Plant-Insect Horizontally Tranferred Interaction between Mirmecophyte Plants and Ants

Figure 1: hollow thorn Mesoamerican Acacia.

Following the idea of the proceses that allow inter-organims interactions to move from facultative to obligate, lets take a look at the amazing case of acacia trees and its Pseoudomyrmex ants asociates.

Among tropical plants, around 100 genera host specialized ant colonies in structures called “domatia” and in part of these cases, plants also provide these ants with food. Ants in this association exhibits intensive territorial and cleaning behavior over the plant. This has as a consequence the expulsion of other herbivores and their eggs, and the detachment of invasive vegetation and sometimes fungi as well. Thus this relationship has been described as mutualistic.

Extensive revision of this case has suggested that the trait making the interaction between myrmecophyte plants and ants obligatory is usually the formation of domatia (nesting structures) on the plant. Domatia usually are located on hollow stem and shoots, hollow thorns (like in the Figure 1), in leaf pouches, petioles or even on fruits. Additionally, some myrmecophytes present plant derived food rewards like food bodies and extrafloral nectar (EFN) (See Figure 2).

Figure 2: Extrafloral nectar producing structures (upper) and food bodies on acacia tree, visited by Pseoudomyrmex ants.

However, despite these plants and ants seems to be vitally dependent on such interaction, the mutualistic association, even for the ones considered obligate, is transferred horizontally: both partners reproduce independently and the association has to be established di novo in each subsequent generation.

Figure 3: Phylogenetic reconstruction of section from Acacia subgenus includying facultative (grey) and obligate ant interacting plants (orange), based on combined data matrix of chloroplast DNA markers, AFLP cluster analysis (from Heil et al. 2004).

Another trait that has been proposed as relevant of the establishment of obligate plant-ant association correspond to the extrafloral nectar production. Inside the subgenus Acacia, both non-myrmecophyte and myrmecophyte plants release extrafloral nectar (see Figure 3). But the details of how this trait is expressed make the whole difference. In non specialized plants extrafloral nectar secretion respond positively to mechanical damage, herbivory or to the exogenous application of 1mM solution of the plant hormone jasmonic acid (also involve in other plant-herbivory chemical responses). By the other hand, in general, specialized myrmecophytes exhibit a constitutive (and comparatively slow) nectar release, irrespectively of whether exogenous stimuli applied. Thus the attraction of non-specialized nectar feeders (like unspecialized ants) seems to be related to the plant herbivory response machinery in non-myrmecophytes plants with EFN production, while on myrmecophytes this trait continuously expressed. Moreover, nectar composition on facultative EFN producers has three main sugars: glucose, fructose and sucrose, while myrmecophyte plants lacks sucrose (Figure 4).

Figure 4: Chromatograms of relative abundance of sugars in the EFN from non specialized (left) and myrmecophyte acacias (from Heil et al. 2005). Peaks identified as G; glucose, F: fructose, S: sucrose. Insert on left of graph is invertase activity in the nectar for each plant expresed as ug glucose released per ul of EFN per minute.

This is the result of post-secretory hydrolysis of the nectar sucrose on the obligate ant-interacting plant due to invertase activity. Sucrose and other di and trisaccharides are identified as a highly attractive sugars for many non-specialized ants. In nectar choice experiments using non specialized ants and myrmecophyte specialized ants it has been demonstrated that the addition of sucrose to the nectar of the derived myrmecophyte acacia, had triggered the attraction of non specialized ants, that previously (without sucrose) will not be attracted to the nectar of these plants but to the non-myrmecophyte ones. Contrarily, specialized ants are significantly attracted to nectar without sucrose. Analysis of digestive enzymes on these ants has repeatedly demonstrated the lower activity of invertases in extracts of the digestive systems of Pseoudomyrmex specialized ants, while the facultative plant interacting ants from the same genus, P. gracilis, showed greater invertase activity, this specie can actually live independently of acacia trees. Thus, this suggest that the obligate horizontally transmitted Acacia-Ant association is also supported by the transference of the hydrolysis process to the host plant in the evolution of this tight plant-insect association.

Cristian Villagra

PS: Follow the link to see a video of this fascinating interaction from the documental series The Secret Life of Plants.

References:

Agrawal AA. 1998. Leaf damage and associated cues induce aggressive ant recruitment in a neotropical ant-plant. Ecology 79: 2100–2112.

Heil M, Greiner S, Meimberg H, Krüger R, Noyer J-L, Heubl. G, Linsenmair KE, Boland W. 2004. Evolutionary change from induced to

constitutive expression of an indirect plant resistance. Nature 430: 205–208.

Heil M, Rattke J, Boland W. 2005. Post-secretory hydrolysis of nectar sucrose and specialization in ant/plant mutualism. Science 308:560–563.

Heil M. 2008 Indirect defence via tritrophic interactions. New Phytologist 178: 41–61.

Predicting the evolution of Theropod arm size

In 1999 I published an article in the (cryptic) monthly news bulletin of the Museum of Natural History of Chile, entitled "Evolution of Arm Size in Theropod Dinosaurs: A Developmental Hypothesis". In this work, which I did as an undergrad, I tackled what seemed a consistent trend among species of theropod dinosaurs, the presence of proportionally smaller arm sizes in species with larger body size. Femur size correlates quite directly with body size in dinosaurs: I therefore took femur size as an indicator of body size and making a linear regression I obtained that Humerus = 0,387 (Femur)^0,6807, with a rather nice determination coefficient, R^2 = 0,89. It is, of course, very remarkable that this negative allometry would so nicely predict theropod humerus size. Rather than the usual adaptive explanations, I presented a developmental hypothesis: The ontogeny of the most recent common ancestor of the theropods presented slower growth of the arm than of the leg, with arms that were proportionally larger earlier in ontogeny, at smaller body sizes. Thereafter, evolutionary variation of different body sizes in different species descended from this ancestor simply reflected conservation of this ontogenetic trait, with smaller- or larger-looking arms as a consequence of body-size variation, rather than any process of "local" adaptation. In this context, the very bird-like dromaeosaurid dinosaurs would owe their proportionally large arms to their small body size. If this were indeed correct, if a dromaeosaurid species would evolve a larger body size, we would expect it to show short arms, unlike those of its small-sized, long-armed ancestors.

The recent discovery of the dromaeosaurid Austroraptor is just that: a pretty large dromaeosaurid, with proportionally small arms, despite being descended from long-armed, smaller ancestors.

