Atheistoclast wrote:

Rumraket wrote:
Bullshit, your tenure on all the various skeptics forums and science blogs betrays a committed doctrinalist. You completely ignore valid rebuttals and intentionally misrepresent the science of of developmental biology (cell-cell signaling and gene-regulatory networks), evolution (with your "degenerative" horseshit and information theory canards). It reeks of doctrinal commitment and a fear of the progess of science. You're fooling noone.

Lol. I am only reporting what other scientists have mentioned:

1) Development is primarily epigenetic, and gene regulatory networks don't determine specific morphological structures.
2) Many instances of adaptation are degenerative in terms of their effect on functionality.
3) Natural selection has no capacity to generate biochemical information.

Atheistoclast wrote:I am not afraid of scientific progress.

Atheistoclast wrote: I am frustrated at the slow pace of science.

Atheistoclast wrote:I know Darwinism will collapse, largely due to its own internal contradictions

Atheistoclast wrote:but realize it will take longer than I am comfortable with.

Atheistoclast wrote:The last 30 years have been a revelation though.

Atheistoclast wrote:Moreover, the publication of my own scientific papers are accelerating the process.

Atheistoclast wrote:I am very excited.

Atheistoclast wrote:

No you don't, you don't even really believe this bullshit yourself. You really want to, but you can't because It's all a smokescreen, and your only motivation is your fear of having to own up to the inevitable conclusions of the advancements of science. Everything you do testifies to this. Your silly Hitler/Nazi canards, the attacks on scientific institutions("money is driving evolutionism", as if being a biologist was a great way to get rich ). You're knowingly peddling manifest falsehoods and misrepresentations.

I realize how many people are uneasy with the fact that the universe did not invent itself

Atheistoclast wrote:and life did not emerge from a primordial soup

Atheistoclast wrote:(i.e the pantheistic creed of ancient pagan religions)

Atheistoclast wrote:but science is inexorably showing that the universe does require a cause for its existence that is extraneous to its own nature.

Atheistoclast wrote:It also shows that the complexity used to advance the idea of a "telelogy" and designing agency is far more than Paley and co could have even dreamed of.

Atheistoclast wrote:And, yes, money (and corruption) is at the heart of modern science.

Atheistoclast wrote:Evolution is big business.

Atheistoclast wrote:

Another intentional misrepresentation. Another total lie. You know physics successfully explains the behavior of matter, so in order to persist in delusion you are forced to deny it's conclusions. You misrepresent the physics of thermodynamics and chemistry at every opportunity, being forced to deny all the various fields of "materialist science" because you know they all supports each other.

I know there are physical laws that determine the behavior of matter. I just don't know the origin of these laws and forces (like gravity).

Atheistoclast wrote:I certainly don't know the origin of the physical constants that fine-tune the universe for order and life.

Atheistoclast wrote:But I think I know who might be responsible for all this.

Atheistoclast wrote:

monkeyboy wrote:

Atheistoclast wrote:
The paradox is that without consciousness there would be no matter since there would be nobody to sense it! This is the argument of idealist philosophy. It was the Buddha who said that the universe exists in the mind and nowhere else.

And if a bear shits in the woods and there is nobody there to see it or smell it, does that mean that there isn't a large pile of excrement out there to avoid stepping in?
This philosophical navel gazing is ok for passing an evening with a couple of mates over a herbal cigarette or two but in the end it amounts to nothing but a whole load of hot air.
If you needs consciousness for reality to exist, don't try sleeping on a cliff top, you might roll off and meet reality at the bottom without ever waking up to realise what a mistake you have made on this issue.

The smelly bear poop only exists when people sense its smelly presence. It does not exist except in the conscious mind of the person sensing it. Remember that it is your mind that generates the world around you.

Spearthrower wrote:

Atheistoclast wrote:
Darwinism is not the same thing as Evolutionism.

Oh! But I've seen you claim that evolutionism is also primed to collapse... and materialist biology, and methodological naturalism, and....

Basically it's a pet-hate list, isn't it Atheistoclast? You really do project your internal states out onto the world: thus sciences you don't like will fall, external reality only exists in so much as its internal representation, and a human-like god made stuff because you can't see how it could have arisen without agency.

Solipsism is just not a healthy mind-state, and it sure as hell doesn't fit into a scientific paradigm!

Atheistoclast wrote:

Rumraket wrote:Ahh, argument by strawman, your favorite apologetic trick. Pretend the opposition is making a specific claim(in this case, that "gene regulatory networks determine specific morphological structures"), then attack it, wait for someone to try and defend it and produce a silly little quotemine in support of your original claim.

Here's what you need to do:
Produce, by citation of peer reviewed literature, a consensus by scientists that developmental biology does not (and can not) explain morphology.

Here's what you can't do:
Exactly that.

As a corollary, here's what happened:
You lost.

I have authored and submitted a paper on this very subject. It is currently under review.

Atheistoclast wrote:It should come out in the next few months - be patient.

Atheistoclast wrote:

Except that they constitute adaptations and thus the "degenerative" bullshit is simply a rethorical trick. The evolution of whale flippers was a degeneration of legs. Another useless strawman argument.

No. The point is that many adaptations, such as the loss of the pelvic spines and armor on freshwater stickleback fish (which prevent them from being grabbed by dragonflies living at the bottom of lakes) are degenerative and thus show how selection promotes functional loss in many instances.

Kitano et al, 2008 wrote:Summary

Faced with sudden environmental changes, animals must either adapt to novel environments or go extinct. Thus, study of the mechanisms underlying rapid adaptation is crucial not only for the understanding of natural evolutionary processes but also for the understanding of human-induced evolutionary change, which is an increasingly important problem [1–8]. In the present study, we demonstrate that the frequency of completely plated threespine stickleback fish (Gasterosteus aculeatus) has increased in an urban freshwater lake (Lake Washington, Seattle, Washington) within the last 40 years. This is a dramatic example of ‘‘reverse evolution,’’ [9] because the general evolutionary trajectory is toward armor-plate reduction in freshwater sticklebacks [10]. On the basis of our genetic studies and simulations, we propose that the most likely cause of reverse evolution is increased selection for the completely plated morph, which we suggest could result from higher levels of trout predation after a sudden increase in water transparency during the early 1970s. Rapid evolution was facilitated by the existence of standing allelic variation in Ectodysplasin (Eda), the gene that underlies the major platemorph locus [11]. The Lake Washington stickleback thus provides a novel example of reverse evolution, which is probably caused by a change in allele frequency at the major plate locus in response to a changing predation regime.

Kitano et al, 2008 wrote:Results and Discussion

Reverse Evolution of Armor Plates in Lake Washington Sticklebacks

The threespine stickleback (Gasterosteus aculeatus) provides a good model system for elucidation of the ecological and genetic mechanisms underlying phenotypic evolution [12, 13]. One dramatic and prevalent phenotypic change in these fish is the reduction of armor plates, which cover the lateral body surface, that occurred repeatedly after freshwater colonization 12,000 years ago [10]. Whereas ancestral marine sticklebacks typically have a continuous row of lateral plates (completely plated morph), freshwater sticklebacks usually have a reduction in lateral plates resulting in a gap in the middle part of the plate row (partially plated morph) or a loss of both the middle and posterior plates (low-plated morph). The major gene responsible for reduction of the stickleback lateral plates across the world is Ectodysplasin (Eda) [11]. There are two major alleles of Eda found in stickleback populations, and they are here referred to as the complete allele and the low allele. Most marine sticklebacks are homozygous for the complete allele, although marine sticklebacks that are heterozygous carriers of the low allele are found at a low frequency [11]. It is proposed that when marine sticklebacks colonize freshwater environments, strong selection results in an increase in the frequency of the low Eda allele, leading to the prevalence of low-plated fish in freshwater.

