Friday Foolery #7 Play Doh World, the Safe and Unexpected

16 10 2009

Seen at the Loom of Carl Zimmer: using Play Doh, Sophia Tintori and Cassandra Extavour talk about multicellularity and the specialization of reproductive cells.

The video, made by the evolutionary biologist Casey Dunn, is from Creature Cast, a collaborative blog produced by members of the Dunn Lab at Brown University. The Dunn Lab investigates how evolution has produced a diversity of life. On this newly evoluted “Creature Cast” you can find short, original and  good quality posts on zoology in the broad sense often with beautiful photos or videos. You can now subscribe to the CreatureCast video podcast through Brown University at  iTunes U.

Vodpod videos no longer available.

more about “CreatureCast Episode 2 on Vimeo“, posted with vodpod
Work provided under a Creative Commons Attribution-Noncommercial-Share Alike license.

Another example of a great post on Creature Cast is the Tale of two holes about why some animals have one hole and others two. Does the single hole in one-holed animals correspond to the mouth or anus of animals with two holes?  Apparently the same sets of genes appear in many different contexts within and across species. In this case there are two distinct modules for mouth and blastopore (the first hole developed in animals during their development) and they can be decoupled. Again there is a terrific photo made by Dunn showing a sea anemone with a single hole for eating, excreting, and shedding eggs and sperm, and an annelid worm with two holes.

This is a Friday Foolery post, thus permit me to show me something completely different: a successful Play-Doh ad-campaign started in Singapore (what a coincidence, the city I left 26 h ago). These ads talk to parents directly, reminding them about the thousand of possible things you can make with the product, but even more so about how safe it is to play with it. (although someone commented: “what if kids eat those pills? Although Play-Doh is non-toxic…)

16-10-2009 16-48-15 play doh ads


LoL: Stop Following Me!

28 06 2009

This picture is so cool.
First seen at ScienceRoll of Bertalan Mesko (@berci); this print is from a T-shirt of Zazzle.
More t-shirts and other prictures can be seen here

Evolution and Medicine. Cancer and adaptive immune responses as evolutions ‘within’.

29 12 2008

I had almost finished my submission for the Grand Round when I took a look at the site of the host, Moneduloides*, to find that this edition had “the interface of evolution and medicine” as a theme.

What should I write about, considering I only had a few hours to write about this difficult theme?

Quite coincidentally (or not, considering the forthcoming bicentenary of Darwin’s birth (1809) and the 150th anniversary of the publication of ‘On the Origin of Species’) the December 2008 Lancet is a Special Issue: Darwin’s Gifts. But it would be to easy to just summarize one or two articles from this Lancet issue…

Evolution and Medicine can be interpreted differently. One can just see it as the evolution of medicine. Enough to write about this theme….

One can also see the theme in the light of consequences of evolution on medicine or illnesses. Indeed there are ample examples of the consequences of men’s evolution on the susceptibility to certain illnesses, e.g. see moneduloides’ blog about the consequence of human bipedalism.

Yesterday @carlosrizo (twitter) pointed out a link to Darwinian Medicine 2.0″. Since this would be of special interest to this web 2.0 audience, I took a look to see if I could ‘use’ this blogpost. However the post appeared to be based on a rather distorted interpretation of natural selection. Darwinian Medicine 1.0. is considered synonymous with eugenics (!), whereas Darwinian Medicine 2.0 is “gentler, interested in finding “evolutionary causes and remedies for diseases.” while leaving out the genocide”. The counterpart blog being it is easy to position their view.

Although this blog merits no further discussion, it highlights the often wrong interpretations of the natural selection theories. Eugenics is “just” a political interpretation by some of Darwin’s theorie (see Wikipedia). Darwin himself thought it “absurd to talk of one animal being higher than another” and saw evolution as having no goal.

As a biologist I grew up with the following definition of natural selection.

Natural selection is the process by which favorable heritable traits become more common in successive generations of a population of reproducing organisms, and unfavorable heritable traits become less common, due to differential reproduction of genotypes.

In other words natural selection genetic alterations are mostly random and chance (environment, conditions) will determine whether the genotype exhibiting a new phenotype will continue to exist or even will be more likely to survive (natural selection).

Antibiotic resistance
During my biology study we did all kind of mini-evolution experiments. For instance, we treated bacteria that were deficient for a specific amino-acid (AA) with mutagens and plated them on solid agar plates with or without that particular AA. Only bacteria with a mutation making them independent of that AA would survive on AA-less plates.