So, how does the Vargas formula work for Austroraptor? The femur length of Austroraptor is 0,56 M, so the predicted humerus length is 0,261 M. The actual length of Austroraptor's humerus is 0, 262 M... not bad, hehehe.

Of course, my hypothesis has another more direct and straight-forward prediction: Within an ontogenic sequence of a theropod species, younger, smaller specimens should present proportionally larger arms than older, larger specimens. Unfortunately, I still don't know of any conclusive evidence for this in a non-avian theropod. However, this is known to have been the case for Prosauropod dinosaurs, the inmediate outgroup of theropods, which presented larger arm porportions at earlier stages of ontogeny. Furthermore, according to Middleton and Gatesy, there is preliminary data that forelimb size decreases in the gull Larus californicus form 43% in hatchlings to 38% in adults...suggesting, by phylogenetic "sandwich", that the same was true for non-avian theropods. I thus renew the validity of my prediction!

Vargas A 1999 Evolution of Arm Size in Theropod Dinosaurs: A Developmental Hypothesis. Noticiario Mensual del Museo Nacional de Historia Natural de Chile 338: 16-19

Novas, F. E., Pol, D., Canale, J. I., Profiri, J. D., Calvo, Jorge O., 2008. A bizarre Cretaceous theropod dinosaur from Patagonia and the evolution of Gondwanan dromaeosaurids. Proceedings of the Royal Society B.

Quick comments on Odontochelys

Odontochelys is the new basalmost triassic turtle, with a plesiomorphic ("primitive") presence of teeth (hence the name) and a most remarkable transitional aspect: It has a perfectly formed plastron yet no carapace. Odontochelys only presents the dorsal midline of the neural plates of the carapace, that are close to the neural spines but remain separate (which is not the case in more derived turtles).
Lets briefly recall what some evil saltationists (paleos and evo-devo's) have said about this. I remember Bob Bakker's book "The dinosaur heresies" (1986). There, he mentions the fact that in turtles the pectoral girdle is actually under the ribs, and points out that this qualitative aspect is hard to imagine to have occurred in more than a single step.
What can development tell us of all this? First, the plastron is derived from the neural crest, unlike the carapace, which is derived from a mixture of dermal bone and ribs. Second, the plastron ossifies before the carapace. Odontochelys reveals that this embryological and temporal separation also reflects a phylogenetic sequence. Scott Gilbert (yes, the book guy) points out that in turtles, the ribs have shifted dorsally, to developing within the dermis, a unique trait within amniotes. If an embryonic rib is experimentally inserted in the dermis of a chicken embryo, the result is ossification of the dermis surrounding the rib. Because of this paracrine effect on the dermis, Gilbert hypothesized that a single-step shift of the ribs to the dermis could have induced the origin of a well-formed carapace.

Some regard this hypothesis as incompatible with the hypothesis that an exoskeleton of separate dermal bones preceded the origin of the carapace. This incompatibility in my opinion is not quite so; dermal bones could have existed or not previous to the shift of the ribs closer to the dermis; the shift could have led to a single carapace. Critics to Gilbert's hypothesis have pointed out that in the carapace of the early (very fragmentary) triassic turtle Chinlechelys, ribs are not "immersed" in the carapace but run immediately below the surface of the dermal plates. However it is possible that this was sufficient for the paracrine effect leading to a single carapace "shell". Unfortunately we cannot know if the pectoral girdle was already under the ribs in Chinlechelys.

Even admitting the possibility of previous ostederms, Odontochelys is certainly something unexpected from the more "gradualist" perspective, which was "hoping" early stages of dermal armor would go back to remote Pareiasaur-like ancestors (see figure below). The full plastron of Odontochelys is pretty derived, yet this species has no "coat" of osteoderms.

From Joyce et al 2007. Odontochelys indicates that "coats" of osteoderms as in a) and b) did not precede the origin of the plastron

Odontochelys is consistent with the notion that a shift in the position of the ribs to greater proximity to the dermis could have induced a"radical" extension of dermal bone, from mere dorsal midline of neural plates, to a full carapace; as a third step, superficially attached ribs and dermal bones, became fully integrated with the dermal bone conforming the "true" carapace.

References:

Li C, Wu X-C, Rieppel O, Wang L-T, Zhao L-J (2008) An ancestral turtle from the Late Triassic of southwestern China. Nature 456: 497-501

Joyce WG, SG Lucas, TM Scheyer, AB Heckert, AP Hunt (2008). A thin-shelled reptile from the Late Triassic of North America and the origin of the turtle shell Proceedings of the Royal Society B DOI: 10.1098/rspb.2008.1196

Cebra-Thomas JA, Betters E, Yin M, Plafkin C, McDow K, Gilbert SF. 2007 Evidence that a late-emerging population of trunk neural crest cells forms the plastron bones in the turtle Trachemys scripta. Evol Dev. 9(3):267-77.

Cebra-Thomas J, Tan F, Sistla S, Estes E, Bender G, Kim C, Riccio P, Gilbert SF. 2005. How the turtle forms its shell: a paracrine hypothesis of carapace formation. J Exp Zoolog B Mol Dev Evol. Nov 15;304(6):558-69.

It's the SAME cell environment, stupid

A recent commentary in Science titled "It's the sequence, stupid" describes the conclusions of an experiment published within the journal's latest issue. Framed as a supposed slap in the face to epigenetics, the experiment describes what happens with some indicators of "gene expression" of human chromosome 21 in mouse hepatocytes; that is, human c21 has been incorporated into the genome of an experimental line of mice. They find that things such as the binding site of several transcription factors, and the general levels of transcription on the chromosome, are for the most (but not entirely) the same as in human hepatocytes. Their conclusion? The sequence of the human C21, rather than the epigenetic cell environment, is mostly responsible for "regulation" of its own expression. Hence, "It's the sequence, stupid".
But, is it? It is well-known that all cells within the body contain the same sequence, but express very differently in different cell types, because of the different cell environments. It is interesting that the people at Science managed to wash this fact out of their brains, since it directly refutes that expression is determined in the sequence. Further, their conclusion is simply not logical because they are comparing cells with the exact same cell phenotype. The image shows micrographies from two liver sections; one is from mouse, the other is from human. Can anyone tell me which is which? The fact is, at the cell-histological level, most homologous tissues of mouse and human are undistinguishable.
Don't expect virtually identical cells to produce great differences in the expression of the same sequence just because you are comparing them in different species. Expect them to produce virtually identical gene expression. As simple as that.