In contrast to the prevalence of the low-plated morph in many freshwater environments [10, 11], we found a high frequency of completely plated sticklebacks in Lake Washington, an urban freshwater lake in Seattle [14–16]. In 2005, we found that all three lateral-plate morphs were present, with 49% completely plated morphs, 35% partially plated morphs, and 16% low-plated morphs (Figures 1A and 2C). Although a previous study had also shown that all three morphs were present in Lake Washington in 1968–1969, only 6% were classified as completely plated morphs (Figure 1A) [17]. Instead, the low-plated morph, with a mode of seven plates, was the most common morph until the late 1960s (Figures 1B and 1C). In 1976, bimodal peaks appeared, one corresponding to fish with seven plates and another corresponding to fish with 32 plates (Figure 1C) [18]. The frequency of fish with 33 plates was even higher in the 2005 sample (Figure 1C). The increase in completely plated fish in the 2005 sample did not reflect bias in the sampling methods (n = 322, χ2 = 6.6949, d.f. = 4, p = 0.1529) or in the seasonal (Figure S1, available online) or geographical (Figure 2C) distribution of differently plated sticklebacks. These data demonstrate that the frequency of plate-morph phenotypes has changed dramatically in Lake Washington within the past 40 years, which is equivalent to 40 generations in this stickleback population [18].

Genotyping of the 2005 samples at the Eda locus revealed a strong association between plate phenotype and Eda genotype in Lake Washington (n = 196, χ2 = 227.0, d.f. = 4, p < 10247) (Figure S2, Table S1). By ANOVA, the Eda genotype explains 75.2% of the variance in plate number in the Lake Washington stickleback. This is close to the percentage of phenotypic variance in plate number explained by the Eda locus in laboratory crosses (76.9%) [19]. Thus, the increase in the completely plated phenotype in Lake Washington is probably the result of an increase in the frequency of the Eda complete allele, given the previously established link between plate phenotype and Eda genotype in stickleback populations across the world [11].

Gene Flow is Not the Primary Cause of Armor-Plate Evolution in Lake Washington Sticklebacks

Most marine sticklebacks in Puget Sound are completely plated (Figure 2C), with high frequencies of the complete Eda allele (Figure 2D). Because marine sticklebacks can now migrate into the lake through the Lake Washington Ship Canal (Figure 2B and Figure S3), which was built in 1917 [14], an increase in migration might have contributed to the increase of lateral plates in the Lake Washington stickleback. In order to test this hypothesis, we collected sticklebacks in neighboring marine environments (Puget Sound), in multiple points in Lake Washington, and in neighboring streams (Figure 2) and genotyped them with 15 microsatellite markers (Table S2). Genetic data were then analyzed with the Bayesian-clustering software STRUCTURE [20]. Within the marine, lake, and stream fish that were genotyped, the most probable number of genetic clusters (K) was three (Figure S4). Estimation of ancestry for each individual revealed that the sticklebacks in Lake Washington have two main genetic sources (Figure 2E). Sticklebacks sampled from areas near the ship canal were genetically similar to marine sticklebacks (indicated with green in Figure 2E), whereas those sampled from areas close to the streams were more similar to neighboring stream sticklebacks (indicated with blue in Figure 2E). However, there was no significant correlation between probability of marine ancestry and plate number (Pearson correlation r = 0.005, p = 0.967) (Figure S5). Multidimensional scaling of the genetic-distance matrix also confirmed the lack of association between genotypes at neutral loci and plate number (Figure S6). Thus, the increase in armor plates in Lake Washington sticklebacks does not result simply from the presence of marine sticklebacks in the lake.

It might be still possible that an increase in long-term migration from Puget Sound has contributed to the overall increase in the completely plated morph in the lake. To test this possibility, we first estimated migration rates (m; fraction of migrants per generation) from the genetic data and then examined whether the empirically estimated m can explain the observed plate evolution. We used both Isolation with Migration (IM) and LAMARC software [21–23] to estimate the m between a Lake Washington population and a Puget Sound marine population (Table S3). The m of Puget Sound sticklebacks into Lake Washington was estimated as 3.03 × 10-4 (IM) or 1.77 × 10-3 (LAMARC), whereas the m of Lake Washington sticklebacks into Puget Sound was estimated as 6.43 × 10-4 (IM) or 1.20 × 10-3 (LAMARC). Then, we developed deterministic numerical simulations to calculate the m required for the observed change of plate phenotype under different selection regimes (Figure S7). In the absence of selection (s = 0), migration would need to be 0.148 to explain the observed change from 1969 to 1976 and 0.035 to explain the observed change from 1969 to 2005. These values are inconsistent with our low (m < 10-3) migration-rate estimates, suggesting that there was a period of selection that favored the completely plated morph in Lake Washington.

Changes in Selection Regime in Lake Washington

By using the empirically estimated values of m, we found that a selection coefficient s (strength of selection for the completely plated morph) of 0.58–0.72 (Table 1) can explain the evolutionary shift from 1969 to 1976 (from 6% completely plated morphs to 40.2% completely plated morphs) (Figure 1A). This suggests that the complete morph had 58%–72% greater fitness than that of the low-plated morph during this period. To explain the transition between 1976 and 2005 (from 40.2% completely plated morphs to 49% completely plated morphs), an s of 0.01–0.03 is required (Table 1). We thus conclude that there was a period of very intense selection for the completely plated morph between 1970 and 1976, followed by a persistent low-level fitness advantage (1%–3%) of the completely plated morph over the low-plated morph.

One of the dramatic ecological changes that occurred in Lake Washington during the early 1970s is increased water transparency as a result of the mitigation of eutrophication in the late 1960s. Water transparency in the lake was 1–2 m Secchi depth (the maximum depth at which a white Secchi disk is visible from the water surface) during 1955–1971, and it increased to 3.4 m in 1973 and then to 6–7 m from 1976 to the present [14, 15]. Previous behavioral experiments have demonstrated that an increase in water transparency significantly increases the reaction distance of visual predators to their prey, thus leading to increased predation pressure on prey fish [24]. Cutthroat trout (Oncorhynchus clarki) are visual predators, extremely sensitive to subtle changes in water transparency [24], and are the primary predators of threespine sticklebacks in both the littoral and pelagic zones of Lake Washington [16, 25, 26]. Therefore, we used a visual-foraging model, which calculates the search volume by cutthroat trout as a function of light intensity and turbidity [27, 28], to
investigate a possible change in the stickleback predation regime. This analysis demonstrated that the increase in lake transparency created an 8-fold increase in the visual-search volume of cutthroat trout and also expanded the depth range over which effective visual foraging could occur (Figure 3). Most of the expanded search volume was achieved during 1972–1975, when the mean Secchi-disk transparency increased to 3.4 m. Although the cutthroat trout population in Lake Washington did not increase between 1971 and 2006 (Figure S8), our model suggests that an increase in lake transparency could have changed the predation regime by increasing encounter rates between sticklebacks and cutthroat trout.

Predation by toothed predators, such as cutthroat trout, is thought to favor completely plated sticklebacks because the posterior lateral plates can protect the stickleback from being injured and swallowed [29, 30]. Reimchen predicted that the completely plated morph would occur in open-water habitats of high clarity where capture rather than pursuit defenses predominate [30]. Consistent with this hypothesis, we have shown that the increase in the frequency of completely plated morphs occurred during the time when the water clarity increased dramatically in Lake Washington, a relatively deep and large lake (with a surface area of 8.76 × 107 m2 and a maximum depth of 65.2 m). Further supporting the hypothesis that an increase in predation by cutthroat trout has contributed to the rapid evolution of Lake Washington stickleback, recent stickleback samples are larger than historical stickleback samples (Figure 1B and Table S4). Larger body size can protect against predation by gape-limited predators such as cutthroat trout [31, 32]. Although salinity and water temperature have also been proposed as factors contributing to lateral-plate evolution [33, 34], we can exclude a role for these abiotic factors in the evolution of Lake Washington sticklebacks (Supplemental Discussion).

