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Author
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Topic: A Model of Genetic Functionality
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warren_bergerson
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Member # 262
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posted 06. June 2002 11:24
[The adaptive approach which I support assumes that evolution is a paradigm, modeled by an LFS operating on adaptive reactions modeled by PCR’s. I am proposing here a view or perspective of genetic material which makes it possible to explicitly model genetic code as PCR’s. ]
In traditional neo-Darwinian genetic theory, the gene or allele is a mechanism for defining and passing between generations phenotypes or ‘heritable traits’. The proposal is offered here to abandon the ‘Gene as heritable trait’ (GHT) model and replace it with a ‘gene as a set of assembly processes’ (GAPI) model.
THE NEED TO SEPARATE GENETICS AND EVOLUTION
The need to need for a new genetic viewpoint is indicated by the inability to construct/identify genotype to phenotype and phenotype to genotype maps. Neo-Darwinian genetics is based on the assumption that "‘genotypes’ are logically equivalent to or map to ‘heritable traits’ which are logically equivalent to or map to ‘phenotypes’ which map to or are logically equivalent to ‘adaptations’". It is possible to precisely define and model genotypes. It is also possible to explicitly model ‘teleological adaptations’. The two are clearly not identical or logically equivalent. Furthermore, there does not appear to be any simple mapping which makes it feasible to treat the two as logically equivalent. It therefore seems appropriate to consider an alternative model of the gene and its function in biological systems.
THE GENE AS ASSEMBLY PROCESSES (GAP) MODEL
Abandoning Darwinian concepts, the proposal here is to describe a gene as a set of assembly instructions. A single assembly process, as proposed here, consists of an input or initiator and a response or reaction. The evidence currently available would suggest that a single gene codes a relatively small number of processes (say less than 100). There are, however, millions, possibly billions of different instructions which can be constructed from different combinations of initiators and responses. As far as I know, this ‘gene as assembly processes’ model fits all existing knowledge of what genes are and how they operate.
THE FUNCTIONING OF A GAP UNIT
The assumed functioning of an individual assembly process is fairly simple. If the initiator factor or factor is present, the reaction is generated. If the initiator factor or factors are not present nothing happens. There are lots of activate/don’t activate mechanisms in nature.
A gene, as proposed here is a set of such assembly processes. It is assumed here that complex assembly processes are defined by these sets of simple processes. A sequence of such instructions might, for example build a protein or a complex flagellum.
The claim that genes are or can be viewed as sets of assembly instructions may to some appear obvious. To others this interpretation may seem very speculative. In either case, it should be apparent that the proposed interpretation is readily testable.
James has on a number of instances raised the question how does information or abstract models translate into action. The concept of gene defined here, IMO, provides a clear illustration of how this translation operates. I am proposing that the gene be modeled as a set of assembly processes. The physical gene, however, actually is the processes. When the appropriate conditions are present the gene doesn’t just define how a protein, for example, is constructed, it constructs it.
EXPLAINING CHANGES IN GENES
Although beyond the scope of this post, once we are convinced that the GAP model is valid and useful, the next question is to demonstrate how these sets of processes can change or evolve and how did DNA or genes evolve in the first place? As mentioned at the beginning, the gene as a GAP is logically equivalent to the gene as a PCR (programmable causal relationship). Both the development of PCR’s, and changes in PCR’s can, the adaptive approach asserts, be modeled or simulated by a mathematical paradigm called an LFS.
SUMMARY
I have proposed here a model of how genes operate of function. The proposed model appears 1)to be consistent with what is currently known of how genes function, 2)the proposed model appears to be verifiable and testable, and 3)the model appears to address the obvious problems that exist with the neo-Darwinian model or interpretation of genes. Comments anyone?
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warren_bergerson
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posted 07. June 2002 10:46
READING THE GENETIC CODE
Above, I proposed a model of genetic functionality. A model, I suggest, that can define, simulate and explain the functions performed by genetic material. The model is called the genetic assembly processes (GAP) model. Today, I would like to discuss how the GAP model will, if it is valid, make it possible to actually read genetic code and translate code into actions.
To begin, it is well known that genetic material contains the instructions that allow cells to construct or assemble product like flagellum and proteins. It is also apparent that in many instances, scientists have unraveled in great detail the assembly processes which produce organelles and compounds. The GAP model proposes a logical explanation of how those assembly processes can be translated into ‘abstract static code’ also called GAP code.
