KBCid wrote:The evidence is plainly showing that there is a system of spatiotemporal positional control functioning within all life.
Pierson5 wrote:I'm not arguing that the system isn't there. I'm arguing that you are jumping to a conclusion when we are still left with a mystery.
'we' aren't left with a mystery. I know precisely what it takes to systematically replicate 3 dimensional formations of matter. This system is irreducibly complex. 'IT' requires a control to form the system and chance alone does not logically explain it. Thus you are left with 2 choices either it arose by a chance occurance or it was designed since only ID has shown the ability to initiate such a complex form.
Pierson5 wrote:Just as Behe had his flagellum. No one was arguing that the flagellum wasn't there, or that it didn't express machine-like characteristics. Even if we didn't know how the flagellum evolved, this would not be evidence for design. You are taking this structure that is not completely understood (an unsolved problem) and claiming it as evidence for design. If you have an unanswered question, you have an unanswered question. Not evidence. Once you and your colleagues have actually discovered evidence for design in this system, then you can claim it is designed.
Behe wasn't arguing simply for the existence of the flagellum. What he was arguing for was that it was irreducibly complex and essentially beyond the possibiity of random chance to generate in small steps. his error was choosing a mechanical formation that is believed to have come into existence after evolution was already underway.
Evidence for historic occurance can only be derived from what is observable in the present. Only one cause has formed the types of systems that even come close to the systems in life.
Have you ever seen natural forces form such a system? Then by what evidence do you presume to infer that such a system is naturally forming?
Pierson5 wrote:People building systems that are similar is not evidence for biological design.
Wrong. People building systems that are similar learn what is minimally required for a system to provide a function. In this case it is the formation of matter into precise 3 dimensional arrangements and since the ONLY cause observed to have formed such systems is ID.
Pierson5 wrote:The citation you gave says NOTHING about ID in the regards of this discussion. Your whole argument is just a rehashed version of Paley's watchmaker argument. Just as Behe used the flagellum (motor), you are using the same argument with 3 dimensional spatial organization. Paley's argument is flawed, Behe's argument was flawed and yours is flawed for the same reasons.
KBCid wrote:Then you should have no serious problems defining how it is flawed just like all the others. Right?
Pierson5 wrote:Sure. For the sake of argument, let's say we have the same amount of knowledge of 3 dimensional spatial organization as we do the flagellum (so removing some information we know about the flagellum). I'll provide analogies through the rest of this post.
In your case you don't have the same knowledge of 3 dimensional spatial organization as I do and really what do you know about the formation of the flagellum? Since it is clear that it requires a system of spatiotemporal control to form the flagellum then the two systems are not the same. The flagellum is the result of programmed spatiotemporal controlled construction. Thus it is simpler than the system that allows it to form and simpler than the system I am pointing out to you.
Pierson5 wrote:Cutting edge research is exciting, I agree. The issue I have is with your conclusion. From the citations you have provided thus far, no one has come to the conclusion you are promoting (biological design). As I said above, I'm not arguing these systems don't exist. You are taking this cutting edge research and jumping to the conclusion about the origin of these systems when the answer is still inconclusive (again, going off your previous citations).
One does not have to provide citations to opinions that match their own. My references are there for the observable evidence being shown in their experiments. Most of them realize that a system exists but don't say anything about how inclusive it may be which is probably because they are not looking for the forest that the trees are a part of.
I am using logic and reason based on already understood scientific understanding of replication and showing that the same system is functioning within life. All you have to do is follow the logic to its rational conclusion.
Tell me what does it take minimally to systematically replicate a 3D formation of matter? remember... no replication, no evolution. If you don't know then you have no business arguing this thread with me as your counter POV would be an argument from ignorance.
Pierson5 wrote:You mentioned before you were working on a bioengineering degree. So I assume you have some sort of affiliation with the biology department, even if you aren't doing research in their particular field. Since your conclusion would have major ramifications in the field of biology, I guess I assumed you would have at least discussed this, researcher to researcher, with others in that field.
I have and as I said they are implementing the concept. Looking scientifically for evidences to back it. Let me tell you their POV in their own words "It is best to start by uncovering as much of the system as possible before stating the implications it will evoke." This system isn't just another flagellum concept. This system would be required before evolution could function. This has paradigm changing extent and since a system which is capable of replicating 3 dimensional formations of matter is exceedingly complex and irreducible then it will pretty much leave chance as a rediculous assumption for its origination.
Pierson5 wrote:The experimental evidence I'm looking for is biological evidence. Not mechanical engineering.
You can no longer separate biology from mechanical engineering since the formations of life works mechanically as well as chemically and electrically. Life is not as simple as you would like rationalise it.
