¡Viva La Evolución!

This week in the Research Highlights of Nature David Wilkinson talks in the journal club about the possible evolution of the aversion to rotten food. He argues that one possible reason for microbes to produce the stinky compounds is to fend off animals, that would otherwise eat the food, probably digesting the previous bacterial dwellers.

I honestly think that this explanation stretches a little bit the “eukaryocentric” point of view. I doubt microorganisms produce a compound to avoid you eating their food. It simply makes more sense that the ability to differentiate between rotten and fresh food arose with the “need” to avoid contaminated aliments that might cause you some disease. I don’t know, that’s what I always thought.

Also one of the main compounds (sulfide) that hits you to the very bone marrow is a waste product from the metabolism of amino acids with sulfur groups so we’re talking about a by-product not an actively synthesized compound.

Tangled Bank 78 is up at About Archaeology.

Wolbachia is an interesting microorganism (like most… like all). To date it was known to be a parasite that it is maternally transmitted. It had been shown that infection with this microorganism reduced fecundity in its hosts.

The way how populations are maintained is through Citoplasmic Incompatibility (CI). CI basically prevents the embryo from developing if the male mates with an uninfected female, or the the females carry a different strain of Wolbachia.

This poses a clear evolutionary question: Would the “virulence” of Wolbachia decrease over time?. This would benefit its hosts which would increase the numbers of the mutualistic strains.

This week there is a paper published in PLoS that describes an example of evolution in action.

A group of researchers have found that in only 20 years Wolbachia has passed from reducing the fecundity of females in a 20% to increasing it a 10%!

Viva la Evolucion!

After some requests from friends and some readers, and also cause I wanted a t-shirt with Carlitos Darwin on it, I have opened an on-line shop at cafepress

The prices you see are the minimum they allow me to charge (they get all the benefits) and I don’t get a penny out of it, but is fun.

So bring your geek out and get a t-shirt to show off the evolutionary within you.

Salu!

B. aphidicola is an endosymbiont of aphids (sap sucking insects). This bacterium lives in specialised cells called bacteriocytes and stablishes an symbiotic relationship with its host. They get shelter and food, and they provide aminoacids that are not found in the aphid’s strict diet.

That’s kind of the straightforward anwser to why the aphids harbor this guys. The interesting thing is that in some other cases the endosymbiont present in other insects don’t show a clear “function”. Basically, other antibiotic treated species of insects that have endosymbionts have been shown not to have any “visible” problem after the removal of them. For instance, this applies to Blochmania floridanus and its ant host Camponotus.

In a recent paper published in PLoS Biology Nancy Moran’s team found an unexpected “function” of Buchnera.

They found that some buchnera strains upregulate a heat-shock protein when exposure to 35C and some strains didn’t. The reason for that, is a single-point mutation in the promoter of the gene that encodes the heat-shock protein. The strains with the missing nucleotide didn’t upregulate the gene.

Here comes the good stuff: When they exposed two groups of juniles aphids (one with each strain) at 35C for four hours, few of the ones with the nucleotide missing strains could reproduce afterwards, whereas the others encountered no problem. Also the aphids bearing bacteria with short promoters weighed less as adults.

Even more interesting! strains from Arizona showed no mutations whereas strains from cooler areas had a third of the populations carrying the shorter promoters.

Might this confer advantage in cooler climates… YES!
They found that the opposite is true when the aphids are exposed at 15C.The aphids with Buchnera strains that carried the mutation produced progeny faster than the ones bearing strains with longer promoters.

That’s absolutely fantastic!

How can the upregulation of heat-shock genes affect so drastically (only four hours of exposure) the aphids?
This is a beautiful example of how the question is the most important part of the research, what do you call function (like in the case of Blochmania and Camponotus? what are the normal conditions?

How much left to be known. How much left to be known. I love it!!

Tangled Bank is up at Aetiology!

…chromosomes.

It is known that humans and Drosophila “buffer” their double dose of sexual chromosomes (females have two X chromosomes whereas males have only one). Basically one of the two X chromosomes becomes inactive during development.

This week there is a paper published in the Journal of Biology that shows that birds behave differently “sexualchromosomicallywise”. In the case of birds, males are the ones with the double dose. But in this case both chromosomes are active, in fact males express sex-linked genes at higher levels than females.

It’s speculated that this might be involved in the generation of sexual dimorfism.

I guess last march could have been called the microbial genomes month. PLoS dedicated most of last month’s issue to the goblal oceanic sampling that the Craig Venter’s institute is carrying out.
Also this week in Science there’s an article mentioning the ambitious program that the U.S. National Academies’ National Research Council (NRC) has outlined: The Global Metagenomics.
I have the feeling that microbiology is getting more and more momentum. The next golden era of Micro is close!!

P.S: By the way, why don’t we have a bacterial genome day? you know, you have days for drivers, bees, unemployed, etc. I guess we deserve one, no? I propose the 28th of July, which was the day that the first bacterial genome was published (Haemophilus influenzae).

In nature’s news there’s an interesting article about Darwin’s supossed reluctancy to publish the origin due to the fear of church’s and people’s reactions.

Interestingly, according to John Van Wyhe there is no reason to think that the delay between the beggining of the writing and the first print was due to fear or external pressures. After reading personal letters from Darwin and colleagues the author cannot find any statement or vague idea that proves the myth. In fact he argues that the 8 years “delay”had more to do with the fact that at that time Darwin was finishing his studies on the barnacles, and also was polishing and putting ideas together to create the masterpiece he wrote.

Viva la evolucion!, and viva Darwin’s cojones!

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