Conclusions

We have reported a dramatic example of ‘‘reverse evolution’’ [9], in which there has been an increase in completely plated sticklebacks in a freshwater lake. Our data demonstrate that selection for the complete morph was particularly strong during the early 1970s, suggesting that the main increase in the frequency of completely plated fish might have occurred during a time period of less than a decade. Armor reduction has also been shown to occur within only a few decades after the introduction of marine sticklebacks into freshwater [35– 37]. Thus, sticklebacks can respond to environmental changes by either an increase or a decrease in lateral plates within a few decades. Rapid phenotypic evolution in sticklebacks provides us with a great opportunity to further investigate the mechanisms by which animals can respond to rapidly changing environments [38].

The rapid evolution of armor plates in Lake Washington sticklebacks might have been enabled by the presence of standing genetic variation at the major plate locus [11]. Without standing variation, a sudden increase in predation might have led to population extinction before a new mutation appeared [6, 39]. Although an increase in gene flow was not the primary cause of armor evolution, gene flow from the marine population might have enabled rapid armor evolution by contributing to standing genetic variation within the lake [7, 40]. This work provides an example of a rapid phenotypic change that does not result from phenotypic plasticity, which has been proposed as a major mechanism of contemporary evolution [4, 8]. Thus, investigation of the genetic mechanisms that underlie adaptive phenotypes is essential for a better understanding of rapid evolutionary change [2, 4, 8, 41].

Although we suggest that reverse evolution in the Lake Washington sticklebacks is probably attributable to the change in water clarity, we still lack direct evidence for this hypothesis, and additional factors might have also contributed. As in many other cases of rapid evolution [5], it is often difficult to tease apart all the potential factors that contribute to phenotypic evolution. We demonstrated, however, that changes in water clarity are able to influence predator-prey interactions; further attention should be given to the influence of water clarity on predator-prey interactions and animal evolution. In addition, this work highlights the importance of investigation of the relationships between environmental changes, species interactions, and the genetic basis of phenotypic evolution, both to better understand the mechanisms of animal evolution and to inform conservation efforts.

Atheistoclast wrote:

Rigorously define "biological information".

Testable prediction: You won't.

Sequence motifs (be they in coding or non-coding DNA).

Atheistoclast wrote:

You're scared shitless and your almost pathological need to attack that very progress everywhere on the internet works as a perfect testament to this fact. Your >99 sockpuppets on the old RD.net forums still sit there as a monument to one guys paranoid delusion.

No. I did not set up 99 concurrent sockpuppets over on RD.

Atheistoclast wrote:I was repeatedly banned for allegedly "insulting" scientists according to moderators like Calilasseia who reveres them.

Atheistoclast wrote:I just kept setting up new usernames after each suspension.

Atheistoclast wrote:In the end, I resorted to proxy servers and IP hopping techniques to avoid being identified.

Atheistoclast wrote:I am satisfied that I played a part in the demise of the RD forum.

Atheistoclast wrote:One of the reasons Dawkins closed it down was the vile abuse directed against people like me.

Atheistoclast wrote:

Ahh yes, soon... soon it will happen.

The next 20 years will see the final nails in the coffin hammered in.

Atheistoclast wrote:

Really? When did that happen? Why hasn't this been pronounced on TV?

It will - be patient.

Atheistoclast wrote:

The Blind Watchmaker dealt with this silly argument better than any book before it.

Funny. The BW actually made me more convinced of the argument for design when it described the sophisticated instrumentation present in bats and how the best engineers seek to replicate it in military technology.

Atheistoclast wrote:

Prove it. How much money are evolutionary biologists making?

I know that a professor at a university can receive a grant of $500,000, of which he only need spend half on research and the rest ....well...

Atheistoclast wrote:

Then it's really weird you have to willfully misrepresent that physics in your catastrophically ignorant pronouncements on thermodynamics on Pandasthumb.org or outright deny the papers on Turing morphogenesis.

I have yet to see how Turing's models are in any way realistic and applicable to actual biological morphogenesis.

Turing, 1952 wrote:It is suggested that a system of chemical substances, called morphogens, reacting together and diffusing through a tissue, is adequate to account for the main phenomena of morphogenesis. Such a system, although it may originally be quite homogeneous, may later develop a pattern or structure due to an instability of the homogeneous equilibrium, which is triggered off by random disturbances. Such reaction-diffusion systems are considered in some detail in the case of an isolated ring of cells, a mathematically convenient, though biologically, unusual system. The investigation is chiefly concerned with the onset of instability. It is faund that there are six essentially different forms which this may take. In the most interesting form stationary waves appear on the ring. It is suggested that this might account, for instance, for the tentacle patterns on Hydra and for whorled leaves. A system of reactions and diffusion on a sphere is also considered. Such a system appears to account for gastrulation. Another reaction system in two dimensions gives rise to patterns reminiscent of dappling. It is also suggested that stationary waves in two dimensions could account for the phenomena of phyllotaxis. The purpose of this paper is to discuss a possible mechanism by which the genes of a zygote may determine the anatomical structure of the resulting organism. The theory does not make any new hypotheses; it merely suggests that certain well-known physical laws are sufficient to account for many of the facts. The full understanding of the paper requires a good knowledge of mathematics, some biology, and some elementary chemistry. Since readers cannot be expected to be experts in all of these subjects, a number of elementary facts are explained, which can be found in text-books, but whose omission would make the paper difficult reading.

Turing, 1952 wrote:1. A Model of the Embryo. Morphogens.

In this section a mathematical model of the growing embryo will be described. This model will be a simplification and an idealization, and consequently a falsification. I t is to be hoped that the features retained for discussion are those of greatest importance in the present state of knowledge.

The model takes two slightly different forms. In one of them the cell theory is recognized but the cells are idealized into geometrical points. In the other the matter of the organism is imagined as continuously distributed. The cells are not, however, completely ignored, for various physical and physico-chemical characteristics of the matter as a whole are assumed to have values appropriate to the cellular matter.

With either of the models one proceeds as with a physical theory and defines an entity called 'the state of the system'. One then describes how that state is to be determined from the state at a moment very shortly before. With either model the description of the state consists of two parts, the mechanical and the chemical. The mechanical part of the state describes the positions, masses, velocities and elastic properties of the cells, and the forces between them. I n the continuous form of the theory essentially the same information is given in the form of the stress, velocity, density and elasticity of the matter. The chemical part of the state is given (in the cell form of theory) as the chemical composition of each separate cell; the diffusibility of each substance between each two adjacent cells rnust also be given. In the continuous form of the theory the concentrations and diffusibilities of each substance have to be given at each point. In determining the changes of state one should take into account:

(i) The changes of position and velocity as given by Newton's laws of motion.
(ii) The stresses as given by the elasticities and motions, also taking into account the osmotic pressures as given from the chemical data.
(iii) The chemical reactions.
(iv) The diffusion of the chemical substances. The region in which this diffusion is possible is given from the mechanical data.

Clarke & Sheppard, 1960 wrote:1. INTRODUCTION

WHEN Bates put forward the mimicry hypothesis which bears his name, Darwin (1872), although accepting it, had some difficulty in explaining the evolution of the mimetic resemblance of several distinct species to one distasteful model by a series of small changes, a requirement of his general theory of evolution. He said "it is necessary to suppose in some cases that ancient members belonging to several distinct groups, before they had diverged to their present extent, accidentally resembled a member of another and protected group in a sufficient degree to afford some slight protection; this having given the basis for the subsequent acquisition of the most perfect resemblance ". Punnett (1915) realised that the difficulty is even more acute when one is dealing with a polymorphic species whose forms mimic very distantly related models. Knowing that, in those butterflies which had been investigated genetically, the forms differed by single allelomorphs he concluded that the mimicry did not evolve gradually and did not confer any advantage or disadvantage to the individual. He argued that an allelomorph arises at a single step by mutation and that therefore the mimicry also arises by chance at a single step. Goldschmidt (x) although not denying that mimicry confers some advantage to its possessors also maintained that the resemblance arises fully perfected by a single mutation of a gene distinct from that producing the colour pattern in the model, but producing a similar effect in the mimic. Fisher and Ford (see Fisher, 1930; Carpenter and Ford, 1933; Ford, 1953) on the other hand have put forward a view intermediate between the extreme ones of Darwin on the one hand and Goldschmidt on the other. They maintain that a resemblance between the mimic and model as good as that often found in nature cannot reasonably be expected to arise by chance. They therefore suggest that a mutant becomes established which gives a sufficient resemblance to be advantageous and that this is gradually improved by the selection of modifiers which alter the effects produced by the mutant.

