Archive for March, 2010

The Red Queen hypothesis in a glass
What factors predominate in evolution? In daily life, the constant evolution of our lives is influenced by our conditions and by external factors. If I want to build a house with my own hands, I have to consider my abilities, some of which are genetic (I am small, thin and I am not strong, so I can’t carry heavy materials), and also I have to check how many money I can spend; hence, the “evolution” of the house, sort of, depends on both factors.

Two hypothesis, the “Red Queen” and the “Court Jester”, view evolution in these terms [1]. The Red Queen hypothesis view evolution as a balance of biotic (intrinsic) pressures, whereas the Court Jester model propose that evolution, speciation and extinction rarely happen except in response to unpredictable changes in the physical environment. Finally, it seems reasonable that evolution proceeds as a mixture of both models, where the Court Jester model operates in a time scale far longer than the Red Queen. Locally, in an ecological niche, the competition (biotic factor) between events en species shapes the local evolution, but in a larger scale, such as earthquakes, rise of mountains, and separation of physical spaces, provide a definitive barrier shaping long-term evolution, although events such as migration in birds and migration between continents should be taken into account.

The Court Jester model seems more logical to be imagined. Darwin viewed evolution in terms of biotic factors, but in his journeys, he observed marked differences in similar species in long distances, being islands a hallmark of evolutionary observation. But the Red Queen hypothesis, in biological terms, remained a challenge to be resolved in a laboratory. In a recent paper published in Nature [2], Paterson and coworkers provided a genetic evidence for the Red Queen hypothesis, using a smart experimental design. They used co-cultures of the bacterium Pseudomonas fluorescens and its viral phage Φ2. The molecular evolution rate in the phage was higher when both bacterium and phage coevolved with each other that when phage evolved against a constant host genotype. Remarkably, the genes that most rapidly evolved were involved in host infection, after 12 serial transfers (being each transfer every 48 hours). Consequently, coevolved phage populations varied in the range and identity of host genotypes that they were able to infect, but phage from evolved populations failed to infect any coevolved hosts.

How fast a bacterium can coevolve inside a human organism? For example, in a hospital, there is a spreading of infectious bacteria. Could be possible a coevolution of the microorganism with its host, allowing the mutation and adaptation of the bacteria in order to be able to infect more hosts? It will be interesting the extrapolation of the findings from Paterson and coworkers, at the clinical level. An example is provided by a brief review in PLoS Genetics [3]. Neisseria meningitidis, a major cause of morbidity and mortality in childhood, in a lapse of three decades of observation showed little variation, but a few loci showed variation, including the gene coding for a transferrin binding protein (tbpB). However, it seems that the genetic variation occurs at expenses of the “transmission fitness”.  It will be interesting to see if this technique can be improved to study more complex and bigger “cosmos” and specially for disease-causing bacterium, or viruses.


[1] Benton MJ (2009). The Red Queen and the Court Jester: species diversity and the role of biotic and abiotic factors through time. Science (New York, N.Y.), 323 (5915), 728-32 PMID: 19197051

[2] Paterson S, Vogwill T, Buckling A, Benmayor R, Spiers AJ, Thomson NR, Quail M, Smith F, Walker D, Libberton B, Fenton A, Hall N, & Brockhurst MA (2010). Antagonistic coevolution accelerates molecular evolution. Nature, 464 (7286), 275-8 PMID: 20182425

[3] Falush D (2009). Toward the use of genomics to study microevolutionary change in bacteria. PLoS genetics, 5 (10) PMID: 19855823

Milk, Prions and Evolution

ResearchBlogging.orgPrion protein (PrP) is the focus of some neurodegenerative diseases. It is believed that misfolded prion protein (PrPsc, or “scrapie”) is the infectious agent responsible for bovine spongiform encephalopathy (BSE), and Creutzfeldt-Jacob disease (CJD), among others. PrPsc propagates by conversion of normal (healthy) prion protein (PrPc).

Several questions arise in the research community. Two of them are: a) can prions be transmitted from domestic animals into humans, and b) how the prion protein propagates inside a healthy subject. Food safety is a major concern. Milk and their derivatives are a subject of study, because of their wide consumption in most countries. A study [1] from Didier and coworkers shows that the normal prion protein is detected in mammary gland and milk fractions of cow, goat and sheep. PrPc protein is detected in all milk fractions (skimmed milk, acid whey, cream) in goat and sheep. Although the authors failed to detect PrPc in bovine milk, they refer to other study that successful detected the protein in bovine milk using a different approach. Some conclusions of this study are that analytical methods to detect the prion protein should be improved (hopefully, at an industrial scale), to avoid the variability between studies, specially considering the high levels of prion protein detected in cream fractions and the widespread use of cream in cooking.

