November 30, 2011 § Leave a comment
I like bees, and for a brief and mostly happy period was the host of the Stern/Rudner Swarm — a pair of hives maintained by Bodo Stern and David Rudner that resided in my garden. My job was to grow the flowers and take a share of the resulting honey. Sadly they failed to make it through last winter. I suspect that the problem for these particular hives was the lack of a convenient water source rather than one of the many diseases that seem to be decimating bees worldwide, but it’s no secret that bees are in trouble— and therefore, perhaps, so are we. Bees are not only responsible for making honey; they also
pollinate agricultural crops, most types of fruit, and many wild plants. In my list of apocalyptic worries, the collapse of the bee population is not at the top — climate change and the risk of sterilizing the oceans are both up there — but it’s not at the bottom either. And so I was interested to see a recent paper (Koch and Schmid-Hempel, 2011: Socially transmitted gut microbiota protect bumble bees against an intestinal parasite. PNAS doi/10.1073/pnas.1110474108) that suggests that the gut microbiota of social bees may give them some protection against certain parasites.
The parasite studied in this paper is a nasty little item called Crithidia bombi, which — if it infects a young queen bee — leads to a ~50% loss in the queen’s ability to found her own colony. In previous work, the authors found that treating bees with antibiotics led to a very high C. bombi infection rate; but these experiments were hard to interpret since bees apparently really don’t like antibiotics. About half of the bees in the antibiotic-treated group died just from the antibiotic treatment, before they ever saw the parasite. So, was the higher infection rate simply caused by the fact that the bees were not very healthy? Or was there some specific interaction between the microbiota associated with the bees and the parasite?
January 14, 2011 § Leave a comment
I wrote a while ago about mate choice in Drosophila being influenced by differences in the bacteria carried by flies fed on different diets.
Now a new paper (Verhulst et al. 2010. Differential attraction of malaria mosquitoes to volatile blends produced by human skin bacteria. PLoS ONE doi:10.1371/journal.pone.0015829) suggests that bacteria influence not only mate choice, but also choice of meal. By mosquitos. Thanks to the advent of
high-throughput rRNA sequencing, it’s now possible to characterize the bacteria found on the skin of individual humans, and it turns out that — funnily enough — we’re all individuals. So, can we use microbiology to explain the fact that some individuals are visibly more attractive to mosquitoes than others?
December 10, 2010 § Leave a comment
A couple of weeks ago I wondered aloud about the question of whether diet-related changes in the nature of gut bacteria could have significant effects in evolution. The paper I was writing about at the time showed that flies fed different diets quickly began to prefer mates who had been fed the same diet, and this preference appeared to be due to a change in the composition of gut bacteria. But is the composition of gut bacteria maintained over evolutionary timescales? A recent paper (Ochman et al. 2010. Evolutionary relationships of wild hominids recapitulated by gut microbial communities. PLoS Biology doi:10.1371/journal.pbio.1000546) suggests that it is; but the role of diet remains unclear.
November 30, 2010 § 1 Comment
When two populations of a species evolve in different directions — perhaps because they live on separate islands, with different food sources or different dangers — at some point individuals from the two populations become unwilling to mate with each other. This can increase the rate at which the two populations diverge, and thus the chance that they will actually become separate species. A recent paper (Sharon et al. 2010 Commensal bacteria play a role in mating preference of Drosophila melanogaster, PNAS doi: 10.1073/pnas.1009906107) suggests that developing a mating preference may be much easier than we thought, and can be due not to genetic change but to changes in the bacteria carried by the population.
August 27, 2010 § 2 Comments
I’m not normally a fan of research that claims to prove that weight gain is anything other than a result of eating too many, and burning too few, calories; it seems too much like wishful thinking. But I have to say that the story around gut microbiota being involved in obesity has been getting interesting. The story just took another intriguing turn with a paper that identifies links between gut microbiota and the endocannabinoid system (Muccioli et al. 2010 The endocannabinoid system links gut microbiota to adipogenesis. Mol Syst Biol. 6 392. PMID: 20664638.)
The endocannabinoid system is, as you might guess, the system of receptors that respond to the active principle in cannabis, and the endogenous ligands that activate them. Endocannabinoid signalling is involved in neurotransmission, memory retrieval, and the control of hunger. [Yes, this is why smoking pot gives you the munchies, and affects your short-term memory; and no, the title isn’t meant to be sarcastic.]