Refs:
Wilson, M.D., Barbosa-Morais, N.L., Schmidt, D., Conboy, C.M., Vanes, L., Tybulewicz, V.L.J. Fisher, E.M.C., Tavaré, S., and Odom. D.T. 2008 Species-Specific Transcription in Mice Carrying Human Chromosome 21. Science 322: 434-438

Coller HA, Kruglyak L. 2008 Genetics.It's the sequence, stupid! Science. 322:380-1.

UPDATE

Check out this site on hepatocyte histology
Left is pig; right is raccoon
Phenotypic plasticity: This is mouse, fasted and glycogen-enriched
And of course, human (from another site):

NOTHING IN EVOLUTION MAKES SENSE BUT IN THE LIGHT OF BIOLOGY

Inverted Dobzhansky (in Chilean Andes)

This phrase was recently uttered at an evo-devo symposium by MQ Martindale. By turning Dobzhansky's dictum on its head, Martindale was referring to how the study of the development of marine invertebrates is crucial to reconstruct the evolutionary history of metazoa (1). However, this phrase can find unsuspected depths in its resonance, quite beyond the reconstruction of natural history. It reminds us of the big crime that was the elimination of developmental biology from the neodarwinian synthesis (buried in the name of population genetics).
In fact, the actual priority that should be given to organismal biology, including development, continues to evade much mainstream evolutionary biology, which continues to show too much adaptationist-reduccionist nonsense as a result of a doctrinary enthronization of population genetics.
Take the case of Richard Lewontin. He gets close to the truth on many counts but does not acknowledge the centrality of having a theory of organism. Without this, placing the focus on population genetics (his field) will always be misleading: the organism is collapsed between the gene level and the population level. In other words, to get a correct view of evolution Lewontin would have to renounce to population genetics as the basic framework and thus be willing to erase the blackboard for a new starting point. Notice that by erasing the blackboard I do not mean to destroy the achievements of population genetics, denying any of its utility for answering specific questions. It is merely not to consider it as starting point of all evolutionary understanding.
In fact, biology is a larger topic than population genetics, even larger than evolution itself. Yet the absence of a generally accepted theory of organism has led to confuse the branch with the root: thus the vaccum at the roots is not properly acknowledged.
This, however, did not happen to Humberto Maturana upon being asked by a medicine student "what happened at the origin of life, such that we can say that life began?". Suddenly realizing he did not have a theory of organism, Maturana blushed and was only capable of promising the student he would think it over and answer his question next year.
The result, as many chilean and brazilian biologists already know, was the theory of autopoiesis, a theory of the basic organization of the living. A systems perpective providing minimal theoretical terms for understanding exactly what is goig on in organisms, such that they exhibit the properties we observe. This is not a definiton made for evolutionary biology; it is a definition for life, and as such, universal to all biology. This is why the notion of auotopoiesis has proven fruitful in the theoretical discussion of fields of biology that would appear completely dispar, for instance, the study of abiogenesis; inmunology; and neurobiology (not to mention a somewhat distorted use of the term that has become very popular in the social sciences).
And it so happens that the systems perspective of autopoiesis, focused on the organism, has implications for the understanding of evolution, too...

(1): Like myself, Martindale proposes a ctenophore-like ancestor of bilateria: See Vargas and Aboitiz 2005.

Is everything OK with Olfactores? A call to properly assess morphological implications

When molecular phylogenies do not coincide with the morphological phylogenies, this is a serious problem. Experience tells us that its not a matter of assuming the morphological data is equivocal; specially if it is completely uncontroversial within (morphological) phylogenetic systematics. Many times the conflict thereafter disappears, specially upon better taxon sampling of molecular data (Note: increasing the number of adequate taxa seems to be of much greater consequence than increasing the number of genes). We all remember that "sharks are teleosts" thing. This is why it is good to know the exact "morphological cost", or extra morphological transformations, that are implied by molecular hypotheses that openly conflict with morphological phylogenies. If the conflict shows no resolution by further studies, it is not a matter of assuming the molecular data must be "the correct one"; or at least, if you are going to make that assumption, KNOW the implications for the evolution of morphology!

Is something smelling fishy about the phylogeny of the chordates? Or is everything OK? At record speed, the evo-devo community has accepted the results of the latest molecular phylogenies, that vertebrates are closer to urochordates than to cephalochordates. Olfactores = Urochordates + Vertebrates. This term was born in the context of a marginal theory of Jefferies (1981) within his interpretation that the fossil Homalozoa ("calcichordates") are the ancestors of chordates (other paleontologists consider Homalozoa to be basal echinoderms).

The recent publication of the entire genome of Amphioxus has further repeated this result for the comparison of an astounding 1090 genes in a phylogenetic analysis (Putnam et al 2008) that included important groups that are frequently left out, such as an acorn-worm, and a larvacean urochordate.
Given that the Olfactores are becoming accepted as some "new truth", it is interesting to review why never before had this notion attained popularity, the most common assumption being that cephalochordates and vertebrates were closest, conforming a clade Euchordata (also called "Myomerozoa" for the presence of somites). Actually, just a glance at amphioxus, a very fish-looking creature, should make us immediately suspect that the olfactores is probably not consistent with the most parsimonious morphological history; that is, that we may have the proverbial case of a clash of molecular vs morphological phylogenies.

Everybody agrees that urochordates have secondarily lost traits. This is obvious when the traits absent in urochordates are present even in hemichordates , such as coelomic cavities, and several (not just one) pairs of branchial openings. However, the list of things lost in urochordates increases substantially if we consider Olfactores to be real: for instance, the loss of somites, and several vertebrate-like gene expression patterns in the developing neural tube.

In this sense, it is important to point out that the exact morphological cost of the olfactores, in terms of assuming extra steps beyond parsimony, has not being adequately discussed or investigated yet. An important conflict with morphology and gene expression is looming, but people are failing to see it.

