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Agathi

Je n’ai pas eu l’occasion de vous présenter Agathi,, qui est devenue membre de ce blog depuis quelue temps, parce qu’elle n’ pas posté quoi que ce soit encore ici (hey, nous somme là 😉 ).

Mais elle a entamé une discussion sur le forum ‘Scepticisme – Zététique » de SLT; le sujet est « Questions sur M. Denton et 2 objections au darwinisme« , lancé par une personne (EmmanuelD) qui n’a pas encore dépassé son premier post, comme ça semble être le cas avec d’autres fils de discussions qui tournent autour de la discussion anti- pro- Darwin.

(suite…)

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by ,
PNAS May 15, 2007 vol. 104 suppl. 1 8567– 8573

’s greatest contribution to science is that he completed the by drawing out for biology the notion of nature as a system of matter in motion governed by natural laws. With Darwin’s discovery of natural selection, the origin and adaptations of organisms were brought into the realm of science. The adaptive features of organisms could now be explained, like the phenomena of the inanimate world, as the result of natural processes, without recourse to an . The Copernican and the s may be seen as the two stages of the one Scientific Revolution. They jointly ushered in the beginning of science in the modern sense of the word: explanation through natural laws. Darwin’s theory of natural selection accounts for the ‘‘design’’ of organisms, and for their wondrous diversity, as the result of natural processes, the gradual accumulation of spontaneously arisen variations (mutations) sorted out by natural selection. Which characteristics will be selected depends on which variations happen to be present at a given time in a given place. This in turn depends on the random process of mutation as well as on the previous history of the organisms. Mutation and selection have jointly driven the marvelous process that, starting from microscopic organisms, has yielded orchids, birds, and humans. The theory of evolution conveys chance and necessity, randomness and determinism, jointly enmeshed in the stuff of life. This was Darwin’s fundamental discovery, that there is a process that is creative, although not conscious.


Il n’y a rien de nouveau dans cet essai de FJ Ayala, mais il est bien écrit, un résumé intéressant qui pourra servir d’amorce pour les discussions avec les jeunes qui sont en train d’apprendre. Bien sûr in serait recommandé pour JS et VF, mais je crois que c’est peine perdue que de le leur proposer. JS ne comprendrait pas de toute façon et je doute que VF veuille le lire; mais VF devrait le lire, conseil amical et sans aucune ironie.

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Jean Staune decided after a long silence (January 23, 2006 to October 3, 2006) to comment on my reactions to his paper “ and : A ”.

Why now ? He is writing a book and probably he will copy/paste his parable concerning the Plutonians (or maybe not).

His comment starts by:

# has failed completely to understand what was my goal in the development of my “Plutonian” story.

When I started discussing this paper I wanted to keep things soft. I learned a lot about Jean Staune, his technique of discussion (fr) and the use of logical illusions (fr) he (ab)use to try to make his point. And that he probably use public discussion spaces (fr) to learn how to present his points of view.

So let’s make it tougher for Jean to make his point by avoiding to provide hints until his book is printed. The Plutonians’ parable is used to make a point:

In conclusion, it seems clear that there is a deep analogy between my Plutonian story and the debate around the mechanism of evolution on Earth, and that Vekris failed completely to understand it[…]

OK then, let’s admit that I’m unable to understand tortured parables. Why not address the evolution problem directly? It would be much more concise and clear, not only for me but for any reader.

There are a few interesting things here:

If ADM‘s explanations are to be used to prove anything, she (or somebody else) must reply to my observation that simple darwinian models can account for directional, non-continuous phenotypic variations; before that, and in respect of the parsimony principle no need to introduce hypothetical and not well documented models, say « harmonic attractors ».

