¡Viva La Evolución!

A couple of weeks ago I was talking about foreign DNA and how to differentiate it from that of the host genome. Well, there were two other ways to identify foreign sequences that I was gonna talk about:

- Genomic dissimilarity
Genomes have another “odd” characteristic: they have a particular frequency for dinucleotide pairs, that is, the frequency of ATs toghether in Salmonella enterica is different from that in Shewanella amazonensisthe same applies for other pairs (AG, GT, CA,…).
When you compare whole genomic dinucleotide frequencies with that of a group of genes from the same organism they should give a very simmilar result (genomic dissimilarity low) so you can estate that the latter (the genes) belong to the former (the whole genome), however if you get high genomic dissimilarity, which means having two groups with very different dinucleotide frequencies, you can say that the genes you have compared with the whole genome might not belong originally to the core genome and might have been horizontally acquired. Or what is the same, three points in the acquired-o-meter!

- Codon and aminoacid usage

Another intrinsic characteristic of the genomes is the codon usage. As you might know, the same
aminoacid can be encoded by different codons (a string of three nucleotides encoding one aminoacid) that is what is called the degeneracy of the genetic code.
Have a look at this
So, again, each organism is going to have its preferences when encoding an aminoacid, for instance, most codons encoding Proline for organism A will be CCT, however, for organism B it might be CCA, this is called codon usage. If you compare the codon usage of the entire genome of your organism with that of a group of genes that you think might have been acquired, you can corroborate whether your hypothesis was true or not, Simmilar codon usage: possible origin in common; different codon usage: possible different origin (acquired).
There is a big drawback for this method: highly expressed genes usually show a different codon usage and they belong to the same genome. So you might get false positives using this method. Another thing to take into account is to check that your genes are in-frame, an extra nucleotide will provoke a frameshift and would completely alter your results.

I think that’s enough!

Viva la evolucion and the genetic exchange!

Tomorrow I’ll be in the U.K.
I’m going to the Sanger institute in Cambridge. Ooole!

So probably there will be not many new posts this week, but a nice summary will be left once I’m back (Friday this week).

Viva la evolucion!

I don’t think so. Many people still argue about this slippery issue, but only at first sight…
My reasons, and those of many other scientists, to say that a virus is not alive are very simple, above all if we take into account Varela and Maturana’s concept of “autopoietic system”for a living thing (see “being autopoietic”).

- Autolimitation in viruses?: well you can consider the capsid of some viruses something that encloses the system, but certainly it doesn’t allow any continuity with the environment, as far as I know. That is to to say DNA/RNA inside the capsid or DNA/RNA outside, that is all you get.

- Autogeneration in viruses?: here comes a big problem, it is easy to think that a virus autogenerates itself: put it close to a cell it can infect and pretty soon you’ll have hundreds of them. The main drawback of this is that you need external machinery to generate yourself (ribosomes,…) so then you are not being autogenerated.

- Autoperpetuation in viruses?: definitely not, there is no energy and carbon source exchange in viruses when not infecting.

If you think that, for instance, Chlamydia needs also a host and is alive why a virus is not?, because Chlamydia “only” need certain compounds from the host not the host itself.

A good point would be if some of this obligate parasites lost someday the ribosomes and all the capacity to replicate independently. But as far as I know this case hasn’t been found yet.

Who knows?

Then here comes my second point: Probably we would have then a virus. So, from either a degenerated ancient parasitic cell or some released DNA in the environment could the first ancestral virus come from. Don’t you think? you can’t be a parasite with nothing to parasitize.

I want to dedicate this post to my friend Tara Kelly and see if I can convince her.

Although sounds weird, all living organisms share one common trait:
According to Humberto Maturana and Francisco Varela they are autopoietic systems.
Poiesis means making, formation, so an autopoietic system is able to make itself, and be maintained partially isolated from the surrounding environment, enough to be regarded as unique.