For instance, a recent comment (Swalla and Smith 2006) says "an extensive cladistic reanalysis of morphological data found strong support for Olfactores ( Ruppert 2005)". However, the cited work of Ruppert is not a cladistic analysis at all, but a "homology analysis", the mere mapping of proposed events assuming that Olfactores is real, for a limited set of traits. Further, the morphological cost of the olfactores is hardly rescued by Ruppert 2005, which cites only a few of the most notorious losses we must assume occurred in the urochordates (for instance, Ruppert fails to mention any of the similarities of gene expression between the neural tube of cephalochordates and vertebrates)

In good faith, we must assume that Swalla and Smith were thinking about another morphological analysis that is cited as support for the olfactores, namely the cladistic analysis of all metazoa made by Zrzávy et al (1998). While indeed Zrzávy et al. is an extensive analysis (238 traits), it does not specifically address the question of the phylogeny of chordates , but of metazoa in general. So actually only a minority of these traits are bound to be relevant to the question of chordate phylogeny. Further, despite the non-traditional placement of the urochordates retrieved by this analysis, Zrzávy et al did not make any mention of this result in their discussion, concentrating on other aspects of animal phylogeny. No list of "Olfactorian" synapomorphies was discussed. The analysis by Zrzávy has been criticized at length by Jenner 2001 on various grounds, such as the assumptions made in the definition and polarization of traits.

With no explicit cladistic analysis of chordates for an alternative phylogeny , the review by Rowe (2004) of chordate phylogeny does not even mention the work by Zrzávy or the possibility of the olfactores. Indeed, the best references for a cladistic analysis specifically focused on the chordates are earlier works (Maisey 1986, and Schaeffer 1987), which support the euchordata, and are largely accepted within the community of phylogenetic systematics. However, these studies will fail to collect numerous newly described traits shared by cephalochordates and vertebrates, from gene expression patterns to fine structure of the nervous system. So, in fact, a new updated cladistic phylogenetic analysis of the cephalochordates is needed to establish the precise consequences of the Olfactoria for the morphological history of the chordates.

It is certainly possible that this new analysis may show the history implied by olfactores to be too absurd, implying too many reversals or convergences. If this is the case, it is not just a matter of going with the molecular phylogeny over the morphological; rather, the possibility of an artifact in the molecular studies must be taken into account (yes, even with 1090 genes! )


This is the tree of the 1090 genes (Putnam et al 2008). Some observations:

1) As usual, the longest branches of the chordates are the Urochordates. Also, notice that this effect is not mitigated by the large amount of genes; that is, abnormally high substitution rates is a genome-wide phenomenon. Is it possible that high substitution rates may distort the phylogenetic signal of entire genomes? Also, notice the low 76.4 % bootstrap value support for the monophyly of chordates. Traditionally, molecular evidence has had some problems retrieving this node, which is, from a morphological perspective, a very straight-forward conclusion

2) Hagfish, morphologically the most basal vertebrates , were not included in this analysis. In fact, the position of hagfishes haunts this entire issue, since it is a case in which a clear conflict of molecules vs morphology still lives on

3) Despite the general trend of nuclear genes to support the olfactoria, the comparison of entire mitochondrial genomes supports the classic hypothesis of euchordata (Bourlat et al. 2006). Further, this is also the case when discussing the relationships of Hagfishes, supporting them as basalmost vertebrates (Yu et al. 2008). Why this diference ? Is it possible that the mitochondrial genomes have been spared from some source of artifact affecting the phylogenetic signal of nuclear genes?

References.

Bourlat et al 2006 Nature 444:85-8

Jefferies 1981 Zool. J. of Linnean Soc. 73, 351-396

Jenner 2001 Syst. Biol. 50(5):730-742

Putnam et al 2008 Nature 453: 1064-1070 doi:10.1038/nature06967

Rowe 2004 In: Cracraft & Donoghue, Ed. Assembling the tree of life. Oxford. pp 384-409

Ruppert 2005 Can. J. Zool. 83: 8–23

Swalla & Smith 2006 Phil. Trans. R. Soc. B doi:10.1098/rstb.2007.2246

Yu et al. 2008 J. Genet. Genomics 35: 285-290

Zrzávy et al. 1998 Cladistics 14, 249 -285

Evo-Devo: The Good, the Bad, and the Ugly.

THE GOOD: Homology assesment evo-devo, and epigenetic evo-devo. Evo-Devo that works on the pretty empirical task of assessing problematic homologies, with tree-based inferences on the evolution of development, continues to greatly help the reconstruction of the evolutionary history of life on earth. Epigenetic evo-devo's, in turn, understand that developmental biology is not genetics. They have realistically confronted the role of higher level and environmental epigenetic interactions in development, and thus also in the origin of evolutionary novelties. Both of these tend to emphasize how standing developmental mechanisms, and not natural selection alone, are essential to the pathway taken by evolution.

THE BAD: Reductionist "regulatory" evo-devo. Dangerous, because it is is upheld by important figures of evo-devo, presenting itself as a triumph and empirical conclusion. Yes, mutations in cis-regulatory regions are commonplace in evolution, but these people seem to have reductionist difficulties in understanding there is anything more beyond finding such a mutation. The notion that only non-coding "regulatory" sequence changes can produce localized expression (in time or space) simply makes no good developmental sense. As Lillie pointed out, all cells have the same DNA content, including the "regulatory" elements; whether a gene is expressed or not still varies from cell type to cell type depending on something else as well. In other words, Lillie's "paradox" forces the question: "who regulates the regulators"? This question reveals that "regulation" is nothing but a sloppy, semi-nonsensical wastepaper-basket term. Both coding and non-coding sequences can be "regulatory". Even environment can "regulate" gene expression. Genes are expressed differentially in cells, NEVER because of their "regulatory" sequences alone, but ALWAYS including the higher-level and environmental interactions at the cell and tissue level, which explain "Lillies paradox". (again: This is why developmental biology is different from genetics!). Focusing only on one type of mutations (cis-regulatory) is just a re-strengthened version of the old reductionist fallacy that genotype=phenotype. This false equivalence ultimately downplays the role of understanding development, the actual mechanisms that relate genotype to phenotype. Without really introducing developmental mechanisms, no serious challenge is made to the hegemony of population genetics as a way of understanding evolution. Yes: The bad is a traitor of development, for love of genetics. Evo-Devo can now become a mere footnote: The largely uninteresting filling-in of superfluous data on "what the specific mutations were".