Ford (1953) has raised serious theoretical objections to Goldschmidt's (1945) hypothesis and he pointed out how the validity of each hypothesis can be tested. He notes that a particular mimic usually varies in appearance in parallel with the local race of its model and that on his own hypothesis one would expect these allopatric mimetic forms of one model to differ multifactorially. However, if mimicry arises by mutation and is not thereafter modified, as is postulated by Goldschmidt, one would expect such local variation in the mimic to be controlled by multiple allelomorphs as Goldschmidt himself predicts. In 1954 we decided to investigate this problem genetically.

Clarke & Sheppard, 1960 wrote:2. MATERIAL AND METHODS

The work has been carried out in two stages. Firstly, it was necessary to understand the mode of inheritance of various sympatric varieties and secondly, to make suitable race crosses to test the two hypotheses. Ford (1953) suggested that the best material for such a study might be the butterfly Hypolimnas dubius since both sexes are polymorphic and mimetic and the genetic status of the forms is relatively well known. However, we decided to use the African butterfly Papilio dardanus Brown. Although it suffers from the disadvantages that it is only polymorphic and mimetic in the female and has an almost bewildering variety of forms, whose genetics were unknown at the time, it had the overwhelming advantages that (a) it can be handmated, (b) it will lay eggs readily in captivity, (c) it has a larva one of whose food plants, Citrus, was known to be available in England, (d) the butterfly is widely distributed and common over much of Africa and (e) it has a large number of relatively distinct races whose distribution has been worked out in detail.

A description of the races and forms can be obtained from the excellent paper by Ford (1936) and the standard works he cites. An account of the forms we have investigated can be obtained from Clarke and Sheppard (1960). The pattern differences between the forms can be described in terms of the numbered areas, and the length of the tails, if present, can be measured by the length BC and that of the wing BA (fig. I). The method of determining these points and of adjusting tail length to take into account variations in the size of the wing itself are given by Clarke and Sheppard (1960).

The details of the breeding techniques are given by Clarke and Sheppard (1959a) and an account of the genetics of most of the major varieties by Ford (1936) and Clarke and Sheppard (i959b, and in preparation). The hippocoonides, cenea, natalica, trophonius, leighi, pale-poultoni and the yellow male-like non-mimetic forms of the female are controlled by a multiple allelomorphic series or by closely linked genes whose effects are sex-controlled. Bright-poultoni, niobe and planemoides are determined unifactorially by genes whose effects are sex-controlled and they are probably members of the same allelomorphic series as all the others. The absence of tails in the females is determined by a single locus not linked to the multiple allelomorphic series and its effect is also sex-controlled.

Clarke & Sheppard, 1960 wrote:Since the genes we are considering do not produce perfect mimicry in all the gene-complexes of the species we must conclude that, if Goldschmidt's hypothesis is correct, an allelomorph producing mimicry can only establish itself if by chance it occurs in a very favourable gene-complex. Moreover, we must also conclude that once established, selection is powerful enough to stabilise the gene-complex so that the good resemblance produced by the gene is maintained. Such an extreme view does not accord with the facts. In P. dardanus the mimetic forms are found wherever the models are common so that on Goldschmidt's view a suitable gene-complex must have occurred by chance (at a time when the mutant was available) in all areas where appropriate models are at high frequency notwithstanding that in other areas, anyhow at the present time, such suitable gene complexes do not occur! Now we know from the work of Brower (1958) that in the laboratory, in circumstances in which birds could examine their prey for two minutes, imperfect resemblances protect to some extent. It is therefore unreasonable to assume that in the wild, when the bird may see the insect for only a few seconds, imperfect mimicry will not confer some advantage. This is in accord with the finding that where the mimic is rare, mimicry is sometimes less perfect. It has already been shown that if we accept Goldschmidt's view we must also assume that selection is powerful enough to stabilise the gene-complex to give good mimicry even if the mimic only accounts for some i o per cent, of the female population. But such powerful selection would also be strong enough to alter the gene-complex to give a better mimetic resemblance if an imperfect mimic established itself. We may therefore safely reject Goldschmidt's hypothesis and accept that developed by Fisher and Ford.

Clarke & Sheppard, 1960 wrote:6. The results support the view that the original mimetic resemblance produced by a new mutant is enhanced by the selection of modifiers and when perfected the pattern is stabilised by selection. In Abyssinia there appears to be disruptive selection which is accumulating modifiers reducing female tail length in the mimics. Owing to the segregation of these modifiers there is greater variance of tail length in the polymorphic Abyssinian than in the monomorphic Madagascan race.

Ford, 1971 wrote:THE study of Batesian Mimicry has contributed considerably to our understanding of natural selection and the nature of the predator-prey relationship. Since the theory of Batesian Mimicry was proposed (Bates, 1862) numerous workers have inferred its existence from the presence of palatable species resembling distasteful and usually conspicuous species with which they occur. There have also been numerous experimental studies on mimicry, but because of the difficulty of observing this phenomenon in nature they have usually been carried out under unnatural conditions (Muhlmann, 1934; Brower, 1958a, b, c, 1960; Schmidt, 1958, 1960; Brower et al., 1960; Sexton, 1960; Brower and Brower, 1962; Reiskind, 1965; Brower et al., 1967; Cook et al., 1969; Morrell and Turner, 1970). Nearly all these experiments have successfully demonstrated the efficacy of the mimetic pattern in protecting the mimic.

However, far fewer experiments have investigated the processes that have led to the evolution of a near perfect resemblance between the mimic and the model. The evolution of the mimetic pattern from the originally nonmimetic form is best explained by the occurrence of a single mutation, giving some resemblance to the model, followed by the selection and fixation of modifying genes gradually perfecting the resemblance (Sheppard, 1959; Clarke and Sheppard, l960a, b).

The experiments of Schmidt, Sexton and Muhlmann (loc. cit.) in the laboratory all show that more protection is obtained by better mimics, though significant protection may also be received by poorer mimics. Studies of this type on wild predators have been few. Morrell and Turner using artificial prey and wild birds also show that poorer mimics, though less frequently eaten than non-mimetic prey, are more frequently eaten than better mimics. Brower et al. (1967) and Cook et al. (1969) found that there is sometimes underpredation of artificial mimics (painted moths) compared with non-mimetic moths.

The experiments described in this paper were aimed to study further the action of mimicry using uncaged predators with artificial prey and to investigate the effectiveness of mimics showing incomplete resemblance to the model.

Ford, 1971 wrote:2. MATERIALS AND METHODS

Artificial cylindrical "caterpillars" made from a pastry mixture (two parts lard to five parts flour) were used as prey. The pastry was coloured by mixing in liquid flavourless food-colouring (from the Scottish Colouring Co., Newington, Edinburgh). Quinine sulphate (0.5 per cent. by weight) was used in the models; at this concentration the baits were very distasteful to people and preliminary experiments showed that birds soon learnt to avoid them. Red and blue were chosen as the initial model and non-mimetic control colour respectively for the following reasons:

1. Preliminary experiments using red, green, blue, brown and yellow prey showed that red and blue were taken in approximately equal numbers, neither being particularly popular or unpopular.