The GAP model asserts or predicts that there is a direct correspondence or mapping between the ‘abstract static code’ of the GAP model and ‘physical genetic material or code’. Using the techniques to be discussed here for ‘reading GAP code’, it should be relatively easy(there are two levels of difficulty in science and mathematics- relatively easy and impossible) to determine if the predicted mapping exists and if it exists the exact form of the mapping.
It is also, useful to note that if the GAP model if valid that it provides interesting and useful insights into what genetic material actually does. Of more general interest to the discussions on this board, if the GAP model is valid, then it provides a rigorous logical basis for analyzing biological evolution. Now to the subject of this post.
ASSEMBLY INSTRUCTIONS
Building, assembling, constructing etc. are complex continuous processes. Even relatively simple construction processes can be broken down into an infinite number of steps, sub-steps, operations and causal relationships. It is also possible to define or model even complex assembly processes using a finite number of assembly instruction. Defining or modeling complex processes using finite sets of instructions is based on the ‘change of state’ concept.
The change of state concept asserts that complex continuous processes can be modeled in terms of the occurrences that change the state or condition of the process. As a simple example, baking a cake is a very complex process involving an infinite number of very complex chemical and physical reactions. Using the change of state concept, this very complex set of processes is reduced to two simple causal reactions 1)turn oven on and 2)turn oven off. [I am assuming at this point that the basic concepts and principles of change of state modeling are understood.]
It may at this time be useful to once again note the distinguish between ‘change of state’ models and ‘change of state’ mechanisms. A model obviously is a set of mathematical/logical notation. A change a state mechanism is a manifestation of such notation. If you take an appropriate system, a cake baking machine for example, and insert the appropriate change of state mechanism(a program for example), the system will produce complex output such as a cake. The assertion here is that if you take an appropriate type of cell (system), and insert the appropriate type of ‘change of state mechanism’ (appropriate DNA sequence) the cell will produce complex output such as a protein or flagellum).
THE COMPOSITION OF AN ASSEMBLY INSTRUCTION
An assembly instruction or change of state process is, or can be viewed as, a causal relationship of the form ‘S causes R’. The S in this relationship is the stimulus or input that triggers some output or reaction R. If, as suggested, genes are sets of assembly instructions, then the gene must contain specific elements that code specific instructions. This means that a gene must contain areas that code for 1)recognition of some stimulus S 2)generation of some response R and 3)stimulus S in the presence of such a section of code would generate response R.
It is useful, at this time, to note that the claim is that the GAP model assumes there is a direct mapping form assembly instructions to DNA code. This doesn’t mean that I would expect to find one section of code for each complex instruction. An instruction of the form ‘S causes R’, can broken down into ‘(s1 and s2 and … and sn) causes (r1 and r2 and … rn)’. For example ‘S causes R’ might take the form "If conditions s1 and s2 are present then s3 causes r1’ . I would expect that complex instructions will involve a hierarchy of sub instructions. As a general rule, such hierarchies are not difficult to de-code once you have a general idea of what you are looking for.
SUMMARY
The technique proposed here for ‘reading genetic code’ is, it appears, a simple extension of the analytical processes currently used. The starting point is to identify some structure or compound generated by a cell. The next stage is to study the process by which an organism generates the identified structure. This process is then modeled using change of states concepts and techniques. For each identified change of state process or mechanism it is then necessary to identify the stimulus or trigger and the response or reactions generated. Finally, the coding for these stimuli and responses are traced backward into genetic material. The processes described are obviously not simple, but from what I have read, I get the clear impression that all, or at least most all of the required information has been or could be obtained. I believe, that all I am proposing is a formal technique for interpreting or expressing what is already known. (I am also suggesting that this interpretation will be useful in understanding how evolutionary change operates. )
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YZ2
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Member # 91
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posted 13. June 2002 06:05
Dear Warren,
I do find this thread very interesting. Is the GAP model widely accepted? There may be a number of difficulties in using GAP in practice though:
1) All the relevant variables may not be known, i.e. hidden variables may affect the pathway;
2) The cause-and-effect may not be deterministic as a if-then sequence, the relationships may be many-to-many, i.e. several factors may produce the same effect and one factor may produce several effects;
3) The pathway may be probabilistic rather than deterministic.