If the « anthropic principle » is to be used as an argument in the discussion, it must be clearly stated that this is an hypothesis without any proof to support it, and it can’t be use to prove anything. And I would like to add that this is an a priori 😉

If points of view of known biologists (say ) are to be used to support non-darwinian points of view, Jean Staune should specifically state the exact point where darwinism fails, not just ask for an explanation. He can use any help he need as he isn’t trained in evolutionary biology and he fails to understand simple models, as the one I presented concerning ADM of the one that it explains the observations about the Kallima butterflies (I keep it as a draft to publish after his book is printed).

Let’s keep the discussion in english. As soon as Jean starts answering this post with scientific rigor I’ll advertise it at Science blogs, The Panda’s Thumb, Uncommon Descent and other places around the Net, as much as possible, in order to show them how brilliant the guy can be.

, , , , , ,

That’s me, hello world 🙂

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post 813 of uncommondescent, by himself:

Here is a brief essay on design by ’s contemporary . Question: are the molecular machines identified by Michael Behe as decisive evidence for design merely analogous to human-built machines or do they fully instantiate the concept of machine?

What is the meaning of this post? That have just a century of science to catch up?

Please, could you push the update button(s)? 🙂

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variations

I received a single reaction concerning ADM-DM series, from a friend; she reproached to my presentation to be too much « preset »:

[translated]…, it isn’t fair to use constant food concentration, preset velo-jump intensities and a particular ratio between the velo-jumps due to d1-d2 and d1-d2-d3. Make them random.

A short discussion followed and she accepted that it is fair to diminish complexity for simple models. Then she argued that it wasn’t « elegant« .

Arguing about elegance isn’t what I expected, then I spend a few minutes my precious time to see how I would add randomness for food concentration and velo-jumps. As it was quite easy, Despite the fact that it was extremely painful, I’ve done it to please the lady.

  • food density varies: df = f ± 0,4 * f and according the optimal value of velocity, for each generation of Specs,
  • and velo-jumps intensity is random,
  • and the effect of d1-d2 don’t influence the one of d1-d2-d3.

I made a hundred runs, overlaid the graphs and sent the image to her. The reaction was almost immediate

wha! quite cute, may I have the same with red rather then blue lines?

100-aleaalea.jpg

While I was preparing and sending the Photoshop file to SunG, so she could fix the colors as she likes them (because there are several reds!), I was reading Behe’s « A Response to the Opinion of the Court in Kitzmiller vs Dover Area School District  » and was at point 13.

(13) As a further example, the test for ID proposed by both Professors Behe and Minnich is to grow the bacterial flagellum in the laboratory; however, no-one inside or outside of the IDM, including those who propose the test, has conducted it. (P-718; 18:125-27 (Behe); 22:10206 (Behe)).

If I conducted such an experiment and no flagellum were evolved, what Darwinist would believe me? What Darwinist would take that as evidence for my claims that Darwinism is wrong and ID is right? As I testified to the Court, Kenneth Miller claimed there was experimental evidence showing that complex biochemical systems could evolve by random mutation and natural selection, and he pointed to the work of Barry Hall on the lac operon. I explained in great detail to the Court why Miller was exaggerating, was incorrect, and made claims that Barry Hall himself never did. However, no Darwinist I am aware of subsequently took Hall’s experiments as evidence against Darwinism. Neither did the Court mention it in its opinion.

The flagellum experiment the Court described above is one that, if successful, would strongly affirm Darwinian claims, and so should have been attempted long ago by one or more of the many, many adherents of Darwinism in the scientific community. That none of them has tried such an experiment, and that similar experiments that were tried on other molecular systems have failed, should count heavily against their theory.

What kind of cognitive impairment strikes IDers, Behe included and given a place of honor as he is a biochemist, to be unable to understand that the probability to reach the same result is extremely low?

Given enough time and money one can expect to build an experiment where some motility system will be seeing evolving; something not even remotely similar to the flagellum, but having the same function, provide motility. And those ressources, time, money and educated people, needed to carry out the experiment, are much better used to develop vaccines, biofuels, bioproducted and biodegradable plastic etc.

