Scanning electron micrograph of Shewanella putrefaciens. Photo by EMSL.
This week at Nothing in Biology Makes Sense!, Sarah Hird explains a new theoretical study proposing that species concepts are hard to define for microorganisms not because just because they reproduce asexually and trade genetic code like playing cards … but simply because they’re small and numerous.
Specifically, the product of mutation rate and carrying capacity (uK) needs to be below a certain threshold for species to form. This is because there needs to be a small amount of variation relative to the amount of niche space available or no clear “best” type will emerge that can outcompete all the other types quickly enough to become established. If mutation rate is high, there are too many available types. If carrying capacity is high, there is no way to limit who’s there at all. Many other things are happening with this paper, but their big conclusion, put plainly, is that if there is too much variation, differentiation cannot occur.
If that sounds as freaky to you as it does to me, you’ll want to go read the whole thing.◼
If you think those tusks are impressive, you ain’t seen nothing yet. Photo by Joe King.
Over at Nothing in Biology Makes Sense! Sarah Hird discovers a case in which Creationists are willing to cite phylogenetic context to make a point, and that point is that God made Eve from the bone in Adam’s penis. What, you didn’t know that most mammals have a penis bone?
Baculum is the technical term for the penis bone. Many mammals have one – presumably to aid in sexual intercourse. For mammals that mate infrequently, prolonged intercourse ups the chances that a particular male sires some babies. For mammals that must mate quickly, the baculum provides immediate rigidity. And for all mammals, keeping the urethra straight while copulating is imperative, so maybe it’s there to prevent a kink in the works, so to speak.
To see the full phylogenetic context of the baculum, and learn some possible reasons why a male walrus has a two-footer but humans have none at all, go read the whole thing.◼
This week at Nothing in Biology Makes Sense!, guest contributor Chris Smith finds something a bit odd in his Google Scholar results:
I recently gave a lecture on the Miller-Urey experiment, and I wanted to pull up the original citation. So, glancing at the clock to make sure I still had five minutes before showtime, I headed over to Google Scholar and entered in the search terms “Miller Urey.” When I started browsing the results I was surprised to find, on the first page, a link to an article titled “Why the Miller–Urey research argues against abiogenesis” published in The Journal of Creation, a product of Creation Ministries International.
To learn what Chris thinks is going on—and how it resembles a phenomenon in evolutionary biology—go read the whole thing.◼
Over at Nothing in Biology Makes Sense, Amy Dapper takes a look at a new study suggesting that thinking about science might promote moral behavior.
In all four experiments, the authors found exposure to scientific thinking led to more moral behaviors. Study participants that were exposed to the scientific priming (or in the first experiment, that had greater previous exposure to science) reported date rape as being more wrong, were more likely to report that they would participate in prosocial behaviors and divided the $5 more evenly between themselves and the anonymous participant.
Of course, I’m flabbergasted by these results, because all of the scientists I know are selfish, amoral hedonists—that’s why we’re all clamoring for cushy, overpaid jobs on the tenure track. But maybe you should go read the whole thing and see what you think.◼
A Joshua tree flower. Photo by jby.
Over at Nothing in Biology Makes Sense! I’ve got a new post discussing freshly published results from my dissertation research on Joshua trees and their pollinators. I don’t have to tell you why Joshua trees are interesting, do I?
Joshua trees are pollinated by yucca moths, which are unusually focused, as pollinators go. Your average honeybee will blunder around in a flower, scooping up pollen and drinking nectar, and maybe accidentally pollinate the flower in the process. A yucca moth, on the other hand, gathers up a nice, tidy bundle of pollen in specialized mouthparts, carries it to another Joshua tree flower, and deliberately packs it into place. She does that because the fertilized flower provides more than a little nectar for her—she’s laid her eggs inside the fertilized flower, and when they hatch her offspring will eat some of the seeds developing inside it.
That’s pretty cool in its own right. But what’s especially interesting about Joshua trees, from an evolutionary perspective, is that they’re pollinated by two different moth species. And it turns out that the flowers of Joshua trees associated with the different moth species also look pretty different. The most dramatically different feature is in the length of the stylar canal in the pistil, the part of the flower that determines how the moths lay their eggs.
In the latest development, my collaborators and I tested for genetic evidence that Joshua trees pollinated by different moth species are isolated from each other. To learn what we found, go read the whole thing.◼
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.◼
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.◼
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.◼
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.)◼
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.◼