¡Viva La Evolución!

…save the world?

This week in nature news there’s an article about the relevance of keeping the microbes that live on earth alive.

Well, if they wanna save the microbes they have a loooooong way to go. But it sounds cool on a t-shirt.

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.

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!

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!!

Pathogens have developed astonishing ways of invading, evading, colonizing etc. hosts and host´s immune system, one of the most widely studied is that of L. monocytogenes. Check this link to an animation in nature reviews microbiology where the cycle of this food-borne pathogen is clearly explained.

What amazes me the most is how the actin polymerization ability might have evolved in this pathogen. Anybody there working with LM can help me out?

Hi everybody!

The summer is finishing (in Ireland somehow neither starts nor finishes), the children go back to school and stop messing around, the leaves fall, bla, bla, bla… and many good posts are around the bloggosphere:

We start with Ruth Schaffer from The Biotech Blog with a post about hydrogen production of Thermatoga neapolitana and the advantages of this facultative anaerobe.

Andreas Baumer posts about the experience he had when he realized of the ubiquitousness of our beloved bugs, particularly focusing on the omnipresence of biofilms in the surrounding world. By the way Andreas, did you trip with the black fungi on the wall? read the post and you’ll understand…

Tara posts about the emergence and outbreak of Antibiotic Resistant Mycobacterium tuberculosis strains.

Endosymbionts is the topic on syaffolee. Are aphid endosymbionts only transmitted vertically (mother to descendants? or there are other ways of transmitting this microorganism? Check out the post.

Sandra Porter has a four part series where she gives useful examples of how we can use AIDS virus to prove evolution. Part I, Part II, Part III, Part IV. Not to be missed.

Mike talks about an outbreak of E. coli O157:H7, emphasizing that most of E. coli strains are harmless inhabitant of our gut.

In my post I give an example of how misleading can be the anthropocentric view of the world focusing on a “well-known pathogen”: Vibrio cholerae.

Hope you all had a nice summer cause I didn’t!

Salu y liberta and
Viva la Evolucion!

As we all know, humans have this tendency to consider themselves as the center of the universe. Some of them, with more imagination, think that they are direct creations of a Omnipotent Entity. Well, I’m delighted to consider myself a simple very ape-like human. Where am I trying to get at? well, a subtler way of anthropocentrism is that of roughly classifying bacteria as pathogens and non-pathogens…of humans of course!

A good example of this anthropocentrism is the bacterium I work with: Vibrio cholerae. You wouldn’t doubt for a second to consider this species as a pathogen. OK, what if I told you that more than 99% of the strains of V. cholerae isolated in an endemic area lacked the genes that allow the bacterium to cause the disease?. You would start thinking that it is not particularly advantageous for the bacterium to carry these genes in that particular environment.

We have published a paper this month in nature reviews about the niche specialization of the Vibrionaceae and how we can infer this from the genome sequences.

In the article we brought this issue a little bit further, trying to find possible environmental uses of the “pathogenic” traits of this V. cholerae isolates.

The main cause of the diarrhoea is what we humbly call the Cholera Toxin (CT). CT basically takes salts out from the intestinal cells, a massive efflux of water follows, due to osmotic inbalance and cholera ensued. This “Toxin” can fit better as an osmorregulator in its natural environment, taking salts out of the crustaceans where VC is ubiquitously found. The second main pathogenicity factor is the Toxin Corregulated Pilus (TCP) which allows the bacterium to attach to epithelial cells… and to other things too… for instance, it’s been found that chitin (exoskeleton of crustaceans) induces TCP production, thus allowing the bacterium to bind to it. So we infer that V. cholerae might stablish a symbiotic relationship with copepods (the crustacean) getting a nice niche with food and providing a powerful osmorregulator.

I think this makes more sense than to cause diarrhoea in humans and get washed out in only one day. So “unfortunately” for our egos they are not here only for us baby.