Take a look at this detail of the figure to get the feeling if you can’t understand the probabilities calculation:

100-aleaaleadetail.jpg

A single gene, a single selection factor and something close to 4*108 possible paths without taking in account the variations of intensity of the velo-jumps.
If you understand the model it’s enough to not even try, not even imagine that one would ask for such an idiot movement.
It would be as if you spent your life making Lotto draws to verify that calculated probabilities meet the fact that a guy named Guy, living at Place and born 100 years later Darwin’s death, won the special-super-hyper-uber Lotto last week. Simulation different guys, with different names, different hair cuts, living at various places etc.
Damn idiot, isn’t it?

Now, it would be interesting if Behe stopped talking nonsense and spend the rest of his life trying to either obtain de novo a flagellum (damn idiot but this could keep him quite) of if he tried to understand what he is talking about (some people may think that this is harder the flagellum experiment).

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ADM-DM-03

Anne Dambricourt MalasséADM DM #0ADM DM #1ADM DM #2 – ADM DM #3

I’ll keep the same here as for parts ADM-DM-01 and ADM-DM-02, Specs in Isle, velo, the gene determining Specs’ velocity, and the same clonal population at time T0.

Let’s consider now three particular mutations of velo gene: velo-d1, velo-d2, which are the same as in ADM-DM-02, and velo-d3.
The genotype d1-d2 is always at the origin of a velo-jump of x%; the genotype d1-d2-d3 produce a velo-jump of n*x%, where n>1. Genotypes d1-d3 and d2-d3 are neutral for velocity.

For equal probabilities of occurrence of the three mutations, p, the probability to observe the triple mutant d1-d2-d3 is p1/2/3 = p3. An event less probable then the double mutant d1-d2, p1/2 = p2.

Statistically the double mutant d1-d2 appears before the triple mutant d1-d2-d3. And the double mutant is necessary to observe a phenotypic impact from the mutation d3.

Once the double mutant d1-d2 present in Specs population it will be fixed as it represents an advantage for the carriers and thus the probability to obtain the triple mutant will increase to p1•2/3 = p !

The step from the initial genotype/phenotype (T0) to the d1-d2 ones (Ts) is expected to be longer then the step from d1-d2 to d1-d2-d3, statistically mean.

The following figure illustrates six runs of the model, with x%, the velo-jump du to d1-d2, equal to 25%, and n = 2, so the velo-jump associated with d1-d2-d3 is of 50%.

d1d2d2-1.jpg

Only the mean velocity of the Specs population is represented. There is a story line where d1-d2 wasn’t observed. The rectangular ROI highlights the two velo-jumps. The circular ROI highlights overflows, where the velocity is above the optimal one, and show that the model is still reversible.

Let’s take a look at a particular line story:

d1d2d2-2.jpg

Arrows point to the apparition of d1-d2 and d1-d2-d3 and the corresponding velo-jumps. And in this particular example the time lapsed between the wild type and the double mutant is longer then the time lapsed between the double and the triple mutants. This graph represents what one expect to observe as a statistical result.

The graph below was obtained with x% = 25% and n = 2, just for better visualization of the velo-jumps.

d1d2d3-3a.jpg

We have here a typical situation of overflow. The pic of velocity (red arrow) is du to the effect of d1-d2-d3. The phenotype will reverse as a higher then the optimal velocity isn’t selected, and the optimal velocity will be reached.

Let’s summarize:

  • A population of Specs, a species with three main activities: sleep, food and sex; duration of sleep is constant so Specs existence may be considered as part alimentation and part sexual activity.
  • At the beginning of the stories lines T0 all Specs share the same genotype and present the same phenotype.
  • At the T0 Specs aren’t perfectly adapted to their environment. There is a selection pressure favoring those able to move faster and thus feed in shorter times; those dispose of larger periods for sexual activity and their genetic variants of velo will be transmitted to descendants. Foods density on Isle determine the Vmax, which is the speed of movement of Specs, making meals so sort that they don’t interfere with sexual activity.
  • During the observation period a single gene is able to mutate, velo, which is the only one modulating velocity, which is the phenotypic trait describing Specs maximal speed; variations on genotype produce equivalent variations on phenotype, directly.
  • From the many variants of velo three are remarkable, d1, d2, and d3. The probability to observe these three mutations is equal and expressed by p, which satisfy to the condition 0velocity, what I called a velo-jump. The same is for genotype d1-d2-d3, which have a more important effect. Genotypes d1-d3 and d2-d3 don’t produce a velo-jump.