Although this is not an experiment of nature, a very similar example of natural selection in action is the development of antibiotic resistance in microorganisms (see wikipedia).


Enhancement of antibiotic resistance by natural selection - modified from wikipedia

Natural populations of bacteria contain considerable variation in their genetic material, primarily as the result of mutations. When exposed to antibiotics, most bacteria die quickly, but some (red in Figure) may have mutations that make them less susceptible. If the exposure to antibiotics is short, these individuals will survive the treatment. This selective elimination of maladapted individuals (lighter colors) from a population is natural selection.

Evolutions within
It is not difficult to see how infectious diseases were driven by natural selection (of the organisms causing these diseases). Because all rules that apply to eukaryotic organisms apply to prokaryotic organisms as well. But I would make a point that evolution and natural selection also takes place at a lower level: that of viruses (non-living organisms, see post about sputnik-virus here) and of “individual cells” within an organism. That is to say: the same mechanisms apply.

Clonal selection and B-cell adaptive immune response.
One example of a cellular evolution is the development of the B cell (and T cell) immune repertoire. B and T cells are cells of
the adaptive immune response. In contrast to the innate immune response, which is always ready to respond to whatever intruder, the adaptive immune response matures throughout life, is antigen-specific and long-living. The specificity of B cells lies in the variable region of their immunoglobulins or antibodies, Y-like molecules, anchored in the B cells’ plasma membrane. There are endless antibody variants and each B cell (and its progeny) produces antibodies with one particular specificity.
How is this diversity established?
In the Pre-B cell phase, when B cells do not produce any immunoglobulins individual gene segments coding for the V, (D) and J regions of the heavy and light chain of the immunoglobulin molecule are randomly assembled to one molecule. The random assembly of 51 V, 27 D and 6 J gene segments provides a minimum of 8.300 different possible combinations for the heavy chain alone, but since the recombination process is not precise and extra nucleotides are inserted the number of possibilities of antibody V region diversity turn out to be greater than that.[2]
(The following excellent animation is recommended: (be sure to choose Open > Antigen Recognition > Recombination)


When an organism encounters a foreign microorganism or other antigen, only those B cells that recognize the antigen are stimulated to divide and to become plasma cells which produce many antibodies specific for the particular antigen. This process is called clonal selection. It results in a B cell repertoire skewed towards the antigens encountered in life. The advantage is that those B cells are selected that have been proved useful. The next time the same antigen is encountered the response is quicker, stronger and more specific, a process called memory.This is also the principle behind vaccination and boostering.

The principle of clonal B cell selection is very similar to the development of antibiotic resistance, discussed above.


Carcinogenesis: Follicular Lymphoma
However, sometimes clones are selected that erroneously react with ‘self’ which results in ‘autoimmunity‘.

Cancer can also be considered as another faulty ‘evolution’, be it within the organism. Cancer cells are better at surviving and reproducing than other cells, because they have escaped the body’s controls. This allows them to increase their population much faster than other cells.

In an interesting editorial, J Breivik comments on the work of Vineis and Berwick[4,5]:

Vineis and Berwick argue that ‘Carcinogenesis, at least for some types of cancer, can be interpreted as the consequence of selection of mutated cells similar to what, in the theory of evolution, occurs at the population level’. Taking a more conclusive stand, I will ague that carcinogenesis is an evolutionary process within the multicellular organism. Evolution by means of natural selection is a scientific principle that reaches far beyond the origin of the species and is applicable to all systems of inheritance, including somatic development.

One example is follicular lymphoma (FL). Follicular lymphoma is characterized by a chromosomal translocation between chromosome 14 and 18, t(14;18), caused by a faulty coupling of the immunoglobulin heavy J chain to the BCL-2 proto-oncogene on chromosome 14 during the normal VDJ-rearrangement process, described above. This mistake leads to a constitutive overexpression of BCL-2, which makes the cell less vulnerable to apoptosis (programmed cell death). Mice bearing a transgene mimicking the BCL-2 translocation have an increased incidence of spontaneous B lymphoid tumors. The lymphomas take many months to develop, however, and the penetrance of disease is low, arguing that BCL-2 overexpression on its own is not highly oncogenic (reviewed in[6]). Indeed our group has shown many years ago that t(14;18) translocations, that were considered specific for follicular lymphoma generally occur in follicular hyperplasias [7] and even in B-cells of healthy individuals [8]. Apparently B cells with the t(14;18) translocation are regularly generated in normal individuals, but only very few cells with the translocation will acquire the additional oncogenic hits necessary to establish the malignant phenotype. Overexpression of BCL-2 only gives the cells a survival advantage. Indeed, according to recent insights [9]:

“Accumulation of genomic alterations and clonal selection account for subsequent progression and transformation. Recently, the role of the immunologic microenvironment of FL in determining clinical behavior and prognosis has been substantiated. Combined genetic and immunologic data may now support a model for the development of FL as a disease of functional B cells in which specific molecular alterations infer intrinsic growth properties of the tumor cells as well as dictate a specific functional cross talk with the immunologic regulatory network resulting in extrinsic growth support.”