The evidence I am bringing to the table with the cited references are showing how the system is an inherent part living systems and they know a system exists. Their major failure is that they have not ever had to form a replication system. This is where I have an advantage. I see the connections from the individual references and recognise that they are all part of one system. Soon they will have to make the same rationalization as they start to connect the dots.
So if you don't accept my references as evidence for an irreducibly complex system of control for spatial positioning then I invite you to define how chance makes it happen at every replication event.
Pierson5 wrote:If we use the same argument Behe had used with regards to the flagellum, it's not hard to see the similarities.
As I pointed out my argument is not the same as Behe's concerning the item constructed. My argument is the same as Behe's as concerns the irreducible complexity of a system. It's not hard to see the differences if you pay attention to what I'm writing.
Pierson5 wrote:The system requires a designer because the flagellum is irreducibly complex. We only have seen intelligent agents give rise to the type of design we see in the flagellum. As our understanding of the flagellum grew, however, this was shown to be false. You can test for these sort of things. For example, if the flagellum evolved, we should be able to see some sort of gradual transition.
Indeed if something was formed by evolutionary mechanism then you should be able to test for it and yet no such test has confirmed such a thing and Behe's rationale still stands. However, since my argument is not the same as Behe's then you have to deal with the specifics that I am pointing out if you hope to refute it.
Again my position is that
1) in order to have evolutionary function as you conceive it to be you must first have alleles and replication.
2) 3 dimensional formations of matter cannot be replicated without a defined system of spatiotemporal control
3) No replication, no evolution.
Unlike Behe's critics you cannot invoke the conceptual magic wand of evolution to bypass the forming of the minimal irreducible complexity of the system I am revealing. You are simply left with 2 choices... It occured by chance or it was designed. I would really like to see you try to formulate how it could have happened by chance.
Pierson5 wrote:This may be a bit lengthy, I'll try to sum it up the best I can. From the trial:
Your attempt to make Behe's argument the same as mine is a strawman argument. You are making a strawman by avoiding the plain understanding of differences that I have repeatedly pointed out.
Pierson5 wrote:And now, from my point of view, the key part of the argument, and I'll continue to read. An irreducibly complex system cannot be produced directly by slight, successive modifications of a pre-cursor system -- and that's how evolution would have to produce it -- because any pre-cursor to an irreducibly complex system that is missing a part is by definition non-functional.
So his argument is that, if you have a multi-part system, and all the parts are necessary to function, you can't produce that system five parts at a time, six, seven, and gradually build up the complex system, because there is no function possible until the last part is snapped into place. And that's why evolution cannot produce that system.
Mostly correct except that in this case you don't get to invoke the (pre-cursor system) conceptual magic wand of evolution since there is no evolution systematically functioning until there is replication. You sir are logically cut off at the pass with your strawman since 3 dimensional replication cannot proceed without the spatiotemporal control system, and evolution cannot begin until replication does.
Pierson5 wrote:They continue to have similar examples such as blood clotting and the immune system, which I don't think I need to go into. The point is, these ARE testable claims. I understand that you are on the cutting edge of the current research being done in this field. But, you are coming to a conclusion (biological design) before your research is complete. When you or your colleagues actually publish your research which concludes biological design, THEN you will have evidence for what you are promoting.
Another point. If you do end up showing this structure is, in fact, irreducibly complex, this is not evidence for design. It is merely a problem for evolution.
You are invited to provide rationale for how my irreducibly complex system came about by chance since 3 dimensional replication cannot proceed without the system, and evolution cannot begin until replication does.
KBCid wrote:Point 2 isn't true... the fact is 'You' don't understand it. I understand it quite well since the type of system you don't understand is what I make for a living and since these systems have only ever been observed as a result of ID I have every right to hypothesize that ID would be required for them to come into existence. What have you observed that forms such a system? really show me what kind of system like this you have personally observed nature forming?
Pierson5 wrote:We don't understand it 'completely.'
What don't 'we' understand completely?
Pierson5 wrote:There are still unsolved mysteries about this system, I think you'll agree.
The only thing not understood completely by anyone is the extent of the paths that the system works through.
Pierson5 wrote:That is what we are arguing about and is what I was referring to. Before we understood a lot of the intricate details of the flagellum, we still had a pretty good understanding of the flagellum itself. Before our further understanding of the flagellum, you could make the same argument in your last sentence. "Show me nature forming this system." And eventually they did. This goes back to my previous point as well. This is merely a problem for evolution. NOT evidence for design.
lol 'a problem for evolution'. yes it is... since 3 dimensional replication cannot proceed without the system, and evolution cannot begin until replication does.
How does one try and invoke a theoretical cause (evolution) that doesn't logically exist prior to the system necessary for the cause to function?