Scrapie in milk?

Another conclusion is that the prion protein exist at low levels in mammary gland and milk. Even detecting PrPc in milk requires hard work (enrichment of protein concentration, for example). But someone expect that PrPsc should exist at even lower levels, specially in asymptomatic animals. Then, PrPsc can be undetected in an industrial quality control. What happens if the common assumption that infectious prion protein is not present in milk is wrong? There is evidence of infectious prion transmission via milk; Timm Konold and colleagues published evidence in lambs fed with infected and healthy milk, but using lambs from a genotype with high susceptibility to scrapie [2], observing high levels of infection. Thinking in human population, if  populations with genetic susceptibility to scrapie are identified, then health measures should be implemented in those populations to avoid the exposure to potentially contaminated milk and cream.

Once inside the cell, then what?

A few days ago, a comment in Science raised the question  “What makes a prion infectious?” [3]. The article referred to two papers published recently. One of them raises interesting questions regarding the possibility of disease development after drinking contaminated milk, for example. A research team from the Department of Infectology in the Scripps Institute, showed that prions in cell culture are able to “evolve” [4]. Prions, viewed as infectious agents, exists as strains, which are a specific conformer of the protein, and they are able to multimerize forming seeds. One hypothesis, called “protein-only”, assumes that each strain is associated with a different conformer of PrPsc, and the infectious agent is composed of a misfolded conformer exclusively (without cofactors). Many strains can exist, since many conformers are able to arise from PrPc misfolding. Experiments from the work of Li and colleagues shows that, indeed, these strains exist, and they were able to identify prions strains sensitive to swainsonine (inhibitor of the formation of N-linked glycans). In a series of experiments they showed that the strains identified in a time-lapse isolated from a cell line infected with a brain homogenate changed over time: in the first days, they identified swa-resistant strains (and competent for R33, a neuroblastoma-derived cell line), but then they identified swa-insensitive and R33-incompetent, after they transferring to PK1 cells. These and remaining experiments suggests that the prion population changed over time, and there are different strains that can “compete” if the growth conditions are advantageous to a specific strain.The authors, based in their results, conclude that prions show the hallmarks of Darwinian evolution: they are subject to mutation and to selective amplification. Obviously, these findings are relevant to Medicine, since drug discovery should consider the fact that, in disease conditions, the raise of a infectious prion can lead to mutation (more likely by binding of a prion to some cellular cofactor leading to a small variations in the misfolded structure) of some monomers, causing strain evolution, some of which can growth in the presence of some drug, replace the remaining strains and lead to resistance.

It is evident that we are far from understand the biochemical and molecular foundations of scrapie disease and mechanism, and the new evidence suggest a complex scenario, specially regarding to the deveolpment of new drugs to fight the clinical symptoms and the CJD and BSE diseases.


[1] Didier A, Gebert R, Dietrich R, Schweiger M, Gareis M, Märtlbauer E, & Amselgruber WM (2008). Cellular prion protein in mammary gland and milk fractions of domestic ruminants. Biochemical and biophysical research communications, 369 (3), 841-4 PMID: 18325321

[2] Konold T, Moore SJ, Bellworthy SJ, & Simmons HA (2008). Evidence of scrapie transmission via milk. BMC veterinary research, 4 PMID: 18397513

[3] Supattapone S (2010). Biochemistry. What makes a prion infectious? Science (New York, N.Y.), 327 (5969), 1091-2 PMID: 20185716

[4] Li J, Browning S, Mahal SP, Oelschlegel AM, & Weissmann C (2010). Darwinian evolution of prions in cell culture. Science (New York, N.Y.), 327 (5967), 869-72 PMID: 20044542

Science predicted the Chile’s Earthquake

I am finally back, repairing some of the damages in our labs. The situation in Chile is not good. The deaths are raising slowly, but continoulsy, over 800 people now. Also, some data regarding thousands of missing people is also of great concern.

Regarding to science, several laboratories have reported serious damages, including lost of data, expensive equipment (you must consider that, due to the location of Chile, far from the manufacturers, equipments and reagents cost three or four times more expensive than in USA or Europe).

The observations and predictions (at a glance)

It is surprising that researchers had predicted the earthquake almost two years ago [1]. Teachers always say to students “nature is unpredictable; you can’t know where an earthquake will occur”. But technology advances, and together with mathematical modeling and observation, just like Darwin did in his travel to Chile almost 170 years ago, describing the earthquake of 1835 [2], researchers can formulate hypotheses about when, and how strong an earthquake will occur.