The theme of this week inspired me to philosophize about immunity and cancer being examples of evolutionary process. While reading I found that this idea is by no means new; a lot has been written about this concept. For instance in “Understanding Evolution” the writer(s) quite nicely explain the process of evolution within a cell lineage. They first explain that the key elements of the evolutionary process – variation, inheritance, and selective advantage – characterize not just populations of organisms in a particular environment, but also populations of cells within our own bodies.
Furthermore they make the interesting statement that

cancer – even within one person – isn’t a single entity. It’s a diverse and evolving population of cell lineages. A single tumor, for example, is made up of a variety of cell types, produced as the cells proliferated and incurred different mutations. All of this diversity means that the population of cells could easily include a mutant variety that happens to be resistant to any individual chemotherapy drug we might administer. To make matters even more difficult, treating the patient with that drug creates an environment in which the few resistant cancer cells have a strong selective advantage in comparison to other cells. Over time, those resistant cells will increase in frequency and continue to evolve. It’s not surprising then that a simple cure for cancer has yet to be developed: treating even a single type of cancer is a bit like trying to take aim at a whole set of moving targets all at once”

Thus, this challenge helps explain why research has not yet provided us with a cure, but also points the way toward new solutions that take that evolution into account ….


  1. Wikipedia (several pages, as indicated)
  2. Kimball Biology Pages: [A] AgReceptorDiversity (very good background information in dictionary-format)
  3. Evolving Immunity – A Response to Chapter 6 of Darwin’s Black Box. Matt Inlay. [blog] Talkdesign: interesting discussion on whether or not clonal selection system could have evolved in the context of irreducible complexity.
  4. Cancer the evolution-within, by Dan [blogpost] on Migrations (2007/04/18) referring to:
  5. Cancer – evolution within. Breivik, J. Int. J. Epidemiol. (2006) 35, 1161-1162.
  6. The Bcl-2 family: roles in cell survival and oncogenesis. Suzanne Cory1, David C S Huang1 and Jerry M Adam. Oncogene (2003) 22, 8590-8607.
  7. Bcl-2/JH rearrangements in benign lymphoid tissues with follicular hyperplasia. Limpens J, de Jong D, van Krieken JH, Price CG, Young BD, van Ommen GJ, Kluin PM. Oncogene. 1991 Dec;6(12):2271-6.(PubMed-link)(
  8. Lymphoma-associated translocation t(14;18) in blood B cells of normal individuals. Limpens J, Stad R, Vos C, de Vlaam C, de Jong D, van Ommen GJ, Schuuring E, Kluin PM. Blood. 1995 May 1;85(9):2528-36.(PubMed-link)(Google Scholar)
  9. Molecular pathogenesis of follicular lymphoma: a cross talk of genetic and immunologic factors. de Jong D. J Clin Oncol. 2005 Sep 10;23(26):6358-63.(PubMed-link)
  10. Another perspective on cancer: Evolution within. [blog] Understanding Evolution with a detailed description on natural selection within, and the evolution of cancer cells plus possible solutions.


  1. Antibiotic Resistance: wikipedia
  2. Clonal Selection:
  3. Recombination: Evolving Immunity – A Response to Chapter 6 of Darwin’s Black Box, adapted from janeway

The Real Sputnik Virus

15 08 2008

I just rewrote the “about” section, saying that this blog was started as part of the web 2.0 SPOETNIK (EN: Sputnik) course, that I saw this blog as an experiment, but that I am now irreversibly infected by the blog/Sputnikvirus.

Coincidentally a real Sputnik virus has been discovered.¹ The virus is called Sputnik (Russian for “travelling companion”), because it “accompanies” the mamavirus, the big ‘mama’ among the recently discovered giant mimiviruses. Both the mamavirus and its satellite were present in an amoeba-species, found in a water cooling tower. Strikingly Sputnik cannot infect the amoeba on its own, but needs the companion of a mimivirus. In fact Sputnik hijackes the ‘viral factory’ of the mimivirus in order to replicate, making the mimivirus less infective. Therefore the Sputnik virus is said to actually “infect” another virus

Wait a minute…!! A virus that ‘lives’ from an other virus and takes over his replicating machinery? This means that the virus that is being ‘infected’ (the mamavirus) is a living organism??? But viruses are ‘dead’, at least that is what I learned.