THE UGLY. Just plain wrong or artifactual topics, mostly born from the lack of proper integration of different fields of research. Specially silly is the "conflict" between microevolution and macroevolution. Doubtless, the study of microevolution offers many advantages. But this does not mean at all that a macroevolutionary study will not be able to derive sound conclusions: when the evidence is there, there is nothing to say about the micro or macro level in which a question is satisfactorily answered. That comparable experiments can only be tested between closely related species is a myth: gene expression experiments can produce the same phenotypic alteration despite hundreds of millions of years of separation.
This follows in an old lab-bench tradition of being purely "experimental" negating any need to know much about natural history and macroevolution. It also relates to "blind" faith in molecular phylogenies, that is, with little capacity for critically evaluating these studies (such as by morphologica implications). As a result, plain artifacts of the tree become the basis for many weird hypotheses (I have argued before this is happening right now, with new supposed clades such as "urochordates+vertebrates"). Studies continue to emerge where well-established facts of natural history are swept aside in favor of some "groundbreaking hypothesis".

Many Evo-Devos have thought that macroevolution is some kind of truly radical "body plan" change with mechanisms quite different from those observed at a microevolutionary level, appealing to some mysterious happenstance of the past for the origin of phyla or higher "grades". However, Evo-devo's are slowly wisening up to the fact that macro and micro evolutionary change proceeds pretty much in the same way, with the simple fact being that lineages diverging earlier can accumulate greater differences (as pointed out before)

Looking for Darwin in all the wrong places

Looking for Darwin in all the wrong places: the misguided quest for positive selection at the nucleotide sequence level

AL Hughes

Heredity (2007) 99, 364–373

Recent years have seen an explosion of interest in evidence for positive Darwinian selection at the molecular level. This quest has been hampered by the use of statistical methods that fail adequately to rule out alternative hypotheses, particularly the relaxation of purifying selection and the effects of population bottlenecks, during which the effectiveness of purifying selection is reduced. A further problem has been the assumption that positive selection will generally involve repeated amino-acid changes to a single protein. This model was derived from the case of the vertebrate major histocompatibility complex (MHC), but the MHC proteins are unusual in being involved in protein–protein recognition and in a co-evolutionary process of pathogens. There is no reason to suppose that repeated amino-acid changes to a single protein are involved in selectively advantageous phenotypes in general. Rather adaptive phenotypes are much more likely to result from other causes, including single amino-acid changes; deletion or silencing of genes or changes in the pattern of gene expression.

Heredity (2007) 99, 364–373; doi:10.1038/sj.hdy.6801031;
published online 11 July 2007

Podrán encontrar el pdf en el grupo yahoo...

Epigenetically Acquired Brain Disorders

Cachense este trabajito (hacer click en titulo)...

Epigenetic Mechanisms in Autism Spectrum Disorders

Parental Care Usurpation as a model for thinking about Developmental Systems

Parental Care usurpators exploit the social behavior of their hosts, this “modo de vida,” it is present in numerous taxa and involve the partial sequestration of the ontogenetic niche of the host species. In this commentary I will mention two cases of parental care usurpation: the avian brood parasites (e.g. cuckoos) and the ant nest usurpations (often called slave-maker ants or pirate ants).

Due to the very emergent properties involved in the evolution of these life styles; these cases are interesting models for thinking about the value of Developmental System Theory or Evolution by Means of Natural Drift as explanatory backgrounds.

Previously in this blog, we have seen comments about the relevance of the “incomplete isolation” of the multicellulars systems processes as a way to understand certain kinds of dynamic changes in the ontogenetic niche. This “epigenetic permeability”, could be suggested as a property that may help to understand why it is not always necessarily an “Internalization” (i.e incorporation of adaptative traits in the genome of the evolving species) for the development of new life styles or lineage changes in order to get an idea of the points when this “epigenetic permeability” may help to explain the establishment and conservation of these life styles, lets compare the steps of the parasite-host interactions.

In avian brood parasites, the female lays the egg in the host nest, which has been recognized by some authors as the only interaction between the parasite and host species. I would suggest to add a second step that is performed by the parasite chick: the expulsion from the nest of the host offspring (this does not always happen though). For the realization of step one of the interaction, the parasite mother had to find the appropriate host nest and the host parents have to be fooled to keep believing that the extra egg belongs to them. Some parasites species present similar egg pigmentation with their main host, but it is not clear, as far as I´ve read, that this is genetically determined and that this trait can vary inter and intraspecies. The second step is very similar to other kind of parasitic interaction where the allocation of resources is diverted to feed the growing parasite (See Sacculina barnacles post in this blog as an example).

In ant nest usurpation species, the first step involves the usurpation of the queen host throne by the parasite ant. The female searching for nest, sneaking in the nest without being detected as alien by the colony, and (as similar as the avian parasite chick) the diversion towards the reproducing parasite.

In the second step, the parasite queen offspring will search for new host colonies, raid them and kidnap host worker’s larvae. Experiments have demonstrated that when two alternative host are available for the queen and she picks one of them in the first step, the parasite sons will also choose that one for collecting more workers.

This two examples suggest to me that the Developmental System is more than the niche variables and the inheritable organism material, and cannot be reduced to the somatic and germinal part as a satisfactory explanatory background but also the construction of these parasitic life styles due to epigenetic permeability are possible thanks to crucial behavioral operations (“conducta” in Maturana’s approach) that allow the emergence of these very externalized and dependent systems.

Cristian Villagra

Conditions of Evolution and Adaptation in Organisms as Autopoietic Systems

Del capítulo de Gerhard Roth en el libro "Environmental Adaptation and Evolution". El artículo entero pueden bajarlo desde los archivos del grupoyahoo de decenio (Roth1982) Provecho!

Deep-time dinosaur phyloepigenetics

West-Eberhardt repeatedly mentions in her book the case of the two-legged goat, born with no forelimbs, that learned to walk bipedally, and developed several hip traits, bipedal "adaptations". Certainly, to understand the development of these hip adaptations, we would be ill-advised to concentrate on the molecular mechanisms underlying cell-death in the embryonic forelimb, who have only indirect "causation", far removed from the actual mechanisms involved in the largely non-genetic influence on this trait. Comprehension can only come from observing the higher-level interactions and the direct developmental effects of emerging epigenetic interactions. It is interesting to think just how many aspects of our phenotype are, like this, only very indirectly related to the genotype (from a systems view, a mutation can be nothing but a "trigger").