2. Both colours are fairly uncommon in the natural food of the predators, except in the berries sometimes eaten by some of the species.

3. They were both conspicuous against the predominantly brown and green background of the experimental lawn.

4. Intermediate mimics would be easily made and their value as mimics could be tentatively estimated.

Two types of mimics were used: bicoloured mimics where half was exactly the same colour as the model (red) and the other half the same as the first non-mimic; (blue) and intermediate mimics, various shades of purple.
These were presented in separate experiments.

Two half-cylinders (made by cutting a whole cylinder longitudinally) were pressed together side by side to make the bicoloured prey.

The predators were suburban birds of the following species;

Blackbird (Turdus merula), Song Thrush (Turdus philomelos), House Sparrow (Passer domesticus) Dunnock (Prunella modularis) and Robin (Erithacus rubecula).

Individual visits of blackbirds and thrushes were observed and each prey taken was recorded as eaten (when swallowed whole) or pecked (when picked up then dropped or when partly eaten). The total number of prey eaten and pecked was termed the number taken. (This is relevant from the point of view of the prey as a peck may or may not be fatal.) In addition, the instances where the prey was regurgitated or where only half of a bicoloured prey was eaten were recorded.

The number of prey eaten by sparrows was usually unobserved since several birds were present at one time, and so it was calculated when missing prey was replaced. Robins and dunnocks only visited the experimental area occasionally and are included with sparrows in the tables as "others" since their predation was usually unobserved. On certain days when separate records of robin and dunnock predation were made the number of prey taken rarely exceeded five and the pattern of predation was never statistically significantly different from sparrows.

The experimental area was divided into 10 squares, each 5 feet by 5 feet, and 5 baits of each colour were put in each square, except in the initial training periods when 10 of the single colour were placed in each square, and in the experiment testing for frequency dependent selection when 15 models were place in each square. The squares were divided into quarters and each bait was assigned to one of the four quarters, using random number tables.

The experimental plan, showing the sequence of presentation of the prey, is laid out in table 1.

Ford, 1971 wrote:3. RESULTS

When equal numbers of red and blue were presented together, both colours were taken in approximately equal numbers, except by male blackbirds who showed a red preference (table 2). When quinine-flavoured red prey were introduced the numbers of red taken dropped rapidly from the first to the sixth day of presentation, till by the fifth and sixth day only a minute proportion of the prey taken were red (table 3).

The bicoloured mimics were then introduced along with the red and blue prey. The results showed that again the numbers of red taken were minimal, and that significantly fewer of the bicoloured mimics were taken than the blue. In addition a greater proportion of the mimics taken were pecked and not eaten (table 4), and sparrows and others ate the blue half of the mimic on 44 occasions and blackbirds three times. A new blue and yellow bicoloured non-mimic was then presented along with the red and blue mimic and the red model. This would compare the predators' behaviour to a new non-mimetic bicoloured type with their behaviour to the new bicoloured mimic. Significantly more of the yellow and blue were eaten by all species although in the case of sparrows and others as many mimics as non-mimics were taken (a greater proportion of the former being pecked and not eaten) (table 5).

In this experiment the frequency of mimic to model was high. It was considered that mimicry would only be effective if the mimic was relatively uncommon in relation to the model, though Brower (1 960a) found that the mimic still receives some protection when it is nine times as common as the model. To test the predators' response to a lower mimic to model ratio the numbers of model were trebled. Sparrows and others ate an even greater proportion of bicoloured non-mimics than before, indicating greater avoidance of the mimic (table 6).

Although this is significant (χ2(1) = 239, P<0.00l) it may still be accounted for by day-to-day fluctuations.

A new colour (purple) of edible prey was then presented together with the red model for four days to train the birds to accept this colour. On the last day of presentation 450 of this colour were taken, indicating the birds' acceptance of this new prey. Subsequently the purple was replaced by reddish purple and bluish purple. The reddish purple were taken far less frequently than the bluish purple by all species (table 7). The red model was then replaced by a blue model, containing the same concentration of quinine. The bluish purple then became the better mimic and the reddish purple the poorer one. A direct comparison of the two days of red model and the four days of blue model shows that the number of bluish purple eaten by blackbird and thrush is in fact greater with the blue models, while the numbers eaten by sparrows and others is not significantly different with the two models (table 8). However, if the individual days are looked at (fig. 1) the proportion of reddish purple taken by sparrows and others appears to drop from day 1 to day 2 of red model and again on the first day of blue model, then to increase on the second and third day of blue model. The difference between day 1 and day 2 of red prey and between day 2 and day 3 of blue model are both significant.

Ford, 1971 wrote:4. DISCUSSION

Although the demonstration of mimicry has been frequently successful using caged predators, few studies have successfully shown it operating in more natural conditions with free living predators. The present study was aimed at examining the response of the predators to artificial prey under mimetic situations. The results showed rapid learning to avoid distasteful models and underpredation of a bicoloured partial mimic. This underpredation of the partial mimic need not necessarily be explained by its mimetic pattern. Three factors may influence the behaviour of a predator towards its potential prey:

(i) Conspicuousness

There is a strong selection in most animals for cryptic colouration, the best hidden individuals being most likely to be overlooked by predators. Red and blue were chosen in these experiments as they should be equally conspicuous against the lawn background. It is possible that the bicoloured prey is less conspicuous, as its pattern may be disruptive, though many warningly coloured insects are bicoloured, presumably to make them more conspicuous (e.g. wasps, ladybirds).

(ii) Previous experience

There is considerable evidence (Tinbergen, 1960; Allen (pers. comm.); Allen and Clarke, 1968; Croze, 1970) that birds develop specific search images for food items. Such search images are most likely to develop for abundant, palatable and conspicuous foods. Alternative foods may not be eaten because they are passively overlooked or they may be actively avoided. New or uncommon foods will fall into the former category, while unpalatable prey and mimics fall into the latter.

(iii) Innate preferences

Coppinger (1969) discussed innate avoidance of particular patterns and avoidance of novel stimuli. He considers that the latter may be important, and it is clearly related to the search image theory.

To clarify the nature of the response, a new mimetic type was introduced to determine how much of the avoidance of the mimic was due to its novelty. Although a higher proportion of the prey taken are mimics, suggesting that some of the previous protection was due to the mimic's novelty, more of the non-mimics than the mimics are taken, showing that at least some of the protection was due to the mimetic pattern of the red and blue prey.

Thus, even in a natural situation, one might expect a mutation, producing a new mimetic pattern, to be selected due to its novelty, in addition to any protection it might obtain from its mimetic resemblance. This may well be an important, and previously rather overlooked, factor in the early stages of the evolution of mimicry.

Increasing the frequency of the model gives increased protection to the mimic compared to the non-mimic. For mimicry to be effective the predator must experience sufficient models, to associate the particular pattern with distastefulness. If the model is rare relative to the mimic, the predator is less likely to learn to avoid it. A model to mimic ratio of 1:1, used in these experiments, is probably higher than usual in nature and it has even been suggested that the mimic needs to be rare in comparison with the model. The experiments of Brower (1960) with starlings and coloured mealworms showed that some protection of the mimic was received even with a model to mimic ratio of 1: 9.

In the situations considered so far resemblance to the model has been achieved by presenting prey showing the model colour on half of the mimic. This is analogous to situations where the pattern of the mimic resembling the model is achieved by a single mutation. Alternatively mimics may show continuous variation with one extreme best resembling the model. This situation was simulated using shades of purple. The mimic most closely resembling the model was eaten less frequently than the one resembling it less well. This shows the effectiveness of mimicry of this type. In this experiment the effect of novelty was the same for both good and poor mimics since they were introduced at the same time. When the model was changed to blue so that the previously poor mimic was now the better one, the results were somewhat confusing; although the now better mimics do not receive more protection overall, the day-to-day changes do suggest a change in preference.