Definition of a virus in one of my studybooks (Genes IV, Benjamin Lewin, 1990, p41).

“Viruses take the physical form of exceedingly small particles. They share with organisms the property that one generation gives rise to the next; they differ in lacking a cellular structure of their own, instead needing to infect a host cell. Both prokaryotic and eukaryotic cells are subject to viral infections; viruses that infect bacteria are usually called bacteriophages”

Thus ‘per definition’ viruses are not alive ànd they do not infect other viruses?!

But what is in a definition/name?
According to Aristotle a definition of an object must include its essential attributes or its “essential nature”. However humans may only observe part of the essential attributes, especially when it concerns the infinitely small or infinitely large (which limitates the accuracy of our observations). Nature made his own definitions/categorizations and we just trying to find the rules, if any, to bring some order into chaos. But in science rules and concepts can be falsified and this rule may be one of them.

That viruses may be at the boundaries of life is no new discussion. According to wikipedia:

Biologists debate whether or not viruses are living organisms. Some consider them non-living as they do not meet all the criteria used in the common definitions of life. For example, unlike most organisms, viruses do not have cells. However, viruses have genes and evolve by natural selection. Others have described them as organisms at the edge of life.

As you can see from the scheme above (from wikipedia) the classification of living organisms has never been rigid and as time goes more ‘kingdoms’ have been discovered.

The Mimivirus seems to be at “the edge of life”, because it

Besides the what-is-a-living-organism-issue the discovery of the Mimi-Sputnik virus couple raises some other interesting points.

  • The paradigm that viruses are evolutionary latecomers, evolving as parasites after the archaea, bacteria and eukaria had formed is challenged by comparative genome-analysis which suggests that the virus world is the most ancient.
  • There is an abundance of Mimi-like genetic sequences in the (virus-rich) ocean leading to a suspicion that giant viruses are a common parasite of plankton.
  • Sputnik-like DNA is also found in the ocean, raising the possibility that satellite viruses could play a role in regulating the growth and death of (Mimi-infected) plankton. Therefore these marine viruses could be mayor player in the global ecosystem
  • Although Mimiviruses primarily infect amoeba, antibodies have been found to the virus in some human pneumonia cases. If these mimiviruses have their own satellites…. then this might perhaps be therapeutically exploited against large DNA viruses in human.

Finally I would like to close this post with an apt poem of Jonathan Swift (often cited in this context):

So, naturalists observe, a flea
Has smaller fleas that on him prey;
And these have smaller still to bite ’em;
And so proceed ad infinitum.

And another coincidence: There is a popgroup sigue-sigue-sputnik that has an number called virus (on the album ray-of-light.)

¹The Sputnikvirus has been detected by the team led by Jean-Michel Claverie and Didier Raoult (CNRS UPR laboratories in Marseilles), the same team that identified the mimivirus as a virus.
²Some of the finding are not completely new, e.g. Sputnik was not the first virus-satellite: Satellite Tobacco Mosaic Virus had been discovered before. Some researches don’t regard a satelite virus as a virus, however, but as subviral

La Scola, B et al The virophage as a unique parasite of the giant mimivirus, Nature DOI:10.1038/nature07218; announced in ‘Virophage’ suggests viruses are alive – Nature News, 2008 august 6th
Other news-coverages:
NRC-handelsblad, 2008-08-09 en wetenschapsbijlage 2008-08-10 2008-08-06
sciencenow daily news 2008-08-06

about the sputnikvirus
: good starting point for further information about Sputnik and mimiviruses with links to other sources
about the mimivirus :
a general overview in (last update 2007)
and “unintelligent-design at

about the origin of viruses and their presence in the sea: again….
Nice overview
Viruses in the sea’ in Nature by Curtis A. Suttle et al(2005)
Hypothesis: The ancient Virus World and evolution of cells by Eugene V Koonin in Biomedcentral (2006) (pdf-open access)
General: Wikipedia, ie about Viruses and Bacteriophages


Ik heb net de “about” pagina herschreven: ik schrijf dat ik dit blog ben gestart in het kader van de web 2.0 SPOETNIK cursus, dat ik dit blog als een experiment zag, maar dat ik inmiddels voor altijd geinfecteerd ben met het blog/Spoetnikvirus.