Rayleigh-Benard convections

Amoeba

The president of the U.S.A

Autopoietic systems have three properties in common:

- Autolimitation
Autopoietic systems are surrounded by a structure (cell membrane, skin,…) that encloses the system, and at the same time allows an energetic and material continuity with the external world

- Autogeneration
The whole system is created by itself

- Autoperpetuation
Even when they are not growing, they are continuously using energy to maintain their relatively complex structure

The most interesting thing to be pointed out is that commonly to describe the Living we used to stress growth and replication, however, the first living thing that possibly merged in this world had more than enough with the maintainance of its fortuitous structure that the endlessly irradiating sun was helping/pushing to create than to grow or replicate, and WAS ALIVE!!.

It is important to note that all living things are autopoietic systems but not all the autopoietic systems are living things. An example is given above with the Rayleigh-Benard Convection, which are the spontaneous structures that “arise” when a certain fluid is heated from below forming a complex autoorganized pattern. Think that the first thing the heat will lead to is to an increase in the entropy of the fluid (call it disorder, I hate this translation but…), that is to say, when you increase the temperature you increase the movement of the molecules and thus reduce (common-sensically speaking) the “order”. But this doesn’t happen when you heat, for instance, a liquid silicone fluid in a certain way. When you do that, you get this unpredictable highly ordered structures coming out from your pan. And this is a property that the system has already!! no designer needed, no anything.

I find this concept very interesting, though does not give a definition ( and I think we’ll never get one of a concept we humans made up- ALIVE ) but helps me to mentally deal a bit with the matter. The living matter!!

By the way: Viva La Evolucion!

Option A) I want my children to be taught creationist “theories”, to undermine their personal decisions and rationality from their childhood, to undervalue other people’s belief, to be unopinionated…

Option B) I want my children to be free to decide their personal beliefs, to be taught SCIENCE in SCIENCE classes, to be taught in an environment of personal freedom of choice…

If your choice is Option A, please don’t keep reading and don’t login here again, thanks.

If your choice is option B, and you want this to happen, please visit this websites and support a free of religion classes Europe:

Europa laica
Andalucia laica

Viva la evolucion!

What do some V. cholerae strains have that make them pathogenic?

Two are the main pathogenicity factors:

-CTXphi: which is prophage (virus inserted in the genome in a “dormant” state) that encodes the cholera toxin, the cause of the fluid accumulation in the gut.

-Toxin Corregulated Pilus (TCP): A type IV pilus ( hairlike structure on the surface of the bacterium) which allows pathogenic V. cholerae to attach to the gut epithelium and was the main entrance for ctx virus to get into V. cholerae.

So basically an anchor and a gun!

TCP is found in a pathogenicity island (VPI-1), which is a big chunk of mobile DNA that can insert in the genome of the bacterium and confer certain pathogenic traits. They don’t know yet the possible origin of VPI-1, but a very interesting answer awaits us.

The moral of the story: there’s no moral in nature… only movement!

Grey Thumb is the new host for the science carnival called “Tangled Bank”, so do not hesitate and get a bath with science.

Bored? Have a look at this
http://www.greythumb.org/blog/

Yes, they have.
Don’t you believe it?

A) Synechococcus carboxysome
B) The same but negatively stained and closer
C) H. neapolitanus carboxysome
D) Negative stain of H. neapolitanus carboxysome, you can even see RuBisCO assemblies inside
E) S. enterica Typhimurium LT2 enterosomes
F and G) Negatively stained enterosomes from S. enterica Typhimurium LT2

From Cannon et al, 2001

To date two different types “organelles” have been found in bacteria: carboxysomes and enterosomes. The first ones present in cyanobacteria and chemoautotrophic bacteria, the latter ones in some enterobacteria such as E. coli and S. enterica.
By definition they are polyhedral inclusion bodies that are bound by a unilamellar protein… so they are coated! it’s not only an agregation of enzymes or some substance produced by the bacteria, say, magnetite in Magnetospirillum, for example.

Carboxisomes are filled with 1,5-biphosphate carboxylase/oxygenase (RuBisCO) and the function could be to prevent the enzyme from being inhibited by oxygen. Anyhow, the catalytic properties of the enzyme are significantly enhanced inside this carboxysomes.