These experiments are similar to those carried out by Duncan and Sheppard (1965), who used coloured solutions and chicks. The strongest solution was associated with an electric shock, and progressively weaker solutions (poorer mimics) received more attention. When a large shock was given on drinking the model solution there was even a significant difference in the responses to the poorest mimic and the uncoloured control.

The experiments carried out in this study all point to considerable advantages gained by the partial mimics. This response of the predators is emphasised by the fact that a large proportion of the bicoloured mimics were either pecked or only partly eaten; and when they were only partly eaten it was always the blue half which was eaten. This could be analogous to an insect where only the most vulnerable parts of the body are mimetic, directing any attack to less vulnerable parts.

The experimental period was not long, and the responses of the birds may be different at different times of the year. This difference may take the form of different colour preferences, or changes in the birds' keenness to discriminate. For example, the experiments were carried out during the winter when food may have been scarce and the birds were perhaps more willing to take unusual or less attractive food. Irrespective of the precise feeding pattern it is clear that the behavioural response of the predators would give sufficient advantage to an initially poor mimic for full mimicry to evolve by gradual improvement of the resemblance.

Nijhout, 2003 wrote:SUMMARY The mocker swallowtail, Papilio dardanus, has a female-limited polymorphic mimicry. This polymorphism is controlled by allelic variation at a single locus with at least 11 alleles. Many of the alternative morphs are accurate mimics of different species of distasteful butterflies. Geneticists have long been interested in the mechanism by which a single gene can have such diverse and profound effects on the phenotype and in the process by which these complex phenotypic effects could have evolved. Here we present the results of a morphometric analysis of the pleiotropic effects of the mimicry gene on the array of elements that makes up the overall pattern. We show that the patterns controlled by mimicking alleles are more variable and less internally correlated than those controlled by nonmimicking alleles, suggesting the two are subject to different degrees of selection and mutational variance. Analysis of the pleiotropic dominance of the alleles reveals a consistent pattern of dominance within a coevolved genetic background and a mosaic pattern of dominant and recessive effects (including overdominance) in a heterologous genetic background. The alleles of the mimicry gene have big effects on some pattern elements and small effects on others. When the array of big phenotypic effects of the mimicry gene is applied to the presumptive ancestral color pattern, it produces a reasonable resemblance to distasteful models and suggests the initial steps that may have produced the mimicry as well as the polymorphism.

Nijhout, 2003 wrote:The evolution of mimicry

Batesian mimicry is believed to originate by means of an initial mutation that has a suffciently big effect on the phenotype to give a passable resemblance to a protected model, followed by the accumulation and selection of mutations in modifier genes that progressively refine the mimicry (Fisher 1930; Carpenter and Ford 1933; Sheppard 1959; Clarke and Sheppard 1960c; Charlesworth and Charlesworth 1975a; Turner 1977; Charlesworth 1994). Charlesworth and Charlesworth (1975b,c) calculated the conditions under which mimicry will evolve, and their calculations suggest that modifying mutations that refine the mimicry will be maintained if they are tightly liked to the gene that conferred the initial advantage, thus providing a plausible explanation for the evolution of a supergene.

In P. dardanus, this simple scenario is complicated by the fact that mimicry is polymorphic and that the various morphs are not equally distributed among geographic races. Among the unresolved questions are (a) whether each of the 14 morphs evolved independently from a common ancestor or (b) whether some morphs evolved from others and (c) whether the geographic distribution of morphs due to independent origins in different regions or (d) to differential dispersal and extinction. Given the complexity and the wide geographic distribution of the polymorphism, it seems parsimonious to assume that each of the alleles arose only once and is identical across its entire geographic range and that the evolution of geographic races occurred after the evolution of the polymorphism. The alternative possibility, that the same polymorphic mimicry arose several times independently in different geographic races of a monomorphic ancestor, seems to be less probable. An intermediate between these two extremes is that a limited polymorphism of perhaps three or four alleles arose first, followed by a geographic dispersal and a subsequent evolution of additional alleles unique to particular geographic races. The latter is almost certainly true for the form ochracea (derived from cenea), hippocoonides (derived from hippocoon), lamborni (derived from trophonius), and of the nonmimetic male-like female morph from Ethiopia (a loss of mimicry). Whether the malelike females from Madagascar represent a primitive condition or are also due to a secondary loss of mimicry remains an open question (Vane-Wright and Smith 1991).

Nijhout, 2003 wrote:Although we know little about the nature and molecular mechanism of action of the mimicry gene, we can nevertheless learn a great deal about how this gene controls various aspects of the color pattern by systematic analysis of how different aspects of the color pattern vary under different breeding conditions. The beginnings of such an analysis, using morphometrics and a comparative analysis of pattern variation in color forms and interracial hybrids, is the subject of this article. This analysis suggests a hypothesis about the first steps in the evolution of mimicry and shows that the subsequent diversification of forms and refinement of their mimicry involved significant changes in the patterns of dominance of the many pleiotropic effects of the mimicry gene.

Nijhout, 2003 wrote:So the first step in the evolution of mimicry could involve only a single locus. The hippocoon-like pattern is likely to have evolved twice (see Discussion), and the planemoides and cenea-like patterns may have originated once each. The further refinement of any one of the female forms could be accomplished by a relatively small number of additional genetic changes.

Nijhout, 2003 wrote:DISCUSSION

The mimetic wing patterns of P. dardanus have different patterns of variation and internal correlation than nonmimetic ones. Mimetic patterns exhibit a higher degree of individual variability than nonmimetic patterns. If the degree of variability is a function of the mutation-selection balance, then these findings suggest that nonmimetic patterns either are under stronger selection or experience less mutational variance than mimetic patterns. It is possible that the greater individual variability of mimetic pattern is due to the fact that these genotypes are more protected against predators and thus less subject to selection and that there is, for some reason, stronger normalizing selection on nonmimetic and male patterns than on mimetic patterns. Alternatively, it is possible that mimetic patterns require the activity of many more genes than do nonmimetic ones and would therefore be more sensitive to standing genetic variation and newly introduced mutational variance.

Mimetic wing patterns exhibit a lower degree of correlated variation among the various elements of the pattern than do nonmimetic wing patterns. If the pattern of genetic correlations resembles the pattern of phenotypic correlations, as is the case in other butterflies (Paulsen 1994, 1996), then these findings suggest few if any genetic correlations among the elements of the color pattern of the mimicking forms. The absence of correlation in the mimicking patterns may be due to the accumulation of the many genes with small effects that have been hypothesized to be responsible for refining the details of the mimicry (the second stage in the evolution of mimicry). If this is the correct interpretation, then it implies that these modifier genes affect the morphology of the color pattern on a spatial scale that is the same size or smaller than the scale at which these measurements were made.

The various alleles of the mimicry gene affect the dimension of the pattern elements to different degrees. Here the effect is rather complex in that a given allele may increase the size of some pattern elements while decreasing the size of others. This is unlike the case in Heliconius, where dominant alleles typically increase the size of a pattern element (Nijhout et al. 1990), although a recent report shows substantial evolution of dominance in Heliconius (Naisbit et al. 2003). In P. dardanus the effect on the size of the pattern is independent of the dominance effect of the allele. Thus, a dominant effect can either increase or decrease the size of an element, with the latter being somewhat more common than the former. This mix of hyper- and hypomorphic pleiotropic effects of a given allele is diffcult to explain on the basis of a common mechanism of action. This effect is consistent with both the supergene and the regulatory gene hypotheses. In either case, it can be best explained if variation in each pattern element is affected by at least some unique genes or by unique combinations of genes. Whether these genes are linked in a supergene, as in the case of Papilio memnon (Clarke et al. 1968; Clarke and Sheppard 1971), or whether they are dispersed across the genome and controlled by a polymorphic regulatory gene remains an open question.