I still remember when it dawned upon me in 2001; ALL vertebrate limbs, universally, grow longer with mechanical stimulation and use. I thought about early theropod dinosaur's reduced forelimbs. Even if bipedality were the result of some mutation enlarging legs or shortening arms (by the way: probably not, but behavioral), the arms would receive less mechanical stimulation when relieved from locomotion, whereas the legs now bear the entire body's weight. There is no way this is not going to decrease growth in the arm , increase it in the leg, and enhance forelimb-hindlimb size differences. Enter here the field of phyloepigenetics, which we previously named on this blog; the recopilation of cases of epigenetic explanation of evolutionary differences. This time I present a case of a deep-time epigenetic apomorphy: The fibular crest of the tibia of Theropod dinosaurs and their living representatives, the birds. Here are some photographs of this rectangular crest, that extends from the large tibia onto the thinner fibula (both elements of the "shank" or zeugopod). Since this is a trait of all theropods, the fibular crest must be at least 230 million years old. Two different birds species illustrating the fibular crest of the tibia, upwards, rectangle-shaped (from Müller and Streicher 1989)

The fibular crest is an apomorphy of theropod dinosaurs. On the left, a theropod; right, a non-theropod dinosaur (Müller and Streicher 1989)

It turns out that this crest is a sesamoid bone, that is, a bone that develops within connective tissue as a result of mechanical stimulation; first cartilage is formed in the stimulated region; this cartilage may thereafter ossify originating the sesamoid bone (The chicken patella and human knee-caps are sesamoid bones that develop from within tendons). We can say that the sesamoid bones are to connective tissue what callosities are to epidermis. All of this with plenty of experimental confirmation, such as mechanical forces in abnormal places, etc.
The fibular crest of the chicken develops as a cartilage in the narrow space between the tibia and the fibula. In theropod evolution the fibula became thinner; this may be the reason why muscles that in other reptiles pull the leg backwards and project exclusively onto the fibula, in the chicken embryo also hit the connective tissue between the fibula and the tibia, provoking the development of a new sesamoid cartilage. This cartilage therafter ossifies into the crest, tightly connecting the tibia and the fibula in the adult. This crest in birds is certainly "adaptive" since it is fundamental to have a functional leg (because the fibula in birds no longer connects distally to the foot!) Yet against the adaptationist intuitions of old-style lamarckism, or of reformed "epigenetic darwinists", nothing in all those millions of years has produced a mechanism for developing this bone without movement. It still relies on the same "good old" mechanical stimulation. If the embryo is paralized , for instance, with a postsynaptic blocker, the cartilage of the fibular crest is no longer formed. The unavoidable effects of higher-level interactions have remained the basic mechanism by which this trait is developed .

From Müller 2003

The authors of the study share some wisdom with us:

"The de novo formation of skeletal elements addresses an important but largely neglected issue in evolutionary theory: the origination of morphological novelty. This generative problem of organismal evolution is sidestepped in traditional accounts that focus on the gradual variation and adaptation of characters and calculate their population genetic underpinnings. The studied characters are usually taken as given, and their origination is tacitly assumed to be based on the same mechanisms as their variation and adaptation. There is growing awareness that this does not need to be the case and that innovation should be treated as a distinct problem of
evolution"

Müller GB and Streicher J. 1989. Ontogeny of the syndesmosis tibiofibularis and the evolution of the bird hindlimb: a caenogenetic feature triggers phenotypic novelty. Anat Embryol. 179: 327-339

Müller GB. 2003. Embryonic motility: environmental influences and
evolutionary innovation. Evol & Dev 5:1, 56–60

Population genetics & game theory are not "The logic of life"

The theoretical disciplines of population genetics and game theory are upheld by neodarwinians as general explanatory frameworks for the study of evolution. These provide explanations that do not require understanding of development, physiology, and practically all mechanistic causation at an organismic level, even if these are acknowledged to be crucial. All organism-level mechanisms can be taken as simple "givens" imposed from the outside as from a completely mysterious black box.
This divorce and alienation of organismic biology from "evolutionary theory" was philosophically formalized by Ernst Mayr. To Mayr, any study at the organismic level, for instance of physiology, or developmental mechanisms, can only answer "how" questions of immediate mechanism; whereas evolutionary science is in charge of a different level of analysis of "why" questions and "ultimate" causation (by long-term selection, of course). Immediate mechanism apparently could be "whatever". Mayr then manages to make evolutionary science autonomous as a discipline....but only by means of turning its back on organismic biology.

The effect is disastrous. Neodarwinists have become addicted to attaching ad-hoc explanations to simply "given" organismal conditions, and destine all that level of causation to a wastepaper basket labeled "NON-evolutionary proximal mechanisms". Indeed the implication is that proximal mechanism is not an important part of properly "evolutionary" explanation. But then, if there is no general theory for biology, with no theoretical notions about all that biology that is going on at organismal level, how can a neodarwinist claim to have found a general framework for evolutionary biology? Indeed, is it even possible to have a general theory for evolution, without having a general theory for biology? A truly satisfactory evolutionary theoretical framework requires good theoretical grounds for handling the organismic level, rather than a philosophical argument to ignore it. Truth is, neodarwinists have no theory of organism.

That something is wrong with the "autonomy" of "evolutionary" science surfaces in many details. Consider, for instance, just how impervious the general frameworks of population genetics and game theory are to any data input from other fields of research, and specially so the more historical such as phylogenetic systematics. Consider, for instance, just how useless population genetics is to explain how reptilian jaw bones ended in the mammalian middle ear. The analogy in physics would perhaps be a theoretical physics-cosmology that won't take any lesson from astronomy and is not too helpful to explain any astronomical phenomenon.

In contrast, the systemic -historic perspective fully acknowledges and further emphasizes the historical nature of evolutionary explanations. Plus, we have the notion of autopoiesis for the theoretical handling of the organism level...

Whereupon Lewontin is criticized, and "Phyloepigenetics" is born

In "The triple helix" Lewontin seems to contradict himself a bit on the importance of genes. Consider this paragraph:

"Of course it is true that lions look different from lambs and chimps and humans because they have different genes, and a satisfactory explanation for the differences between lions, lambs, chimps and us need not involve other causal factors"
(Italics are mine)

Since Lewontin in his next breath talks quite a bit about the importance of environment and random noise in development, we are forced to wonder why they would not count as causal factors when it comes to explaining inter-species differences.