If a GAP model is to be estimated from data, I believe the general case may be NP-hard.
If the GAP model is applied to relate processes from genotype to phenotype, then the Darwinian's mechanism of natural selection can be looked at as processes from phenotype to genotype (the reverse process). Am I correct to say this? Therefore, your comment about GAP model being testable is certainly correct.
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warren_bergerson
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Member # 262
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posted 13. June 2002 08:14
David,
As far as I know, the GAP model or hypothesis is a new concept that developed from my adaptive approach to analyzing the evolution in biological systems. Unless the same concept has been developed under a different label, it is clearly not widely accepted at this time. To address the specific issues you raise.
QUOTE: 1) All the relevant variables may not be known, i.e. hidden variables may affect the pathway; 2) The cause-and-effect may not be deterministic as a if-then sequence, the relationships may be many-to-many, i.e. several factors may produce the same effect and one factor may produce several effects;
The available evidence suggests that 1)most cellular assembly mechanisms are relatively precise and dependable, 2)such assemblies are controlled by genetic code, and 3)genetic code can carry only a limited volume of information. If the GAP model is valid, these three observations would suggest that ‘cellular assembly involves a limited number of relatively precise change of state instructions’. It should be relatively easy to spot missing instructions. It also seems likely that in most instances instructions will be highly deterministic - i.e. within a controlled cellular environment the result produced will be relatively precise. There will obviously be some noise, inefficiencies, or statistical fluctuations in the processes. The noise or uncertainty of a genetic instruction would undoubtedly increase dramatically with even small changes in the cellular environment(there is lots of evidence for this).
QUOTE: 3) The pathway may be probabilistic rather than deterministic.
The GAP model involves modeling assembly processes as deterministic processes rather stochastic processes. In a deterministic model, statistical fluctuations are viewed or treated as noise, or inefficiency.
QUOTE: If the GAP model is applied to relate processes from genotype to phenotype, then the Darwinian's mechanism of natural selection can be looked at as processes from phenotype to genotype (the reverse process). Am I correct to say this? Therefore, your comment about GAP model being testable is certainly correct.
The GAP model is designed to address the issue of ‘what do genes code?" The GAP model hypothesizes the existence of a direct mapping from genetic coding to assembly instructions. This is not a genotype to phenotype map. The GAP model is, in fact, consistent with the claim that there is no genotype/phenotype map in the sense required for neo-Darwinian genetics.
The GAP model is part of or consistent with a model that assumes selection operates to change genetic code. The ‘selection’ processes are, however, considerably different, considerably more complex, and considerably more powerful than the Darwinian Natural Selection mechanisms.
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YZ2
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Member # 91
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posted 13. June 2002 22:14
I still have difficulty appreciating the difference between the two models. Are you saying this:
GAP:
genotype
| unknown mechanism
V
instructions
(black box)
| unknown mechanism
V
phenotype
neo-Darwinian:
genotype
| unknown mechanism
V
phenotype
[ 13. June 2003, 10:41: Message edited by: YZ2 ]
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warren_bergerson
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Member # 262
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posted 14. June 2002 09:35
David,
You are asking, "What is the difference between the GAP model’s definition of the genotype to phenotype map and the Neo-Darwinian definition of the mapping?" In order to answer that question, it is first useful to consider how the adaptive approach defines the issue compared to how the Neo-Darwinian approach addresses the issue.
First, we know that there exist processes (mutations) which create multiple forms of a gene. We also know that only a small portion of the genotypes created actually survive in any significant number in a population. We must therefore conclude that there exists ‘selection processes or mechanisms’ which eliminate some genetic forms.
Second, the genetic forms which survive appear to be associated with, ‘adaptive traits’, ‘adaptive states’ or traits which increase the likelihood the organism will survive. It therefore follows that there must be some type of logical relationship or mapping between ‘genetic forms that survive’ and ‘adaptive states’. This, in Darwinian terms, is the genotype/phenotype map. I would more appropriately label it the genotype/adaptive state map. Genotype/adaptive state maps are definable using the GAP model. More specifically, the GAP model defines a portion of the mapping.