Hi everyone!
Welcome to Mendel’s garden #3, as can be seen 40 celsius of temperature has not been enough to stop our bloggers. My apologies for the one day delay, but yesterday there was a power cut in half of the city that prevented me from using the computer.
Well, let’s see what comes from the melting blogs, by the way, I have ordered the posts timewise, so the first that I got is the first in the list, and so on. No preferences:

We start with Maggie Kirk from Genomics policy blog, whose post entitled “Mendel’s Garden – blog carnival on genetics: Some thoughts on the value of peas” reminds us a bit of history and social implications of genetics.

David Ng from the World’s fair shows an alternative way of using DNA… to make music!

Like birds? then have a look at Joe Kissel’s post at interesting thing of the day about the kakapo, a flightless parrot from New Zealand whose naive behaviour is putting the species at the edge of extinction.

Tara at aetiology has a post about the diverse foci where H5N1 appeared in Nigeria, and how phylogenetic analysis helps us to understand the origins and spread of the disease.

Rich at evolgen shows why mitochondrial DNA (mtDNA) is not as reliable as previously thought to infer certain characteristics of a population.

In genetics and health we have got a four parts story of a woman (Rica Lode) and her search for preimplantation genetic diagnosis.

From RadicalHop comes a particular “comparison” between…

In salamander candy we have a interesting proposal : that of stimulating people interested in science to browse sequence data and mine it in search for the secrets stored in the net.

At Migrations we can find a comment of an article about the evolution of phosphoinositol 3-kinases in eukaryotes.

My post is about polyploidy in prokaryotes.

I hope everything is fine and if not try to find me in the sunny beach of the south of Spain where I am… I’m the hairy and tanned one…

One last comment: It is starting to be annoying the amount of ads that some blogs have. I didn’t start a blog to pay my bills.

Salud y Libertad! (health and freedom for you all!)
…and Viva la Evolucion!

The first story comes from the sea. There is a group of phages that specifically infect cyanobacteria, guess the name… cyanophages… which are divided into three main families: Podoviridae, Myoviridae, and Siphoviridae. Well, it’s been found that these phages carry genes that encode two photosystem II* core reaction-center proteins. By expressing their own copies during infection these phages can manage to enhance photosynthesis. Interestingly, cyanophage production is optimal when photosynthesis is maintained during infection.

I’m only guessing, but I suposse that during infection the host cell stops photosynthesizing, due to the stress conditions, and for some reason the virus needs this machinery working. Why? not a notion! Do you know anything about this, help me. By the way there’s a paper studying the evolution of this genetic exchange between bacteria and virus.

* Photosystems I and II are the two reaction centers in photosynthesis

The second story is about viral trade-offs. Marianne De Paepe and François Taddei from the University of Paris have published an article about the increase in the decay rate* of coliphages when certain conditions are given. They found that this decay rate increases with the density of the packaged DNA (into the phage), so, higher internal pressure higher mortality. This also increases when surfacic mass decreases, so the bigger the better. And finally, and this is the main reason of this comment, they found the highest correlation between decay rate and multiplication rate in the bacterial host.

So, interestingly for phages, survival rate is inversely proportional to multiplication rate. The reason behind this is yet to be known but will be fascinating for sure.

* It is not very accurate to say death since they are not alive

Every scientific field has its highly assumed dogmas. In microbiology, one of them is the fact that prokaryotes have a single circular chromosome and an haploid genome ( only one copy of it ). There are several examples of bacteria with several chromosomes, among them the Vibrionaceae, which I work with. Also, it’s been found that some groups carry linear chromosomes like Borrelia or Agrobacterium.
A group of researchers in Chicago have shown that Neisseria gonorrhoeae contains several copies of its genome, therefore it is NOT haploid as previously assumed.

This polyploidy might help to explain the high gene conversion* required for antigenic diversity among these human pathogens. In the case of N. gonorrhoeae that variability enhances pili protein diversity, which “masks” the microorganism diminishing the likelyhood of being detected by the immune system.

*One gene incorporates DNA from a variant copy that carries slightly different information.