Ruegg and coworkers published a paper in “Physics of the Earth and Planetary Interiors” (Ruegg JC, 175:78–85, 2009). The team made observations in a range from 1996 to 2002, focusing in the area from Constitución to Concepción, since no major earthquakes occurred in that space since 1835 (described by Darwin). They measured the displacement of the plate (more exactly, the velocity of the movement). The results (at a big glance, since I am not a geologist) showed that coastal regions had a higher velocity compared with regions in the Andes area. Assuming that no major earthquakes released the accumulated force since 1835, a deficit of horizontal displacement of 10 m will have accumulated.

To Ruegg and coworkers, this could mean, in a worst case scenario, “that the southern part of the Concepción–Constitución
gap has accumulated a slip deficit that is large enough to produce a very large earthquake of about Mw = 8.0–8.5”.

What happened in Chile?

This February 27, at 3:34 am (Chile’s time), an earthquake with a magnitude of 8.8 in Ritcher scale occurred in a site very close to Cobquecura, located between Concepción and Constitución (see map below). The plates moved 8 m, and since Ruegg and coworkers calculated a 10 m of slip deficit, either the calculations are overestimated or the earthquake should have been even worse.

Figure 1. Earthquake and areas affected. Notice the location of the epicenter, just as predicted by Ruegg and coworkers.

Nonetheless, the prediction of Ruegg and his team is shocking. They were right about the epicenter and magnitude. The final phrase of the abstract is: “… in a worst case scenario, the area already has a potential for an earthquake of magnitude
as large as 8–8.5, should it happen in the near future”.

Interesting Data

Earthquakes in Chile show a striking regularity: every almost 17 years, a major earthquake (above 8 in Richter scale) occurr. Even more, the majority of the most destructive earthquakes ocurred in the chilean summer:

Figure 2: Major earthquakes in Chile since 1906. The box around 1939 and 1943 shows that the average (1941) was considered to calculate the years between the events (between 1922 and 1941, and between 1941 and 1960). 50% of the events occurred in summer or beginning autumn.


An obvious conclusion for our country, Chile, is the following: scientific observations can assist to make predictions about the most probable sites of a future earthquake, including information about the magnitude. Ideally, a global network across the identified seismic gaps in Chile (one at the north, one near to Valparaiso, one located between Concepción-Constitución and one near to Valdivia, epicenter of the greatest earthquake in the last 200 years) and some other regions , could help to be better prepared for a new earthquake. I don’t know of such an approach is being used in other seismic regions on Earth.

1. Ruegg, J., Rudloff, A., Vigny, C., Madariaga, R., de Chabalier, J., Campos, J., Kausel, E., Barrientos, S., & Dimitrov, D. (2009). Interseismic strain accumulation measured by GPS in the seismic gap between Constitución and Concepción in Chile Physics of the Earth and Planetary Interiors, 175 (1-2), 78-85 DOI: 10.1016/j.pepi.2008.02.015

2. Richard A. Kerr (2010). Did Darwin Help Predict Chilean Quake? Science Now

This post was chosen as an Editor's Selection for

Earthquake in Chile and Science

Four days later, I finally have internet connection in my house. I am surfing the web, watching photos from my country. As you probably know, an earthquake stroke Chile at 3:34 am, February 27. It was 8.8 in the Ritcher scale, according to the U.S. Geological Survey Program. The second most strong earthquake in Chilean history (whereas the first most strong earthquake was in Valdivia, also in Chile, 1960, the highest earthquake in history).

The devastation in Chile is overwhelming. More than 720 deaths (and rising), 500 injured people, more than half of the country striked by the earthquake, and thousands of houses and buildings falling apart. The effects of the earthquake is big; tsunamis crashed over chilean cities, destroying them. The tsunamis reached Australia, Japan and Hawaii.

As a science’s blog, I have to say something about the effects of this earthquake over research. Preliminary data inform about Science’s Faculties destroyed. A Chemistry Faculty was burned entirely, in a city very close to the epicenter of the earthquake. Here, in Santiago, we have several damages in laboratories from many research centers and universities. My lab was full of water the morning after the earthquake. A big amount of data was almost lost. Fortunately, equipment was unharmed. Some damages in structures and walls is also observed, but maybe they can be repaired in a few weeks. In other laboratories, where some of my friends are pursuing their Ph.D. research projects, the damages are more extensive, with chemical emergencies, equipment lost, structural damage…

Conicyt, the Government agency funding science, already declared a flexibility in some deadlines for applications and submission of results from research projects. We still don’t have news from other laboratories and research facilities in the areas more affected by the earthquake. The hope and faith that we all have is not only for science. It is also for the entire Chile.

Soon more news and photos.

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