What could we get from such a simple model:

  • Directional evolution of the phenotypic trait velocity, under selection pressure which is related to the actual Specs characteristics and the optimal value of velocity. The selection factor is a combination of Specs characteristics, velocity and available food resources density. Inversely proportional to velocity, it is difficulty observable when the population reach a mean velocity value equal to the optimal. The directionality of evolution of the phenotypic trait is reversible; if the population reach a mean velocity value higher then Vmax, it will tend to decrease, stabilizing around Vmax.
  • Sudden increases of the value of the phenotypic trait, velo-jumps, are possible, when d1-d2 and d1-d2-d3 genotypes are produced by random mutations. If one can evaluate the probability to see those genotypes, it’s impossible to predict when they will occur. It is also impossible to predict the time laps between d1-d2 and d1-d2-d3, but one can calculate probabilities:
    The probability to obtain d1-d2-d3 is p1/2/3 = p3
  • before the apparition of genotype d1-d2,
    the probability to obtain d1-d2 is p1/2 = p2, and
    the probability to obtain d1-d2-d3 becomes p1•2/3 = p after the apparition of genotype d1-d2.
    Thus, p1•2/3 > p1/2 > p1/2/3, which means that the more probable path is to get d1-d2 first, then after a relatively short period d1-d2-d3 (which may be considered as an acceleration of the evolution of velocity).

  1. Directionality of evolution of velocity is respected, at the phenotype level.
  2. Discontinuity of evolution of velocity is respected, at the phenotype level.
  3. Reversibility of evolution of velocity is respected, even at the phenotype level.
  4. Randomness, as builded in the model, is respected, at the genetic level.
  5. The selection factor is a combination of physiological and environmental characteristics, inversely proportional to the phenotypic trait, and it would be quite difficult to determine once the optimal value reached or by fossils examination.

The model is darwinian, the observations similar to those reported by ADM.

Maybe she could spend some time considering this option before the evocation of Unknown Factors, Internal Plans or any thing else.

To do so, it is necessary to dispose of molecular (genetic) data. A first step would be the determination of genes expressed during the cranium build at the sphenoid region; gene arrays to determine which ones then in situ hybridization, to validate and dispose of a spatial repartition overview. And this for both Homo sapiens and a closely related species, which genome is known, say Pan troglodytes.
If that fails, then something else may be considered.

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ADM-DM-02

Anne Dambricourt MalasséADM DM #0ADM DM #1 – ADM DM #2 – ADM DM #3

I’ll keep the same here as for example #01, Specs in Isle, and velo, the gene determining Specs’ velocity, and the same clonal population at time T0.

Let’s consider a particularity of gene velo. If two specific mutations are present on the same molecule, velo-d1 and velo-d2, they act synergistically and the velocity of the individual is Vmax. velo-d1 and velo-d2 independently don’t affect the velocity trait, thus they aren’t selected, and they aren’t punctual mutations.
Say that this occurs at time Td1-d2, and this is in a stage of Specs history that gives it a clear advantage, substantially increasing the movements of carrier Specs, this particular combination will spread rapidly in Specs population, as the carriers have plenty of time available for sex.

The history of Specs will be determined from the occurrence of this particular random event. It represents a jump in the evolution of the particular phenotypic trait, velocity.
A jump which amplitude will be inversely proportional to Td1/d2-T0.