Neo-Darwinian theory, not logical necessity, suggests that the ‘genetic selection processes’ MUST involve Darwinian Natural Selection operating on adaptive states or phenotypes. This theory, not logical necessity, suggests that there must be also be a (phenotype or adaptive state) to genotype mapping. The adaptive approach to evolution suggests that most biological selection processes do not operate on phenotypes or adaptive states, and that the process with do operate on adaptive states are not limited to Darwinian Natural selection. The Neo-Darwinian phenotype to genotype mapping need exist, and the adaptive approach asserts that such a logical/mathematical mappings does not exist.
Eliminating the necessity of phenotype to genotype maps, it is possible to consider far more complex, one to many, genotype to phenotype or genotype to adaptive states mappings. The adaptive approach, in fact, suggests that genotypes map to very large numbers of adaptive states( at least on the order of billions of adaptive states per gene).
Given the above background, the genotype to adaptive state mapping suggested by the adaptive approach would look something like:
(Genotypes) map to (assembly instructions) map to (physical chemicals or organelles) map to (adaptive reactions at points in time) which lead to (an increased chance of survival). The GAP model addresses the genotype or physical compounds portion of this mapping.
The basic difference between this and the neo-Darwinian (genotypes) map to (phenotypes) is that (genotypes), (assembly instructions), (physical chemicals or organelles) and (adaptive reactions at a point in time) can all be precisely defined and enumerated.[For the most part, the techniques already exist to identify and enumerate the members of each of these sets]. For the neo-Darwinian approach, there is no known technique to define and enumerate phenotypes. There is not, therefore, any actual basis for developing, defining, and testing a genotype or phenotype or phenotype to genotype mapping.
As you point out, the actual physical mechanisms and processes responsible for the hypothesized (genotype) to (assembly instruction) map are unknown. The physical mechanisms for the hypothesized (assembly instruction) to (physical chemicals or organelles) map are also unknown or partially unknown. However, it seems to me that it would be relatively easy to 1)demonstrate the existence or non-existence of the hypothesized mechanisms and 2) ultimately to identify the mechanisms involved. Because ‘phenotypes’ are not defined, and (in my opinion) probably not definable, there is no way to test and identify the mechanisms underlying genotype to phenotype mappings.
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James A. Barham
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posted 14. June 2002 11:25
Warren:
I know you are critical of neo-Darwinism, but I wonder if you are not ceding them too much ground. (Or, perhaps I am not understanding you correctly.)
For example, you wrote:
"First, we know that there exist processes (mutations) which create multiple forms of a gene. We also know that only a small portion of the genotypes created actually survive in any significant number in a population. We must therefore conclude that there exists ‘selection processes or mechanisms’ which eliminate some genetic forms."
Now, it may be true that "only a small portion of the genotypes created actually survive" if by that we mean over geological eons, because as we know most species eventually go extinct. But if you mean that there are more nonviable teratologies produced than viable phenotypic variations, that is simply not true (at least, I don't THINK it is true).
On the contrary, nearly all point mutations are actively suppressed by the cell, in a variety of ways, and almost all births are viable. This fact alone demonstrates the absurdity of the Darwinian viewpoint. Whatever variation occurs, occurs already within the context of a fully functioning system. So there is no way the Darwinian mechanism can explain how such a system can come to exist in the first place.
[ 14 June 2002, 11:26: Message edited by: James A. Barham ]
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warren_bergerson
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posted 14. June 2002 12:50
James,
When I say "only a small portions of genotypes survive" I am saying exactly the same thing as "nearly all point mutations are actively suppressed (selected out)by the cell". I my comments were meant to point out, is that ‘selection of genotypes’ is not logically the same as ‘selection by Natural selection’. Also as I point out, it is the neo-Darwinian assumption that selection means selection by Natural Selection that leads to unsupportable claim of a phenotype to genotype mapping.
It might be useful to note, that, in the adaptive approach, genotypes and/or assembly instructions are teleological or purposeful (this seems rather obvious). The definition of teleological causation I use requires the existence of a selection process, but such selection processes are not limited to Darwinian mechanisms. The GAP model provides a useful means of illustrating some of the concepts involved.