The alleles of the mimicry locus have a complex set of pleiotropic and dominance effects on various features of the forewing pattern. Each allele affects a different combination of pattern elements, and the size of each of the pattern elements affected by a given allele is altered to a different degree. Within a geographic race, the different alleles show a clear and unambiguous pattern of dominances, in which the degree of dominance is the same for all elements affected by a given allele. This stands in contrast to the mosaic pattern of dominance observed in interracial crosses, where a given allele may have a dominant effect on some elements and a recessive effect on others. The similarity of dominance effects within a race may be a manifestation of the so-called coadaptation of genes within a population. The mosaic of dominances in interracial crosses would then be due to a breakdown of this coadaptation when an allele is placed in a genetic background that is different from the one in which it evolved. If this is the correct interpretation, it suggests that the similarity of dominance effects within a population is an evolved property.

It is possible that when a mimicry allele first originated, it had a mosaic of dominant and recessive pleiotropic effects on different portions of the pattern, just as modern alleles have a mosaic of morphic effects on different parts of the pattern. Perhaps initially all dominant effects were associated with increases in the size of pattern elements and all recessive effects with decreases in size. A favorable combination of hyper- and hypomorphic pleiotropic effects could then be stabilized by the evolution of a genetic background that made all those effects dominant (e.g., Gilchrist and Nijhout 2001). This process would be repeated with the origin of each new mimetic locus, resulting in the order of dominance observed. This scenario for the evolution of dominance relations is different from the traditional Haldane’s sieve, which suggests that a new favorable allele can be established most easily if it is dominant than if it is recessive so that new phenotypes tend to be dominant over preexisting phenotypes (e.g., Clarke et al. 1985). Under both scenarios, the order of dominance is likely to reflect the order of origin of the phenotypes, but under Haldane’s sieve this would be a purely statistical effect, whereas under the alternative scenario suggested above, dominance is an evolved adaptation.

The hippocoon pattern group is the largest and most diverse of the three pattern groups in P. dardanus (Fig. 1). The fact that the cenea allele (Hc) is dominant to some alleles in the hippocoon group (Hh and Hna) and recessive to others suggests that the hippocoon-like phenotype may have evolved independently more than once. This interpretation is supported by the finding on the dimensions of the phenotypic effects of the various alleles on the pattern. Application of the big phenotypic effects to the presumptive primitive pattern of the P. dardanus ancestor suggests that a hippocoon-like mimic can be achieved in one step but that a cenea-like mimic most likely requires at least two evolutionary steps and is probably derived from a hippocoon-like pattern rather than independently from the ancestral pattern. It is possible, then, that the cenea allele (Hc) evolved from the group that led to the hippocoon (Hh) and natalica (Hna) alleles, to which it is dominant. The other alleles in the hippocoon group may have been derived independently and at a later time, and this may explain why they are dominant to the cenea allele. This scenario is in accordance with the suggestion of Turner (1963) that the hippocoon form probably arose before any of the other mimetic forms. Clarke et al. (1985, 1991) argued that in Papilio phorcas, the male-like pattern of the female is the derived form. This suggests that the species may initially have been sexually dimorphic (with brown/yellow females and black/green males) and that a so-called transvestite evolutionary step (Vane-Wright 1976; Clarke et al. 1985) produced male-like females and was the origin of the female color dimorphism.

Rauch & Millonas, 2004 wrote:Abstract

The Turing mechanism (Phil. Trans. R. Soc. B 237 (1952) 37) for the production of a broken spatial symmetry in an initially homogeneous system of reacting and diffusing substances has attracted much interest as a potential model for certain aspects of morphogenesis (Models of Biological Pattern Formation, Academic Press, London, 1982; Nature 376 (1995) 765) such as prepatterning in the embryo. The two features necessary for the formation of Turing patterns are short-range autocatalysis and longrange inhibition (Kybernetik 12 (1972) 30) which usually only occur when the diffusion rate of the inhibitor is significantly greater than that of the activator. This observation has sometimes been used to cast doubt on applicability of the Turing mechanism to cellular patterning since many messenger molecules that diffuse between cells do so at more-or-less similar rates. Here we show that Turing-type patterns will be able to robustly form under a wide variety of realistic physiological conditions though plausible mechanisms of intra-cellular chemical communication without relying on differences in diffusion rates. In the mechanism we propose, reactions occur within cells. Signal transduction leads to the production of messenger molecules, which diffuse between cells at approximately equal rates, coupling the reactions occurring in different cells. These mechanisms also suggest how this process can be controlled in a rather precise way by the genetic machinery of the cell.

Sekimura [i]et al[/i], 2002 wrote:Abstract. We inverstigate pigmentation patterns in the butterfly wing of Papilio dardanus by numerical simulations of a reaction-diffusion model on a geometrically accurate wing domain. Our results suggest wing colouration is due to a simple underlying stripe-like pattern of some pigment-inducing morphogen. In this paper, we present some of our numerical results and discuss the validity of our model by comparing our results with pictures of male and female wing patterns of the butterfly.

Nijhout [i]et al[/i], 2003 wrote:Abstract

Butterfly pigmentation patterns are one of the most spectacular and vivid examples of pattern formation in biology. They have attracted much attention from experimentalists and theoreticians, who have tried to understand the underlying genetic, chemical and physical processes that lead to patterning. In this paper, we present a brief review of this field by first considering the generation of the localised, eyespot, patterns and then the formation of more globally controlled patterns. We present some new results applied to pattern formation on the wing of the mimetic butterfly Papilio dardanus.

Sekimura [i]et al[/i], 2000 wrote:The butter£y Papilio dardanus is well known for the spectacular phenotypic polymorphism in the female of the species.We show that numerical simulations of a reaction diffusion model on a geometrically accurate wing domain produce spatial patterns that are consistent with many of those observed on the butter£y. Our results suggest that the wing coloration is due to a simple underlying stripe-like pattern of some pigment-inducing morphogen. We focus on the effect of key factors such as parameter values for mode selection, threshold values which determine colour, wing shape and boundary conditions. The generality of our approach should allow us to investigate other butterfly species. The relationship between these key factors and gene activities is discussed in the context of recent biological advances.

Madzvamuse [i]et al[/i], 2002 wrote:Previously, we have proposed a mathematical model based upon a modified Turing mechanism to account for pigmentation patterning in the butterfly wing of Papilio dardanus, well-known for the spectactular phenotypic polymorphism in the female of the species (Sekimurea et al, Proc. Roy. Soc. Lond. B 267: 851-859 (2000)). In the present paper, we use our model to predict the outcome of a number of different types of cutting experiments and compare our results with those of a model based upon different hypotheses.

Sekimura [i]et al[/i], 2000 wrote:

2. MODEL AND NUMERICAL RESULTS

(a) Model equations

Since the seminal work of Turing (1952), which showed that a system of reacting and di¡using chemicals could evolve from an initially uniform spatial distribution to concentration profiles that vary spatially - a spatial pattern - many models have been proposed exploiting the short-range activation, long-range inhibition mechanism used by Turing. One of the earliest models is that of Gierer & Meinhardt (1972). They, in fact, proposed a class of phenomenological models in which the reaction kinetics were chosen to be of activator-inhibitor type. These models all take the general form:

ut = f(u,v) + D1 ∇2u

vt = g(u,v) + D2 ∇2v

where u(x, t) and v(x, t) are chemical concentrations at position x and time t; D1 and D2 are diffusion coefficients; and f, g are polynomials or rational functions of u, v which describe the kinetics. These equations are solved on some spatial domain with imposed boundary conditions, and initial chemical concentrations are prescribed. These types of model have been analysed in depth mathematically. Using standard linear analysis, conditions can be derived on f, g, D1 and D2 under which diffusion-driven instability can arise (see Appendix A). From this analysis, it can be shown that in the vicinity of a primary bifurcation point (where the spatially uniform steady state loses stability) the chemical pro¢les of u and v are either in phase or 180° out of phase (see, for example, Dillon et al. 1994).