KBCid wrote:Ok let's review what I have been saying "The evidence is plainly showing that there is a system of spatiotemporal positional control functioning within all life" and I further state that "a system of spatiotemporal positional control is required for 3 dimensional replication" here is a sampling of the evidence provide to back these statements;
http://genesdev.cshlp.org/content/24/11/1086.full
http://nar.oxfordjournals.org/content/e ... lowres.pdf
So in your opinion none of these references says anything like what i'm saying right?
Pierson5 wrote:No, because that is not what we are discussing. As I've said many times, I am not arguing these things don't happen/exist. I am arguing that you are jumping to a conclusion. Your first statement left out: "Therefore, biological intelligent design." THAT is what you are saying and is NOT mentioned in ANY of your reputable citations.
I am discussing an irreducibly complex system of spatiotemporal control which could not evolve since it's existence is required before evolution can proceed. The logical inference is that it must be designed since it is far beyond a chance ability to form such a complex interacting system. You of course are free to assert that chance could form such a system and then I will begin laying out all the necessary components of the system that would have to arise and interact "by chance".
KBCid wrote:Behe's mouse trap arguement is not mine nor is the stone archway. These are your strawman arguments. How about you define where my arguments are wrong.
Pierson5 wrote:lol. Come on. You were the one citing the reference with the mouse trap analogy, as you said later to "define irreducible complexity." You could have just taken an excerpt from Behe's book and given a short definition instead of citing multiple articles that you claim have nothing to do with what you are arguing now.
The references show how irreducible complexity is being applied. You are choosing to try and use the objects that it was applied to as a means to refute.
Pierson5 wrote:Couldn't I use this same argument against your "evidence" for ID? Have you ever seen something built by humans that has 3 dimensional spatiotemporal control systems and was also able to replicate itself with slight modifications?
Pierson5 wrote:I don't see any mention of 3 dimensional spatiotemporal control.
The post mentions quite clearly "They manufactured a new chromosome from artificial DNA in a test tube, then transferred it into an empty cell and watched it multiply – the very definition of being alive."
How do you suppose it multiplies?
by chance maybe?
Pierson5 wrote:If I may point to the post directed to neo and ask you to expand on this? My point about the arch-way may have fell through, but this still says nothing about biological design. It's interesting evidence about human innovation for sure.
Expand on my entire post to Neo?
Pierson5 wrote:This may be relevant: CONCLUSIONS:
The genetic separability of spatial and temporal control modules in Caulobacter reflects their evolutionary history. DnaA is the central component of an ancient and phylogenetically widespread circuit that governs replication periodicity in Caulobacter and most other bacteria. By contrast, CtrA, which is found only in the asymmetrically dividing a-proteobacteria, was integrated later in evolution to enforce replicative asymmetry on daughter cells.
KBCid wrote:In what way is someones opinion of what may have happened relevant? Do you or they have any evidence from scientific method?
Pierson5 wrote:Here is the full publication:
http://www.ncbi.nlm.nih.gov/pmc/article ... ool=pubmed
They define the background/observation, perform tests and published their conclusion. It doesn't appear to just be "their opinion" if it's supported by experimental testing. I have yet to see any of your research conclude biological design... In what way is your opinion relevant?
They gave an opinion on how a part of the system they see may have occured without having any understanding of how replication itself could begin. My proffesional opinion is relevant since it is based on evidence from existing designed replication systems. You have two options to explain it chance or design. I choose the most logical choice, Design, which is refutable by showing logically how chance could have done it.
Pierson5 wrote:Now, if you are claiming that 97% of scientists who accept evolution are mistaken in their evaluation of this sort of evidence, we now have a testable claim!! Feel free to re-evaluate the methods used by evolutionary/molecular/geneticists and other scientists and prove them wrong.
KBCid wrote:ok... how many genetic markers do they use to ascertain relatedness?
You should by all means continue since you have not shown how the 16S rDNA/ 16S rRNA method is the equivalent to a paternity test.
INTERNATIONAL JOURNAL OF SYSTEMATIC AND EVOLUTIONARY MICROBIOLOGY
How Close Is Close: 16S rRNA Sequence Identity May Not Be Sufficient To Guarantee Species Identity
Abstract
16S rRNA sequence comparisons were conducted with the following three psychrophilic strains: Bacillus globisporus W25T (T = type strain) and Bacillus psychrophilus W16AT, and W5. These strains exhibited more than 99.5% sequence identity and within experimental uncertainty could be regarded as identical. Their close taxonomic relationship was further documented by phenotypic similarities. In contrast, previously published DNA-DNA hybridization results have convincingly established that these strains do not belong to the same species if current standards are used. These results emphasize the important point that effective identity of 16S rRNA sequences is not necessarily a sufficient criterion to guarantee species identity. Thus, although 16S rRNA sequences can be used routinely to distinguish and establish relationships between genera and well-resolved species, very recently diverged species may not be recognizable.
http://ijsb.sgmjournals.org/content/42/1/166.full.pdf
Ribosomal RNA or protein sequences for phylogenetic inference?
