984), who’s in his third fourth year of medical school, led off with a post on a new study of “herd immunity”—the effect whereby people who haven’t been vaccinated benefit from reduced risk of disease if they’re living around lots of people who have been vaccinated. Then Prosanta Chakrabarty (@LSU_FISH) continued the NiB tradition of blasphemy by explaing why creationism is not—and can never be—science. And finally, we announced that Nothing in Biology will be hosting the March 2013 Carnival of Evolution—you can see how to submit your evolution-related blog posts and other online content right here.

Then, over at the Molecular Ecologist, Tim Vines posted Molecular Ecology‘s first-ever list of top reviewers to provide some recognition for the volunteer labor that goes into a good peer-review process. And I wrote about a cool new study that goes looking for the “missing” heritability in quantitative trait locus studies—and finds a lot of it, with the help of lots of statistical power. (It turns out that a lot of the missing heritability is hiding in genes of small effect, which is exactly what some folks have long speculated.)◼

Have yourself a scientific Christmas

The love makes beautiful. frosted landscape for christmas xmas and happy new year pour noël et le nouvel an Photo by Thierry.

Have yourself a scientific Christmas,
May your teaching load be light!
Next year maybe funding will not be so tight.
Have yourself a scientific Christmas,
Pipette your last lane …
Don’t stir the reagents with that candy cane!

You’re done with your holiday shopping and ready to read about selective breeding of Christmas trees, right? Well, then the Molecular Ecologist has just the post for you. Or maybe you’d rather check out an old Denim and Tweed post about mistletoe population genetics?

And a happy midwinter celebration of your choice to all!◼

Nothing in Biology Makes Sense: Making sense of same-sex orientation in humans

This week over at Nothing in Biology Makes Sense, I’m taking a look at a much-heralded new journal article that purports to solve an evolutionary puzzle that has particularly personal interest to me: how same-sex sexual orientation could evolve in the face of its selective costs. Of course, I’ve previously discussed a long list of possible answers to this question — but the new paper suggests that the best solution may lie in the epigenetics of sexual development.

Epigenetics is an appealing explanation for same-sex attraction because we have, at best, a fuzzy picture of the genetic basis of sexual orientation. Homosexuality definitely “runs in families”. That is, people with gay or lesbian parents, siblings, aunts, or uncles are more likely to be gay or lesbian themselves; and pairs of identical twins, who share pretty much all their genetic code, are more likely to have the same sexual orientation than pairs of fraternal twins, who share only half their genes.

Yet more sophisticated methods to identify specific genes associated with sexual orientation have failed to find any consistent candidates. (Though, as a caveat, the only genetic association study [PDF] I’ve seen suffers from small sample size and considers a very small number of markers by modern standards.) Moreover, while identical twins share sexual orientation more than fraternal twins, they don’t share it with complete fidelity — only about 20% of gay men who are identical twins have twin brothers with the same orientation.

For an explanation of what exactly epigenetics is, a full description of the new study, my evaluation of it all, and even some gratuitous — if, I hope, educational — beefcake, you’ll have to go read the whole thing.◼

The Molecular Ecologist: The Carnival of knowing what I know now

This advice won’t even cost you five cents. Image via nola.com.

That carnival of advice based on personal experience from previous career stages? Yep, it’s online today at The Molecular Ecologist. Head on over for a heaping helping of introspection, snark, and (mostly) sober reflection from across the science blogosphere.◼

Nothing in Biology Makes Sense: Making the jump from the mitochondrion

SEM_mitochondria A mitochondrion. Photo by Jay Reimer.

This week at Nothing in Biology Makes Sense, Amy Dapper discusses co-blogger Devin Drown’s new study of the two not-quite separate genomes within every cell in your body:

Unlike our other organelles, mitochondria carry their own separate, circular genome. Furthermore, mitochondria are maternally inherited via the cytoplasm of the egg. This means that unlike the rest of the genome, the mitochondrial genome is inherited only from mom. Interestingly, over time, some of the genes that are important for the function of the mitochondria have moved from the mitochondrial genome to the nuclear genome.

That movement of genes from the mitochondria to the nucleus has some interesting evolutionary consequences, as you’ll find out if you read the whole thing.◼