If you observe the increase of velocity of the Specs and don’t know anything about their genetics, you may have the feeling that there is some Unknown Factor making them faster and faster. And that at time Td1/d2 another Unknown Factor changed the rules and produced the jump of the velocity’s increace. Then you have two solutions: considering some Mysterious Internal Blueprint due to Supernatural Causation being the cause of the velocity’s increase and some Mysterious Change of the Internal Blueprint at time Td1/d2, or inventing genetics and understand how Specs evolved from Spec SlowMotion (those Specs present at T0) to Spec AsFastAsPossible (those Specs living at time Ts, including the velocity’s sudden increase at Td1/d2.

And this is a third observation: Phenotypical traits may evolve in a directional way and by jumps, while mutations are still perfectly random.

But a jump at Vmax isn’t very probable. Let’s say that this is a smaller jump, an increase of x% of the initial velocity, V0, and this particular event I’ll call a velo-jump from now on; the plot of velocity versus time (generations) will be something like that :

velojump-simpel.jpg

Concommitant to the velocity’s increase there is a drop of the selection pressure (they are correlated) and then the evolution of the phenotype will follow the same path as in example 1, reaching a plateau.

The coexistence of the two mutations in a single velo molecule is a random phenomenon. So it’s impossible to say « when » and « if » it will happen during the Specs history. I run a few simulations, and I had a very pleasant surprise; a velo-jump above Vmax. I wasn’t expecting to talk here about the reversibility of the model, but here is what I got at the second run of the model:

overflow.jpg

There are two graphs in fig above. Both represent the same data, the one at the right isn’t versus time, but log(time), this is useful to see more clearly early events. The blue curve represent velocity and the red ones selection pressure. The genotype d1-d2 appears relatively late and the velocity gain set Vs above Vmax. This phenotype isn’t privileged, as in the case where food’s density increased, I presented in example 1. So it will be progressively lost, either by reversion or by apparition of new mutations. I was glad to see that « happen », the model used for simulations seems to be well constructed.

Reversibility is conserved.

I gave it a few more runs and I overlaid a series of graphs to show alternative Specs histories:

point-overflow.jpg

There are three series presented here, a, b and c, corresponding to velo-jumps of 10, 20 and 40% of V0 respectively. For each series I show graphs with the x axis as time or log(time). The red arrows at « series c », points to a story where the d1-d2 genotype didn’t appeared. The duration of Specs history is normalized here. I’ll come back to this.

While Vmax is reached for every run, which mean that the Specs will be optimized for their environment, the path, trough which this is achieved, is as random as the occurrence of the d1-d2 genotype; it may even not contain this particular event.
Now, why did I normalized the histories lengths? It’s only a matter of better visualisation. Let’s see at what generation d1-d2 appeared for a set of 1000 runs :

1000-set.jpg

Quite random, ranging from 5 to 53777. To make it visible, without making a particular choice, the simplest way was to normalize the duration of the stories.

One may evaluate odds that d1-d2 appears during the Specs history; this is a simple probability calculation, predicting that d1-d2 may appear. If the probabilities are equal for both mutations, and p is the probability for each one, then the probability to get both simultaneously is pd1-d2 = p2.
It doesn’t say when.
On the other hand, you may evaluate what is the probability for d1-d2 to appear after n generation and that will be n * pd1-d2 = n* p2.

Randomness is preserved at the mutations level, and thus at the genotype level, the phenotype evolves directionally as long as it doesn’t exceed the optimal value (otherwise the direction change), and a particular genetic event may produce jumps of the phenotypic trait.
One couldn’t predict the history of the Specs otherwise then in terms of probabilities; the single predetermined element is Vmax, and this is only to facilitate calculations, the real value being a function of the Specs physiology and foods density.
The probability to have two identical histories (runs of the simulations) is low. Some cases are present (difficult to see on the graph, but there are 42 repetitions! Now, that the genotype d1-d2 occurs at generation g twice (or more) that doesn’t mean that the paths where identical!

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