posted 01. March 2003 22:49                    

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How do you intend to differentiate careful planning from selection/mutation since both would seem to be indistinguishable other than the fact that we do observe mutation and selection.

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You mention that humans were the end result but were they the goal? So far there does not seem to be any evidence that humans were the goal of evolution. In fact there are far more succesful species than humans on this world.

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posted 03. March 2003 02:59                    

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Even if is somewhat low probability, there is a chance of a “design-segment-duplication” that divides the hull cross-section outline into control by separate “design-segments”. So before the change we have a single unitary hull pattern, after the change we have the exact same hull pattern -- but with control of the upper fraction of the hull cross-section by one “design-segment”, and control of the lower fraction of the hull corss-section by another “design-segment”.

The key point here is that we have a division, but no outward change. ...

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What would be an example of hypervolumetric change? You have only been as specific as

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I've listed them in the paper and discussed them earlier on this board: the origin of multicellularity (the origin of many new gene "contexts"), the origin of bodyplans, the origin of sexual reproduction, the origin of eukaryotes, and certainly the origin of life.
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This are very hard problems. If you want detailed evolutionary solutions to these, obviously we first have to understand the details of how these systems work! If that is the case, you want the study of biology to be essentially complete. But it's not complete, is it?

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Biologically, what I'm saying is that changes in a single gene only move about within a hypervolume (this goes for changes in duplicated genes as well!) and the only thing which adds dimensionality to the hypervolume is if the entire "context" of a gene changes to something new. By "context" I mean the genetic regulatory interactions in which a given gene is imbedded, and which give that gene a "meaning". In other words, fundamental changes in the wiring diagram of an organism are what constitute inventive changes. Once a wiring pattern is established for an organism, a given space of evolutionary possibilities is mapped out in which the Darwinian process can operate. However, re-wiring the genetic network itself (the context in which genes are interpreted) requires teleological input to ensure that multiple components are all changed in ways that produce the novel functionality (which I'm defining as an inventive change).

Bottom line: none of the examples presented in this thread as counterexamples to my arguments have been this sort of inventive change. Simply showing that genes can duplicate and evolve is not enough. The question is: can gene CONTEXTS evolve such that genes are imbedded in the regulatory networks in ways that produce novel structures?

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1) Given the known types of variations that occur in genomes when organisms reproduce, all possible genomes are reachable via the types of variations that occur during reproduction. Now I realize that this leaves off the question of functional intermediates, which is, of course, vital. My point is just that it is possible, given what is known of reproduction and mutation, that all genomes are in one hypervolume.

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posted 03. March 2003 16:13                    

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Thanks for your comments. I appreciated your response. You are correct that all genomes are in-principle encodable in DNA. But this is a rather trivial observation, like the fact that all possible inventions can be made from matter. The question is not whether such inventions can be made from matter, but how such inventions come to be made at all. In other words, it is the exploration of the space of possibilities which seems to be constrained in some way, and that is what gives rise to the hypervolumes of possibilities that I am talking about. In terms of inventions, the constraining factor is "psychological inertia"--the tendency of the human mind to get stuck in a rut, thinking about things that already exist and how to modify them to new uses. This tends to drive the imagination down certain paths and away from true novelty. That's why oftentimes inventions are associated with "eureka" moments when a flash of insight occurs and a genuinely new invention is made. TRIZ theory is all about how to jump to new hypervolumes of possibilities by facilitating this flash of insight. My application of TRIZ to biology suggests that the factor that limits the topology of the possibility space in biotic systems is the developmental process of organisms. While it is true that all possible genomes can be encoded in DNA, it is not true that all possible genomes can be generated by small steps from any given starting genome. The reason is that there is a process of biological development that translates a genome into some sort of functional organism that must survive and reproduce. The constraints of development, coupled with the constraints of survival, serve to put limits on what can be generated from a given starting system. As I've argued earlier, mutations that interfere with essential genetic processes are going to result in a nonviable organism that will be weeded out of the gene pool, hence defining a boundary of the hypervolume. My argument is that development plus environmental constraints serve to slice up and constrain the possibility space, and hence the ability to move from one hypervolume to another requires intelligent input.

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posted 03. March 2003 17:40                   

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This is an interesting example because it illustrates my thesis so nicely. The flaw in this example is that it incorporates inventiveness in the re-working of the "genetic" regulatory system such that different regulatory networks result. Gedankin calls them "extra design segments" but as far as I can tell these are separate regulatory modules controlling the shape of separate parts of the hull. This is precisely the sort of inventiveness I'm talking about

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• Hox genes
• Eng1a/b
• DNT enzymatic pathway (you can consider it as regulating the chemical environment and cellular energy)
• (and so on--read back through the thread!)

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I'm weary of the repititious error in which evolution within a hypervolume (via gene duplication, and subsequent mutation of that gene) is conflated with the re-engineering of the hypervolume itself.

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posted 03. March 2003 17:45                   

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Contrary to your assertions, I haven't changed terms or definitions. I never intended a hypervolume to refer to the number of genes or number of basepairs in a genome, and I've made that abundantly clear from the very beginning (go back and read the ARN thread where I deal with this if you doubt me).