The patterning properties of these models have, in the main, been studied on simple geometrical shapes (for example, rectangles) with zero flux boundary conditions on both species or with both species fixed at the steady state. It is also typically assumed that the domain responds homogeneously to the chemical, i.e. there is a spatially uniform threshold level of chemical concentration above which cells differentiate. In this paper, we begin to extend these studies to consider non-standard cases. For the purpose of illustration, we focus on the activator-inhibitor mechanism suggested by Gierer & Meinhardt (1972). This mechanism has been used in a variety of modelling situations (see, for example, Meinhardt 1982, 1995). The reaction kinetics in the Gierer-Meinhardt model are defined as

f(u,v) = k1 - k2 + k3u2/[v(k6 + k7u)]

g(u,v) = k4u2 - k5v

where u(x, t) and v(x, t) are activator and inhibitor concentrations, respectively, at spatial point x and time t, and k1, ... , k7 are positive rate constants. The reaction diffusion system can be non-dimensionalized in the standard way (see, for example, Murray 1993) to yield the system

ut = γ(a - bu + u2/[v(1 + Ku2)]) + ∇2u

vt = γ(u2-v) + d ∇2v

where a, b, d, K and γ are positive parameters, ∇ is the non-dimensionalised spatial operator and, for simplicity, the non-dimensionalised chemical concentrations and time are denoted, as before, by u, v and t respectively.

In the simulations below, we fix the values of a = 0:1, b = 1:0 and K = 0:5, while the values of γ and d are determined from the Turing space according to the mode which would be selected on a unit square domain (see Appendix A). The numerical simulations show the plots of v only. The profiles of u can easily be deduced from these plots as they are in phase with those of v.

Atheistoclast wrote:

For example, I predict that you will either ignore or outright misrepresent this paper:
http://www.mendeley.com/research/turings-next-steps-mechanochemical-basis-morphogenesis/#page-1

No, I cited it in my latest paper.

Atheistoclast wrote:

You mean lots of space, sand, rocks, gas, dust and black holes?

No, the physical constants:

http://en.wikipedia.org/wiki/Physical_constant

Atheistoclast wrote:

Rumraket wrote:

Atheistoclast wrote:As for sequence motifs:

http://en.wikipedia.org/wiki/Sequence_motif

The best example of one is the homeobox:

http://en.wikipedia.org/wiki/Homeobox

So tell me in what way it constitutes information and produce an example of the quantity.

Technically, my prediction has now been confirmed.

It is qualitative, not quantitative. Data is a quantity, information is a quality.

The homeobox motif is information because it confers functional specificity that allows proteins to perfectly bind to the major and minor grooves of the DNA molecules, as one would expect from an intelligently designed sequence.

Atheistoclast wrote:

Anyway suffice it to say, your earlier posts of delusions of grandieur were much better trolling than this. I guess I was wrong about you, definitely no Da Vinci after all.

The real Da Vinci code is in DNA.

Atheistoclast wrote:Oh, please! I get called much worse by everyone. Sorry, but Rumraket said something patently stupid when he equated data with information. I get very angry when I hear people talk such nonsense with a great deal of misplaced confidence.

Atheistoclast wrote:

chairman bill wrote:

Atheistoclast wrote:You wanted to prosecute me. But God had other plans, and intervened to close down the Sodom and Gomorrah of cyberspace. If you mess with Clastie, you mess with the higher power that protects him. You have been warned.

Surely a piss-take. This must be the point where Atheistoclast reveals his true colours - a Poe. Really, nobody posts pathetic shit like that, and means it.

Everything is the will of the Creator, including the demise of the RD forum. Let that be a lesson to you all.

Atheistoclast wrote:

chairman bill wrote:

Atheistoclast wrote:You wanted to prosecute me. But God had other plans, and intervened to close down the Sodom and Gomorrah of cyberspace. If you mess with Clastie, you mess with the higher power that protects him. You have been warned.

Surely a piss-take. This must be the point where Atheistoclast reveals his true colours - a Poe. Really, nobody posts pathetic shit like that, and means it.

Everything is the will of the Creator, including the demise of the RD forum. Let that be a lesson to you all.

MrFungus420 wrote:

Atheistoclast wrote:

chairman bill wrote:

Surely a piss-take. This must be the point where Atheistoclast reveals his true colours - a Poe. Really, nobody posts pathetic shit like that, and means it.

Everything is the will of the Creator, including the demise of the RD forum. Let that be a lesson to you all.

Thank you for admitting that your god, if he exists, doesn't just watch children be raped, but it is his will that they be raped.

Calilasseia wrote:One of which was "thou shalt not kill". Apparently they didn't have the brains to write that as "thou shalt not kill, except when Magic Man orders it", and give themselves the escape clause they needed before going out and committing mass murder. Not that this has ever stopped supernaturalists from interpreting that commandment in that very manner since, and acting brutally upon that interpretation.

Basically, the Abrahamic Magic Man was a convenient fabrication of the imagination of semi-literate, superstitious, pre-scientific humans, who moreover were amongst the most backward and savage members of the species, even by the standards of the age. The magic man they fabricated was fabricated in their image: backward, homicidal, anti-intellectual, fatuously ignorant of even basic real world facts, and shot through with a host of utterly repugnant traits, many of which centre upon bigotry of one sort or another. The only people who can possibly pay homage to such an entity, without shutting down large parts of their thinking brains in order to do so, are the sort of people who secretly yearn to inflict nameless horrors upon those who fall foul of their own petty little bigotries, and latch onto this entity as a convenient pseudo-justification for their psychotic urges, revelling additionally in the narcissism inherent in believing that an entire universe was made just for them. Supernaturalism in all its forms has been founded upon made up shit, resulting in the need to peddle lies in order to perpetuate the original made up shit, but the Abrahamic brand of made up shit, with its bloodlust, misogyny, and the insidious venom of ruthless enforcement of conformity to doctrine, is the most diseased of all, increasingly attracting to its ranks with the passage of time, deranged, unbalanced, clinically efflorescent individuals who, in any rational society, would be hospitalised for the safety of themselves and the rest of us. You only have to look at some of the kooks, loons, sociopaths, and in some cases, convicted criminals, who populate the American fundamentalist landscape, in order to see this repulsive trend becoming ever more correlated, ever more entrenched, and ever more virulent. The Abrahamic Magic Man, held up for millennia as a purported icon of perfection to aspire to, is in reality nothing more than an invented excuse for murderous malfeasance 3,000 years ago, and the perversity of insisting that this ideological blow-up doll is real, is long overdue for inclusion in clinical texts, with appropriate warnings with respect to the level of contagion, virulence and neurotoxicity of the doctrinal pestilence in question.

Atheistoclast wrote:
You wanted to prosecute me. But God had other plans, and intervened to close down the Sodom and Gomorrah of cyberspace. If you mess with Clastie, you mess with the higher power that protects him. You have been warned.

Nebogipfel wrote:

Atheistoclast wrote:
You wanted to prosecute me. But God had other plans, and intervened to close down the Sodom and Gomorrah of cyberspace. If you mess with Clastie, you mess with the higher power that protects him. You have been warned.

This is hilarious.

Poor old Yahweh! Back in the glory days, he slew the first born, parted seas, drowned mighty armies, turned people into pillars of salt and annihilated cities with fire and brimstone. These days, he´s reduced to shutting down internet forums. Deities just ain´t what they used to be.

Regina wrote:
He must be taking the piss, I'm convinced of that.

chairman bill wrote:

Atheistoclast wrote:You wanted to prosecute me. But God had other plans, and intervened to close down the Sodom and Gomorrah of cyberspace. If you mess with Clastie, you mess with the higher power that protects him. You have been warned.

Surely a piss-take. This must be the point where Atheistoclast reveals his true colours - a Poe. Really, nobody posts pathetic shit like that, and means it.