I suspect this is the result of a typically neodarwinian mistake born from the circular logic of their definition of evolution. Because "evolution is genetic change of populations", when observing a difference that is species-level (evolutionary) they get confused and think they can assume that difference to be the result of natural selection for genetic mutations (unless it is a very obviously a non-adaptive difference, in which case it is still genetic mutations, and drift rather than selection) . This argument in fact is repeatedly encountered in the discussion over whether human "intelligence genes" exist or not. "Evolutionary" psychologists (ultradarwinians) argue that the fact the human brain has evolved from smaller, less-smart brains like those of other apes implies natural selection for "intelligence genes" must have occurred in the human line, and thus that genes capable of increasing fitness through intelligence must indeed exist (The fact being that their effects are difficult to detect. Only using lots of data, statistical correlations for only very small increases in IQ scores is all that is ever detected for an alleged "intelligence gene)"

This argument, that seems so impeccable to those accustomed to thinking with a neodarwinian cap, can be exposed for the misleading definition-game it is when we stop to analize a few case-studies. The human trait of bipedism for instance. Below is the photograph of one of two "wolf girls", Amala and kamala, that were raised by wolves in India and then "rescued" into civilization in the 1920's. Extensive written and photographic documentation were produced by the priest who took care of them. As you can see in the photograph, the girls used quadrupedal, rather than bipedal, locomotion. The priest tried hard but made little progress training them into walking like people. They did not speak and and had obviously subnormal cognitive capacities for human standards .


You would think that genetic influences over general human anatomical structure would be sufficient to lead to bipedality. However, let us remember that in our ontogeny we do, in fact, learn to walk bipedally. This important difference between humans and other animals seems to not come about without an appropiate context, provided by interactions among humans, which are in fact required for preserving the behavior of bipedal walking .

Let's talk about symbolic language, another difference between humans and other species. Beyond Amala and Kamala, it is clear from numerous documented cases of feral or cruel upbringing of children, that children deprived from human interaction will not learn to speak and will develop a severely subnormal intelligence. But perhaps more interesting is the reverse experiment, that is, not only is it possible that a human may not learn to speak despite of any "language genes", but also, it is a fact that non-human primates can learn sign language and use it to communicate, despite any lack of "language genes". In this case, an important part of that species difference has been phenocopied in the other species, once again, with the aid of an adequate environmental context.

So, there definitely is an epigenetic component to the explanation of cross-species differences. A purely genetic causation could never be a satisfactory explanation. We will find that, as we compare the terminal taxa of a phylogentic tree, we will be able to see nodes in which clearly different epigenetic conditions have become established and can be directly responsible for great phenotypic differences or epigenetic apomorphies ; the sublime confirmation of everything is, of course, the experimental phenocopy or reversal through alteration of the suspect epigenetic factor.

I can think of several confirmed examples from non-human organisms and simple phenotypic traits, as well as several epigenetic hypotheses that have never been discussed before as explanations of differences between species, perhaps for lack of a more formal approach. I thus propose we begin by calling this approach Phyloepigenetics.

The intention of this post is to start several posts where we will be studying and discussing probable cases of epigenetic differences at the species-level, and thus make ourselves with a litte more "cultural baggage" to defend this new approach. I invite everyone to share examples!! I will soon be posting one about ...dinosaurs! Phyloepigenetics can be paleo, too.

Reference:
Lewontin, R. 2000 The triple Helix: Gene, Organism and Environment. Harvard University Press.

Systemic vitalism, or the distinction of teleonomy from teleology

The concept of "vitalism" has been traditionally associated to pseudoscience, a metaphysical concept away from any empirisism. It is often referred to as the action of a "vital force" or "entelechy" proper to organic matter, that governs and directs living processes. However, Ortega y Gasset (see the post below) defines vitalism as "any biological theory that considers organic phenomena irreductible to physico-chemical principles" and states that it can be conceived from two radically different points of view: a) the assumption of a special form of entelechy or "vital force" distinct from physicochemical forces, or b) a rigurous empiric approach to study vital phenomena in the feral peculiarity they manifest, without assuming any mysticism, but avoiding a dramatic reduction to its physical properties.

In light of this distinction it is worthwhile to recall some concepts such as "emergence", a core notion of complex systems. "Emergent properties" are not properties of any component of the system, but of the system as a whole. Examples vary from "hurricanes" to "swarm intelligence" and "consciousness". As opossed to pseudoscientific vitalism, emergence is not restricted to organic matter, but is proper to systems.

Teleonomy is a term coined for the "apparent purposefulness" of living processes, as contrasted from "teleology", a concept that indicates intention of an external agent. We may well accept the distinction, although it is a common vice in scientist to confuse them, but an important question still remains: what is the biological process that lets us, as observers, to recall teleonomy?

Ernst Mayr (1965) have said: "It would seem useful to rigidly restrict the term teleonomic to systems operating on the basis of a program of coded information", but do we need to recall "information" to explain "apparent purposefulness"? It seems to me that to invoke "coded information" is as finalist as invoking an entelechy's "intention", so it would not be an acceptable biological answer.

It seems that our mechanicist tradition has forced us to reduce causes to the physico-chemical conformation, rather than to the organization. This reductionism has not only been uncapable of explaining biological phenomena, but has kept biologists in an Aristotelian "formal cause" reasoning, where genetic information is the entelechy able to determine the parts and relationships within organisms, thereby equating the metaphysical and organisational forms of vitalism.

A systemic answer to the "apparent purposefulness" dilemma can be envisioned by recalling the ontogenic phenotype/ontogenic niche relationship (the particular manner of living of an organism of a certain lineage). So when an investigator is observing an organism she recognizes a particular behaviour and can visualize a response for a given situation: she is bringing forth an operational congruence (adaptation) of the organism with its niche, that although pertains to the virtual domain of her observations, would seem to respond to an "apparent purposefulness". However, the organism is free to display behaviours distinct from those expected by the observed, as long as it maintains its adaptation, so the "apparent purposefulness" is only an observational artifact proper to the mind of the investigator accostumed to observe configurations.

Rodrigo Suárez

The "Palau man" paper: The return of precladistic paleontology?

I have just posted this message on the blog of the online community manager of PLOS:

Hi Coturnix,
I haven' heard yet much criticism of the Berger et al. paper, so I guess I'll be one of the first.