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Erik then argues that if genes define the hypervolume of a genetic algorithm, my claim that the hypervolume is fixed ahead of time is trivially refuted. This is true, if I had claimed that the genes define the hypervolume. However, a careful reading of my paper will show that I consider the hypervolume to be determined by the functions of the genes operating upon embryological development. The duplication of genes is of no consequence unless those new genes are somehow modified and integrated into the existing structure and process of development such that novelty is produced. This is what Richard Dawkins notes when he comments that angel wings will never sprout from a human's back.

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Trends Genet 2002 Aug;18(8):399-405

Gene duplication at the achaete-scute complex and morphological complexity of the peripheral nervous system in Diptera.

Skaer N, Pistillo D, Gibert JM, Lio P, Wulbeck C, Simpson P.

Dept of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK.

The number of achaete-scute genes increased during insect evolution, particularly in the Diptera lineage. Sequence comparison indicates that the four achaete-scute genes of Drosophila result from three independent duplication events. After duplication, the new genes acquired individual expression patterns but, in Drosophila, their products can compensate for one another, which raises the question: why retain all four genes? The complexity of the spatial expression of these genes on the notum increased in the lineage leading to the higher Diptera, allowing the development of stereotyped bristle patterns. This probably coincided in time with gene duplication events, raising the possibility that an increase in gene copy number might have provided the flexibility necessary for more complex transcriptional regulation.

Dev Biol 2002 Dec 1;252(1):31-45

Transcriptional heterochrony of scute and changes in bristle pattern between two closely related species of blowfly.

Skaer N, Pistillo D, Simpson P.

Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, United Kingdom.

Temporal shifts in the expression of regulatory genes, relative to other events taking place during development, can result in changes in morphology. Such transcriptional heterochrony can introduce dramatic morphological changes that involve rather few genetic events and so has the potential to cause rapid changes during evolution. We have shown previously that stereotyped species-specific bristle patterns on the notum of higher Diptera correlate with changes in the spatial regulation of scute expression. scute encodes a proneural gene required for the development of sensory bristle precursors and is expressed before pupation in discrete domains on the presumptive notum at sites where the macrochaete precursors arise. Thus, for Ceratitis capitata and Calliphora vicina, species separated from Drosophila melanogaster by about 80 and 100 million years respectively, the domains of sc expression differ. In all three species, a second phase of ubiquitous sc expression, after pupation, precedes formation of the microchaete precursors. Here, we describe sc expression in Phormia terranovae, a species belonging to the family Calliphoridae that is closely related to C. vicina. We find that spatial regulation is almost identical between P. terranovae and C. vicina, in spite of their different bristle patterns. The timing of sc expression differs, however, between the two. The first spatially restricted phase of expression is slightly delayed and the second ubiquitous phase remarkably accelerated, such that there is a period of overlap. As a result, the last precursors from the first phase of expression arise at the same time as the first precursors from the second phase of expression and are morphologically indistinguishable from the late-arising microchaetes. These observations illustrate the power of developmental heterochrony in bringing about rapid morphological change.

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As for wiring diagrams, perhaps you ought to talk with Eric Davidson at Caltech, who has produced an overall wiring diagram of the sea urchin embryo developmental process. Perhaps you would be more comfortable with the concept of a gene regulatory network instead of "wiring diagram"--I don't care what you call it, but it's clearly defined and in the literature.

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Evol Dev 2002 Mar-Apr;4(2):111-23

Gene expression and larval evolution: changing roles of distal-less and orthodenticle in echinoderm larvae.

Lowe CJ, Issel-Tarver L, Wray GA.

Department of Ecology and Evolution, State University of New York at Stony Brook, 11732, USA.

We describe the expression of the homeobox genes orthodenticle (Otx) and distal-less (Dlx) during the larval development of seven species representing three classes of echinoderms: Holothuroidea, Asteroidea, and Echinoidea. Several expression domains are conserved between species within a single class, including Dlx expression within the brachiolar arms of asteroid larvae and Otx expression within the ciliated bands of holothuroid larvae. Some expression domains are apparently conserved between classes, such as the expression of Dlx within the hydrocoel (left mesocoel) in all three classes. However, several substantial differences in expression domains among taxa were also evident for both genes. Some autapomorphic (unique derived) features of gene expression are phylogenetically associated with autapomorphic structures, such as Dlx expression within the invaginating rudiment of euechinoids. Other autapomorphic gene expression domains are associated with evolutionary shifts in life history from feeding to nonfeeding larval development, such as Otx expression within the ciliated bands of a nonfeeding holothuroid larva. Similar associations between evolutionary changes in morphology and life history mode with changes in regulatory gene expression have also been observed in arthropods, urochordates, and chordates. We predict that recruitment of regulatory genes to a new developmental role is commonly associated with evolutionary changes in morphology and may be particularly common in clades with complex life cycles and diversity of life history modes. Caution should be used when making generalizations about gene expression and function based on a single species, which may not accurately reflect developmental processes and life histories of the phyla to which it belongs.