An ‘assembly instruction’ can be described as a causal relationship of the form cr = (sx causes ry) where sx is the environmental property which triggers the instruction, and rx is the reaction which produces a change in state in the assembly process. The causal relationship cr is defined as teleological (contributes to the goal gz- the assembly of the compound or organelle ) if 1)cr is a member of some larger set ‘CR’ of possible causal relationships and 2)there are selection processes which select cr from CR is such a way that the cr selected increases the likelihood the goal gz will be achieved.
If, as suggested by the GAP model, genes code assembly instructions from a defined set S of possible triggers, and a set R of possible reactions, then a cell could have a mechanism or mechanism that eliminates any mutation that doesn’t result in an assembly instruction involving one of the existing stimuli and one of the existing responses. Such a relatively simple mechanistic selection process could contribute significantly to the purposefulness of assembly instructions and could significantly reduce the complexity of evolutionary change processes.
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James A. Barham
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posted 14. June 2002 15:20
Warren:
Thanks for that clarification. I think I see better now what you are getting at with GAP.
The vocabulary threw me off (the word "selection" in particular), and on top of that, everything having to do with genes is conceptually slippery. (A propos, see Paul E. Griffiths' new review article, "Lost: One Gene Concept. Reward to Finder," Biology and Philosophy, 2002, 17: 271--283.)
Here is one more aspect of the matter that might require clarification.
There are a number of folks out there who would argue that everything can be modeled in a Darwinian manner. For instance, the clonal selection theory of the immune system, and also Gerald Edelman's "neural Darwinism". A good source for this sort of pan-selectionism is David L. Hull et al., "A General Account of Selection: Biology, Immunology, and Behavior," Behavioral and Brain Sciences, 2001, 24: 511-573 (with critical peer commentary, and replies).
Now, it seems to me that your GAP might be close in spirit to these ideas, if I am understanding you correctly. That is, by retaining the vocabulary of "selection," you seem to be aligning yourself with a sort of Edelman-style model of the genome itself ("genomic Darwinism," one might say).
Now, that is a very interesting idea (although, depending on how it plays out, someone like Dawkins might say it just reduces to the "selfish gene" concept). But, I wonder, is this consistent with your views on teleology? It seems to me that the idea that the cell is intelligently "choosing" is diametrically opposed to the idea that the appearance of intelligence arises out of a "selection" process imposed on "dumb" elements thrown up in a purely stochastic manner.
Part of the problem may be that we do speak of "selectivity" in molecular biology, but in a very different sense from "selection." "Selectivity" is a lock-and-key concept. One can argue whether such "selectivity" can be reduced to mechanism, or requires positing an irreducible teleological component to explain how keys come to match locks, but either way, it is very different from "selection" as that word is commonly used in biology. A Darwinian might want to argue that "selectivity" can be explained by "selection," but even he would have to admit that these are two distinct phenomena.
Now, my question to you is, Does your GAP model really involve "selection," or does it rather invoke a kind of "selectivity"? Thanks for the additional clarifications.
James
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warren_bergerson
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posted 15. June 2002 10:49
James,
You raise a number of points relating to the issue ‘how does the GAP model fit into the bigger picture?"
To begin, IMO, the high level question being addressed is ‘What is life?" or more specifically "How does science explain life?". This leads to "Why is life purposeful or teleological?" which leads to two questions
1) What is teleological causation as it relates to life forms? and
2) What creates and modifies teleological causal relationships?
The center piece of my work and the adaptive approach is a unique mathematical/logical/scientific model/theory to answer to these questions. Two features of the adaptive approach are of immediate concern to the discussion here. First, the adaptive approach asserts that any life form can be defined and modeled in terms of a finite countable set of teleological causal relationships. Teleological causal relationships are the ‘atoms’ of the adaptive approach. Although a life form is assumed to involve large numbers of these atoms, there are only a very limited number of different types of teleological causal relationships. Genetic material identifies or defines one such type of teleological causal relationship. The GAP model is designed to describe or define genetic material as teleological causal relationships.
The second relevant feature of the adaptive approach is the assertion that the all of the creation and modification of teleological causation in life forms can be modeled and simulated by a single paradigm. This single paradigm has been explicitly expressed by a single mathematical/logical model (Called an LFS). The references you listed are evidence that my claim that biological evolution, learning, and cultural evolution can all be described by a single paradigm is not original. However, the adaptive approach differs rather dramatically from these other approaches in that the LFS is very different, and far more complex than the mutate-select mechanism of neo-Darwinian genetics(NDG).
