I loves me my fruit: It may explain my big brain (sic)

Passion fruit and mangoes are enough reason to move to Australia.

Sure, there are American versions, but not like these.

Bret Stetka of Scientific American writes that compared with other mammals, and along with those of a few other notably bright creatures—dolphins, whales and elephants among them—the brain to body-size ratios of monkeys, apes and humans are among the highest.

For decades the prevailing evolutionary explanation for this was increasing social complexity. The so-called “social brain hypothesis” holds that the pressures and nuances of interacting and functioning within a group gradually boosted brain size.

Yet new research suggests otherwise. A study conducted by a team of New York University anthropologists, and published Monday in Nature Ecology & Evolution, reports diet was in all likelihood much more instrumental in driving primate brain evolution. In particular, it appears that we and our primate cousins may owe our big brains to eating fruit.

I love my fruit.

In Guelph, I was the hockey coach who always ate a grapefruit during the game. I still do when I coach in Australia, but more towards the sweeter fruits.

That must be why I’m so smart (not).

Much of the research exploring the social hypothesis has rendered inconsistent results. And as many in the field have noted, a number of oft-cited studies in support of the theory suffer from small sample sizes and flawed design, including out-of-date species classification. The new work is based on a primate sample more than three times larger than that used in prior studies, and one that used a more accurate evolutionary family tree.

In over 140 primate species, the study authors compared brain size with the consumption of fruit, leaves and meat. They also compared it with group size, social organization and mating systems. By looking at factors such as whether or not a particular primate group prefers solitary to pair living or whether they are monogamous, the researchers figured they should theoretically be able to determine if social factors contributed to the evolution of larger brains.

And it appears they could not. Dietary preferences—especially fruit consumption—seems to have been much more influential. The researchers found that fruit-eating species, or frugivores, have significantly larger brains than both omnivores and “foliovores,” those that prefer eating leaves. “These findings call into question the current emphasis on the social brain hypothesis, which suggests larger brains are associated with increased social complexity,” explains Alex DeCasien, a doctoral candidate in anthropology and lead author of the study. “Instead, our results resurrect older ideas about the evolutionary relationship between foraging complexity and brain size.”


The evolution of dangerous E. coli

Enterohemorrhagic Escherichia coli (EHEC) is the causative agent of bloody diarrhea and extraintestinal sequelae in humans, most importantly hemolytic-uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP).

dangerBesides the bacteriophage-encoded Shiga toxin gene (stx), EHEC harbors the locus of enterocyte effacement (LEE), which confers the ability to cause attaching and effacing lesions. Currently, the vast majority of EHEC infections are caused by strains belonging to five O serogroups (the “big five”), which, in addition to O157, the most important, comprise O26, O103, O111, and O145.

We hypothesize that these four non-O157 EHEC serotypes differ in their phylogenies. To test this hypothesis, we used multilocus sequence typing (MLST) to analyze a large collection of 250 isolates of these four O serogroups, which were isolated from diseased as well as healthy humans and cattle between 1952 and 2009. The majority of the EHEC isolates of O serogroups O26 and O111 clustered into one sequence type complex, STC29. Isolates of O103 clustered mainly in STC20, and most isolates of O145 were found within STC32. In addition to these EHEC strains, STC29 also included stx-negative E. coli strains, termed atypical enteropathogenic E. coli (aEPEC), yet another intestinal pathogenic E. coli group. The finding that aEPEC and EHEC isolates of non-O157 O serogroups share the same phylogeny suggests an ongoing microevolutionary scenario in which the phage-encoded Shiga toxin gene stx is transferred between aEPEC and EHEC.

As a consequence, aEPEC strains of STC29 can be regarded as post- or pre-EHEC isolates. Therefore, STC29 incorporates phylogenetic information useful for unraveling the evolution of EHEC.

Highly virulent non-O157 enterohemorrhagic Escherichia coli (ehec) serotypes reflect similar phylogenetic lineages, providing new insights into the evolution of EHEC

Applied and Environmental Microbiology, October 2015, Volume 81, Number 20

Inga Eichhorn, Katrin Heidemanns, Torsten Semmler, Bianca Kinnemann, Alexander Mellmann, Dag Harmsen, Muna F. Anjum, Herbert Schmidtf Angelika Fruth, Peter Valentin-Weigand, Jürgen Heesemann, Sebastian Suerbaum, Helge Karchc, and Lothar H. Wieler