Enterosomes contain enzymes involved in the degradation of ethanolamine or propendiol. Some bacteria, like S. enterica, are found to have both types of enterosomes (they are independent) Havemann et al, 2003. A recent study done by Sriramulu et al (personal communication) introduced in E. coli the genes needed to produce the enzymes and the proteins of the coat for propendiol enterosomes. E. coli naturally only has the genes to produce enterosomes for ethanolamine degradation. And, Voila! they got nice and round enterosomes when they cultured the mutant on propendiol as an only source of carbon.

Personally, I’m not much convinced whether to call this an organelle or not, at least semantically they seem to be. The thing is that they are only temporary, so when the source starts being added they produce them and after the supply finishes they disappear. So, to put it bluntly, we have enzymatic pots in here!

All of this came because I was wondering, how come that bacteria don’t have organelles, in fact, after reading about this I still have a similar question, How come that bacteria don’t have biphospholipidic-layer organelles? It only takes a bit of invaginated membrane to get some sort of “lysosome”.

If anybody has found the missing link in the organelle issue, please let me know.
Anyway if not, place your bets…

Vibrio cholerae is the bug of the month.
As most of you might know, V. cholerae is the etiological agent of cholera, a serious diarrhoeal disease that causes deaths across the world. But, what many of you might not know is that this bacterium is the natural inhabitant of brackish estuarine waters, and in fact only few serogroups produce the disease, only two as far as we know.

Some basic characteristics of this bacterium:
Is a Gram negative
A gamma-proteobacterium
Belongs to the family Vibrionaceae

This bacterium is the one that I’m working with! and I find it fascinating. Under my point of view, two important things to take into account when dealing (mentally…) with this pathogen are:

- As aforementioned, lives nicely in coastal warm waters and most strains are NON-pathogenic

-The family which it belongs to,Vibrionaceae, is a very diverse group, with aquatic bacteria ranging from pathogens to symbionts to piezophiles. Interestingly, they are very similar genetically.

What I mean by stressing these two points is that we usually see pathogenesis from a very narrow-minded point of view. This f***ing baterium is there to kill us!!!! arrggh!. But sometimes we should be slightly more humble, since, as I already said, they were here before you and me and they don’t care whether you are there or not. So, I’m sorry but we are secondary for this lads, whether you like or not!.

What are the molecular “gadgets” that make a strain become pathogenic??
Many more about VC soon! The same BLOG, at some stage

By the way don’t drink a flask with a V. cholerae culture… just in case!
and Viva la Evolucion!

Ever wondered how does anybody know that
ATGCCACTTGACTAATGCC
doesn’t originally belong my organism but
ATGTAACGGTAACCATGA
does?
In other words, how do you know that a gene has been horizontally acquired?
Well, as far as I know, there are several ways of knowing that:

1) Location of our gene or cluster of genes
For instance if our gene is located close to a tRNA ( hot-spot for insertions) and has mobile elements surrounding it-> then you have 1 point in the acquired-o-meter

2)Incongruent phylogenetic trees
So if I build a phylogenetic tree of my protein or gene in question together with some other homologous genes and I compare it with the 16s rRNA tree of the species included in the analysis and they don’t match we have another big point in our acquired-o-meter. For instance, if my gene encoding gorilate decaiguasilase from E. coli is clustering with streptococci and other gram positives, then you should be happy (provided that many other things are right too, but I don’t want to bring you down now…).

3)Aberrant G+C content
Each microorganism has its own G+C content, and it remains pretty constant across the genome (to a certain extent), so if my bug has, say E. coli, 50% G+C content and my possibly foreign DNA has 40% of G+C, it is highly unlikey that this group of genes belong to E. coli. So… another point in the acquired-o-meter

4)There are other ways of finding out whether my gene’s been acquired or not, I’ll explain them next week:
Genomic signature
Codon and amino acid usage

If you wanna know more about this, a very good and summarized paper is: Samuel Karlin’s “Detecting anomalous gene clusters and pathogenicity islands in diverse bacterial genomes” Trends in Microbiology, 2001.

Hope this might be helpful