The fact that the LFS and the NDG models both involve selection processes is not surprising since both have their origins in the ancient Greek concept of teleological causation. But to answer your question, my approach includes mechanical/naturalistic operations of the type "if f(A) >f(B) then replace or substitute B for A". When you consider specific applications, I think the differences and similarities between the adaptive and Darwinian concept of selection will be clear.
As couple of final notes. My analysis suggests many of the ‘popular’ Darwinian concepts like ‘selfish genes’ and ‘selection of the fittest’ are very inaccurate descriptions of what actually happens. Finally, to modify your terminology, the adaptive approach would be consistent with the idea ‘intelligence-the ability to generate adaptive solutions and creative adaptive solutions, arises out of selection processes imposed on dumb elements which arise systematically’
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YZ2
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posted 16. June 2002 23:34
James and Warren,
Two points for discussion:
1) There is enormous conservatism observed in the genome(s), both between individuals of a species, and between species in a "taxonomic class". This can be calculated quite precisely using mathematics. One example of calculating this is to evaluate the within-class and between class variations. This means that impact of mutations and variations within a species on a species may be over-estimated.
2) Should there be a distinction between (1) random selection, without leading to advantage, stability and long-term purpose and (2) intelligent selection, which has a long-term purpose? My opinion is that the distinction is an important one. That is, if evolutionary process is to have important role, it must demonstrate that it uses intelligent selection, and not just random selection (as I define them).
[ 13. June 2003, 10:42: Message edited by: YZ2 ]
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warren_bergerson
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posted 17. June 2002 08:59
David,
To address you second point first, I believe you are referring to the distinction between 1)so called random genetic drift, what the adaptive approach calls devolution, and 2)purposeful or teleological selection.
The adaptive approach predicts that if a section of genetic code (a gene) is not purposeful or functional in a species, if it is what is commonly called selection neutral, then the code will undergo ‘destruction divergence’. Evidence apparently indicates that organisms have mechanisms for removing such non-functioning DNA with different species or groups of species tolerating different levels of non-functioning DNA.
The GAP model, if you think about it, provides a mechanism/explanation for how a cell can differentiate between functioning and non-functioning DNA at a very early stage and using mechanical processes. If a section of DNA codes a stimulus from set S and a response from set R, then any code which does not contain both a member of S and a member of R would be non-functioning. This mechanism could potentially explain some gene repair mechanisms.
It is useful to note that the adaptive approach predicts very different behavior under selection neutral conditions than the NDG genetic drift predictions. Although beyond the scope of the discussion here, it is interesting to note that despite its widespread acceptance, the NDG genetic drift model appears to be clearly inconsistent with known genetic mechanisms.
As I discussed in a previous post, the adaptive approach recognizes a wide range of purposeful, teleological, or intelligent selection mechanisms in addition to the rather weak Darwinian selection mechanisms.
I note you used the expression ‘intelligent selection which has a long-term purpose’. This suggests a view or perspective of intelligence which is very different that the perspective used in the adaptive approach. Intelligence, in the adaptive approach, can be defined as "the capacity to very quickly find solutions to immediate adaptive problems". Survival, the adaptive approach suggests, depends on being able to very quickly deal with immediate, short-term threats.
Since many of these short term threats are recurring, it is much more efficient to store adaptive solutions than to re-solve adaptive problems each time they recur. A rapidly changing dynamic environment and the storage of multiple adaptive solutions is one of the basic differences between NDG and the adaptive approach. The NDG views a species as a single solution to a single adaptive problem. The adaptive approach views an organism as ‘the ability (or intelligence) to quickly find billions of adaptive solutions to billions of moment by moment threats to survival’. [One of the basic techniques for falsifying the NDG model is to demonstrate that it doesn’t work in a dynamic environment. An organism with an evolutionary process based on the NDG model would be very unlikely to survive even a single lifetime, and would have no chance of ‘evolving’.]
The adaptive approach suggests that the ability/intelligence to solve large numbers of relatively mundane moment to moment survival problems, leads almost coincidentally to long term strategies and solutions that work over millions of years.