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I have heard Davidson speak, and he actually alludes to the types of questions I'm getting at. For instance, a starfish wiring diagram has some fundamental, deep-rooted differences from a sea urchin (which it is supposed to have evolved from),

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in terms of how genes are plugged into the network. When Davidson came and spoke to the biology students and faculty at our annual retreat last fall, he even commented that "we have a real problem here" and more or less dodged the question of how the wiring diagram of two organisms came to be so differently wired.

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posted 03. March 2003 23:35                    

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How would ID solve to problem? What would make it an obvious solution?

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Carl: The above test should also support the goal of humans as the end product of creation.

How?

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posted 04. March 2003 00:10                

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Nelson:
Actually this is a lot worse then what you wanted. As the Force paper shows, instead of the function and capability of the gene being duplicated, what we get is a partitioning of function. There is no evidence for the assumption that this faciliates the evolution of greater complexity. Again, thats simply begging the question.

With the Force paper consider the consequences if the DDC model is correct. In each part a module was lost, whereas in the classical module a module is gained. After all, I am more than content with bringing a scissor that can also act as a calculator to the patent office. Meanwhile, all Ged will get for bringing a scissor and a calculator to the patent office is a lump of coal.

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This model is quite distinct from the classical model, under which degenerative mutations can only lead to gene loss and beneficial mutations are the only route to gene preservation.

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posted 04. March 2003 01:13                   

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For each program, there is an n-dimensional hypervolume of possibilities in which that program operates, with n equal to the number of variable parameters. In the language of William Dembski's design inferential machinery, this n-dimensional hypervolume is equivalent to the reference class of possible outcomes, Omega 10.

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This observation suggests that we may consider any genetic algorithm to be operating within a certain n-dimensional hypervolume, and certain fixed parameters completely determine that hypervolume ahead of time. Furthermore, any particular n-dimensional hypervolume is completely isolated and separate from any other m-dimensional hypervolume (m .ne. n).

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The essential insight is that trial and error may only operate within a given hypervolume—but it may never jump to a new, higher-order hypervolume. The unbridgeable gaps between hypervolumes correspond to the technical contradictions in TRIZ theory.

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This hypervolume is fixed by certain non-varying parameters (In Dawkin’s Biomorph example, the number of genes and the rules regarding how the integer values of each gene are interpreted) that an intelligent agent must set and which are not allowed to vary.

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take-home lesson is that selection and mutation processes can operate within pre-set hypervolumes to find solutions that we know exist but which may be intractable given our current knowledge. However, they cannot find the hypervolume or the fitness function apart from intelligence—we still have to do the design work (getting the program into the right hypervolume where a solution may be found, and then finding the right fitness function over that hypervolume) before the algorithm can take over and sift through the vast possibilities to find a workable solution.

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in computational terms, can be defined as the designing activity that occurs when one or more new variables is introduced into the design. Processes that carry out this introduction are called “creative designing processes”. Such processes do not guarantee that the artifact is judged to be creative, rather these processes have the potential to aid in the design of creative artifacts. Thus, creative designing, by introducing new variables, has the capacity to produce novel designs and as a result extends or moves the state space of potential designs.

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This paper has demonstrated that genetic programming can be used to automatically create both the parameter values tuning and the topology for controllers for illustrative problems involving a two-lag plant and a three-lag plant.

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It is expected that the performance of a circuit will fall with rising temperature, but Figure 5 reveals that the evolved circuit's behaviour also degrades as the temperature is decreased from 340mK. This kind of behaviour had never been seen in such proposed `single electron' circuits before, and indicates that the circuit actually exploits or relies upon the thermal noise of the electrons at 340mK. This is not necessarily desirable, and perhaps by evaluating across a range of temperatures during evolution a thermally robust solution could be found [7], but we see immediately that evolution is exploring a previously inaccessible part of design space/

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In designing a state space of possible designs is implied by the representation used and the
computational processes that operate on that representation. GAs are a means of effectively
searching that state space which is defined by the length of the genotype’s bit string. Of
particular interest in design computing are processes that enlarge that state space to change
the set of possible designs. This paper presents one such process based on the generalization
of the genetic crossover operation.

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To generate the echinoid system would then require only that the pmar1 gene (itself a member of a gene family; our unpublished data) be brought under the control of maternal factors localized at the pole of the egg, and that a single key regulatory link between it and the gene encoding the global repressor be installed. This evolutionary hypothesis suggests that despite its great elegance, the whole micromere specification system that we see in Fig. 7 is basically a jury-rigged add-on, which except for the role of pmar1, is all made of preexistent parts. Whatever its connection with evolutionary reality, the argument suggests that comparative network analysis will someday provide the means to test directly the pathways of regulatory evolution, so that we can understand not only how developmental systems work, but how they got that way.

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There may be other proposals to account for many simultaneous mutations, but I have not been able to find one. That would leave ID as an excellent candidate, as it fits all the evidence.

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