Toevallig las ik afgelopen zaterdag in het NRC dat er een echt Spoetnik virus is ontdekt.¹ Van de Spoetnikcursus weet ik nog dat Spoetnik in het Russisch metgezel betekent. Het virus kreeg deze naam omdat het zich samen met het mamavirus, het grootste virus onder de reusachtige minivirussen, in een amoebe ophoudt. Opmerkelijk genoeg is het Spoetnik virus helemaal niet in zijn eentje in staat om de amoebe te infecteren, maar heeft jij daarbij de hulp van het mimivirus nodig, in die zin dat Spoetnik de virusfabriekjes van het mimivirus inpikt om zichzelf te vermenigvuldigen. Met andere woorden, het Sputnik virus is in staat een ander virus te infecteren.

Wacht even?!……… Een virus dat een ander virus infecteert en ‘ziek maakt’? Dat betekent dat het virus dat geinfecteerd wordt ‘leeft’. Maar virussen zijn dood, dat heb ik tenminste zo geleerd.

Definitie van een virus in een oud studieboek (Genes IV, Benjamin Lewin, 1990, p41).

“Viruses take the physical form of exceedingly small particles. They share with organisms the property that one generation gives rise to the next; they differ in lacking a cellular structure of their own, instead needing to infect a host cell. Both prokaryotic and eukaryotic cells are subject to viral infections; viruses that infect bacteria are usually called bacteriophages”

Dus viruses leven per definitie niet en kunnen andere virussen niet infecteren?!

Maar “what is in a definition/name”?
Volgens Aristoteles moet een een definitie van een voorwerp/begrip essentiële elementen of de ware aard omvatten. Maar mensen zien misschien maar een deel van deze kenmerken, vooral als het om oneinig grote of oneindig kleine dingen gaat. De natuur maakt zijn eigen indelingen en wij proberen om wetten te achterhalen, voor zover deze er zijn, om orde in de chaos aan te brengen.
Volgens de regels der wetenschap zijn wetten en concepten echter toetsbaar en falsifieerbaar. Dat virussen levenloos zijn zou dus ook ontkracht kunnen worden.

Het al dan niet ‘levend zijn’ van virussen is geen nieuwe discussie. Sommige biologen zien virussen als niet-levend, omdat ze niet àlle belangrijke kenmerken van leven hebben, ze hebben bijvoorbeeld geen cellen. Virussen hebben echter wel genen en evolueren door natuurlijke selectie waardoor ze volgens anderen wel op het randje van het leven balanceren.

Het Mimivirus lijkt nog het meest op het randje te balanceren. Het

Behalve bovenstaande implicaties voor wat we ‘leven’ noemen, maakt het Mimi-Spoetnik-koppel nog meer discussie los.

  • Op basis van vergelijkend genoomonderzoek lijkt het onwaarschijnlijk dat virusen evolutionaire nakomertjes zijn, maar meer dat ze aan de voet van de archaea, de bacteriën en de eukaryoten hebben gestaan.
  • Er is heel veel Mimi-achtige genmateriaal in de oceanen gevonden, hetgeen zou kunnen betekenen dat reuzevirussen wel eens een algemene parasiet van plankton zouden kunnen zijn.
  • Spoetnik-achtig DNA wordt óók in de oceaan gevonden. Misschien dat satelliet-virussen wel een slutelrol spelen in de regulatie van de hoeveelheid plankton.
  • Hoewel Mimivirusen vooral amoeben infecteren, zijn antistoffen tegen dit virus ook bij enkele patienten met longontsteking gevonden. Als deze mimivirusen hun eigen satellieten hebben, kunnen deze wellicht ingezet worden tegen de ziekteveroorzakende virussen.

Tenslotte een zeer toepasselijk gedicht van Jonathan Swift (veelvuldig in deze kwestie aangehaald):

So, naturalists observe, a flea
Has smaller fleas that on him prey;
And these have smaller still to bite ’em;
And so proceed ad infinitum.

Nog een toevalligheid Er is een band sigue-sigue-sputnik met een (vrij heftig) nummer virus (album ray-of-light).

¹het Spoetnik- en het mimivirus zijn ontdekt door Jean-Michel Claverie en Didier Raoult (CNRS UPR laboratories in Marseilles) en zijn team.
²Niet alle bevindingen zijn echt even nieuw. Vòòr Spoetnik waren er al andere virussatellieten ontdekt, zoals de satelliet(virus)van tabaksmozaïekvirus. Door velen wordt zo’n virus niet als ect virus gezien, maar als subviraal beschouwd.