I consider that Berger hasn't really established that these tiny Palauans are H. sapiens. This could be a species close to H. sapiens (perhaps the closest known so far and thus "sister" species) that has retained some plesiomorphic traits yet shares several apomorphies with H. sapiens (until now thought to be "autapomorphies", exclusively of sapiens)

To discard this possibility and prove that tiny Palauans are H. sapiens, Berger et al. would have to show that their tiny Palauans are phylogenetically nested within H. sapiens (and not "right outside"). However they did not make a phylogenetic analysis (despite disposing of several specimens and good morphological data)

Without that, they are simply preferring hypotheses of convergence or reversal rather than homology for the primitive traits, which is contra-parsimony unless further evidence is provided; and for that, they would need phylogenetic analysis.
A little PAUP on the morphological traits, that's all I'm asking for. This is standard procedure in systematics and paleontology when describing a new fossil of evolutionary relevance. Statements such as "We feel that the most parsimonious, and most reasonable, interpretation of the human fossil assemblage from Palau is that they derive from a small-bodied population of H. sapiens" do not substitute for actual phylogenetic analysis using parsimony.
If Berger et al did that analysis, they would KNOW, rather than FEEL, whether "tiny palauans are H. sapiens" is REALLY the most parsimonious hypothesis or not.

Quick change, then stasis, is not evidence for adaptive directional selection

Gasterosteus taken from Henry (2008) see ref

In scenarios that consider positive, directional selection as the main cause of adaptation, mutation is abundant, such that there always is available genetic diversity for selection to act upon. If on the contrary, adaptive mutations are rare, no matter how intense, selection is powerless to produce adaptation. In a classic scenario of directional selection, change accumulates steadily as genetic variation is not restrictive to the action of selection. Quite different is a scenario where evolution stops each time selection is done with the existing variation, left waiting for the advent of new mutations.

It is at this point that I wish to emphasize an important conceptual distinction that fails to be made when "positive selection" is reported from the sequence of a single gene. We are talking that each allegedly beneficial mutation lies within a single gene here; it is not a bunch of mutations spread out in different genes within the standing variation of a population, ready to be accumulated by selection. Rather, "positive selection" at the gene sequence level must by force obey an "episodic" scenario. Even if selection immediately imposes each beneficial mutation in the population, the change would be episodic and restricted to the occurrence of the next mutation. It is important to make this clear since this can be easily confused with the classical scenario of positive selection: continuous, and unrestricted by genetic variation. Sequences with "positive selection" don't provide any evidence of that.

Directional selection is also not "episodic" because it is supposed not to depend on more than a single episode of environmental change; that is, you have a new selective condition, and from then on, directional selection is supposed to produce the gradual betterment over time of adaptation to that selective condition. In theory it only requires abundant genetic variation and competition; evolution occurs, despite no further ongoing changes of the environment. However, short episodes of evolution followed by stasis, rather than continuous evolution, suggest that episodes of evolution may be restricted to events of environmental change.

Even within the neodarwinian synthesis, Simpson, their most notorious paleontologist, had attempted a proposal for a saltational mode of evolution, where stasis was interrupted by short periods of rapid evolution. Wright had also provided theoretical reasons for such an evolutionary pattern. The reasons of Simpson were quite understandable: This is the pattern that can most readily be discerned from the fossil record. However these views were pushed into the background pretty much until Gould and Eldredge re-established the fact decades later under the name of "punctuated equilibrium". Cases of gradual transformation of one species into another are rare in the fossil record, and so are the cases where we could suggest directional selection is producing adaptation.

I wish to thank Gustavo Ramos for bringing to my attention a commentary in Nature (Henry 2008) regarding this classic difficulty for detecting directional selection in the fossil record. Researchers with an explicit preference for darwinian explanations are showing frustration because currently available statistical tests for detecting directional selection never deliver positive results from the fossil record. The emblematic case in point is a population of sticklebacks in an environment with low predation, where exquisite fossil documentation and temporal resolution shows a trend across time to reduce the average number of spines in their armor, from about 1.4 to 0.9 (see figure below). When the tests were negative for directional selection, some felt that observable trend means the tests MUST be wrong. What they did was to change the requirements of the tests for detecting directional selection, now retrieving positive results for the stickleback population.

Says the article: "Previous tests have tended to treat directional selection as a reasonably consistent force driving average phenotypes in a given direction. This model is obviously unrealistic in the absence of any force expected to sustain selection in a particular direction over such long time frames. Instead, adaptation should often involve the asymptotic approach of phenotypes towards a particular optimum, near which the average should then remain until the optimum is perturbed. That is, environmental change should cause initially strong directional selection that should gradually grade into stabilizing selection, a ‘hybrid’ selection model if you will. This particular process is what would be expected for heavily armoured sticklebacks colonizing a lake where predatory fishes are rare, and the hybrid model provided an excellent fit to the fossil stickleback data"

Now wait a minute. Isn't this more or less what people like Simpson, Wright and Gould had in mind? An episode of quick change followed by stasis. Henry's comment has placed all the change at the moment of environmental change, and further envisions a different, negative and stabilizing selective pressure after this episode. This is hardly the scenario by which positive selection is suppose to produce adaptation.

Rather, this looks more like fairly typical change in conditions of negative selection, like the peppermoth: population averages change dramatically at the beggining, when the change in the environment is new; as time goes on, the population settles on the new average and stops changing. This is not "creative" selection. It's a shift in the populational frequencies of fishes with either 3, 2, 1 or 0 spines (more than 3 spines are never observed). No new morphologies are produced or even lost, despite the fact the average number of spines clearly moves into a new range.

Can we then confidently say that adaptive directional selection is responsible for what was on average the rapid loss of about half a spine, with stasis therafter? In my opinion, this pattern is suggestive of a shift in conditions of negative selection, specifically, a relaxation of negative selection. When transferred to an environment with less predators, since selective pressure is released, forms with 1 or 0 spines rapidly become more frequent and drag the average down to a new low. Before the environmental change there was little intergenerational oscillation in the average of spines, suggesting strong negative selection. After the episode of rapid change, and as a result of more relaxed negative selection, the averages became lower, AND there is also much greater intergenerational oscilation in average spine number (indeed, much LESS "stabilized" than before the environment changed!) . We go from fairly straight lines to a more wildly zig-zagging pattern. This to me suggests the relaxation of selection; quite according indeed with the shift to a lower presence of predators.
Hardly a compelling case of adaptive directional selection, no matter what the new tests may say.

Ref:

Bell MA, Travis MP, and Blouw MD. 2006 Inferring natural selection in a fossil threespine stickleback. Paleobiology 32(4): 562–577

Henry AP 2008 Darwin in the fossils. Nature 451: 779-780