It is, IMO, one of the many ironies of Darwinian evolution, that although Darwin placed great importance on small gradual changes, he developed a theory that addressed the grandiose goal or purpose of long term survival and basically overlooked the short term day to day goal or purpose of surviving. It appears that many ID advocates commit the same error in trying to explain how intelligence in nature can help solve the problem of ‘surviving a million years in the future’ and to a large extent overlook the issue of how ‘intelligence is used by a cell to survive in the next milli-second’.
Now back to the first point you raised, conservation of genetic material. There are two features of this phenomena that are important to consider. First, the conservation of genetic material suggests that the primary goal or purpose of genetic mechanisms or processes is to preserve, maintain or conserve genetic code and the ‘identity of a species’, rather than to change it.
In focusing on genetic/evolutionary change, it easy to overlook how incredibly difficult it is for organisms and groups of organisms to maintain what I refer to as a ‘species identity’. It is easily demonstrated mathematically, that in the absence of very powerful counter-forces, the genetics of the cells of an individual multi-cell organism and the genetics of different members of a species would diverge very rapidly. The key to understanding genetics, IMO, is understanding how organisms maintain, and apparently in some cases even revert back to a species identity once divergence has occurred. As should be obvious, NDG does not offer an explanation of active processes to maintain species identity.
The second important feature of genetic conservation is to note that ‘adaptive variance or diversity’ and ‘genetic diversity’ are very different phenomena. Contrary to the NDG genetic determinism concept, a single set of genetic code represents not a single adaptive solution, but a very large set or range of adaptive solutions or potential adaptive solutions. The simplest examples of this set of solutions involves ‘genetic programming’ based on activating or inhibiting specific genes so a cell can create an adaptive solution to a specific set of conditions. I predict that additional, and more complex, genetic programming mechanisms will be discovered once we start looking for them.
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James A. Barham
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posted 17. June 2002 18:23
David:
I agree with most of what Warren said, which he said anyhow better than I could, so I will pretty much leave it at that.
I just want to reiterate the point Warren makes about the distinction between "short-term" and "long-term" teleology.
It is perhaps risky to even insist on using the word "teleology," as I do, for this very reason. It invites misunderstanding between these two ideas---which I usually call "immanent" and "transcendent" teleology. But I insist on using the word, because I believe in calling a spade a spade, because "teleology" just means "principle of goal-seeking" which is exactly what is involved, and because euphemisms like "teleonomy" have excess Darwinian and mechanistic baggage.
So, how should we think about the distinction between immanent (or internal) and transcendent (or external) teleology? Just like Warren said, all living things have innumerable short-term goals. These are the force driving evolution. We are still fundamentally ignorant of the way in which goal-directed coherent, coordinated action is possible, and we are even more ignorant of the way in which transitions from one functional ability to another are possible. But whatever the ultimate explanation turns out to be, I agree with Warren that it will have to do with the direct, short-term goal-seeking behavior of organisms. It is the intelligent striving of organisms to adapt that is the motor behind evolution, NOT "random mutation"---of that much, we may be certain.
I have called this principle "tatonnement", which is the French word for "groping" about blindly. (This is a parody of "bricolage".) Groping is trial-and-error, but it is not "random" in any meaningful sense, because it is goal-directed. The groping behavior occurs until the desired solution is found, or at least a good-enough solution ("satisficing"), and then it ceases, for the time being. I don't pretend we understand how individual striving translates into genetic change, and hence into "tatonnement" over generations. But it is better to admit ignorance than to feign understanding we do not really have.
One other example I like to use is this. One ought to think about the evolution of more complex creatures over the course of evolution by analogy with the evolution of more complex elements over the course of stellar nucelosynthesis. Just as most matter remains hydrogen, so too most of the biosphere still consists of prokaryotes. But that does not mean that eukaryotes are not "really" more advanced than bacteria. Of course they are, just as gold is more complex than hydrogen. But we do not say that there is an external telos or Omega Point pulling the elements up the periodic table. And we should not say either that there is an external force pulling organisms up towards more sophisticated, more intelligent forms. Rather, we must posit that there is some underlying structural principle, analogous to the quantum mechanical principles (e.g., Pauli exclusion principle) that explain increasing chemical complexity, that can account for increasing biological complexity. I am saying that that principle, which we do not yet know, must be something internal to life as such.
[ 17 June 2002, 22:07: Message edited by: James A. Barham ]
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