Comparative analyses of rRNA sequences, initiated in the 1970s, suggest that the living world is divided into three domains:
Eucarya, Archaea (formerly archaebacteria), and Bacteria (formerly eubacteria).
...recent data using phylogenetic methods based on protein-coding genes have shown that classical methods of molecular phylogeny using rRNA genes may fail to delineate phylogenetic relationships between domains or between major lineages of these domains.
During the last five years, investigators have analysed an increasing number of protein sequences from Archaea, Bacteria and Eukarya, furnishing many more representative examples from each of the domains. At first, these new trees were expected to support the idea of amitochondriate Archaezoa to have preceded all mitochondriate eukaryotes. However, much of the new information does not support this idea. As data accumulate, a drastically different pictures emerges.
http://www.icp.ucl.ac.be/~opperd/private/tree_o_l.html
RNA Editing
The DNA sequence doesn't always translate into amino-acid sequence. The pre-mRNA may require alteration of its coding sequence before it can be translated into a funtional protein. This is called post-transcriptional editing. In post-transcriptional editing several different mechanisms are known. These are:
RNA editing in the Kinetoplastida.
This involved the insertion or deletion of one or more Us in the pre-mRNA, using guide RNAs as templates. This way non-coded initiation codons or amino acids are added or coded amino acids are removed during the editing process. This could lead to major differences between DNA and mature mRNA sequence. In some extreme cases (in Trypanosoma brucei sometimes more than 50% of a genes is edited. Such genes are called pan-edited genes). DNA and mature mRNA do not hibridise anymore to each other. Nevertheless this leads to roughly the same protein sequence after final editing. (Some details about editing in Trypanosomatidae can be found here or on the RNA editing site of Larry Simpson).
Post-transcriptional base modification in some gene products.
Examples of these are: Modification of rRNAs, Modification of tRNAs Modification of the apo-lipoprotein B mRNA creating an additional termination codon
Conclusion: Peptide sequences are not always identical to what is predicted by the corresponding genes!
http://www.icp.ucl.ac.be/~opperd/private/arguments.html
Comparison of biochemical and molecular methods for the identification of bacterial isolates associated with failed loggerhead sea turtle eggs
Abstract
Aims: Comparison of biochemical vs molecular methods for identification of microbial populations associated with failed loggerhead turtle eggs.
Methods and Results:
Two biochemical (API and Microgen) and one molecular methods (16s rRNA analysis) were compared in the areas of cost, identification, corroboration of data with other methods, ease of use, resources and software. The molecular method was costly and identified only 66% of the isolates tested compared with 74% for API. A 74% discrepancy in identifications occurred between API and 16s rRNA analysis. The two biochemical methods were comparable in cost, but Microgen was easier to use and yielded the lowest discrepancy among identifications (29%) when compared with both API 20 enteric (API 20E) and API 20 nonenteric (API 20NE) combined. A comparison of API 20E and API 20NE indicated an 83% discrepancy between the two methods. Conclusions: The Microgen identification system appears to be better suited than API or 16s rRNA analysis for identification of environmental isolates associated with failed loggerhead eggs.
http://cat.inist.fr/?aModele=afficheN&cpsidt=20291825
Guidelines for interpretation of 16S rRNA gene sequence-based results for identification of medically important aerobic Gram-positive bacteria
Abstract
This study is believed to be the first to provide guidelines for facilitating interpretation of results based on full and 527 bp 16S rRNA gene sequencing and MicroSeq databases used for identifying medically important aerobic Gram-positive bacteria. Overall, full and 527 bp 16S rRNA gene sequencing can identify 24 and 40% of medically important Gram-positive cocci (GPC), and 21 and 34% of medically important Gram-positive rods (GPR) confidently to the species level...
Since its first use three decades ago, 16S rRNA gene sequencing has become one of the indispensable pillars in the polyphasic approach to bacterial classification and novel bacteria discovery (Woo et al., 2008a). In the last decade, the technology has further developed beyond the research realm and matured into a clinical application for bacterial identification. Despite its increasing use in reference laboratories, one of the major limitations to its wider use is the difficulty associated with interpretation of 16S rRNA gene sequence results. The use of 16S rRNA gene sequencing for bacterial identification depends on a significant inter-species difference and a small intra-species difference in 16S rRNA gene sequences. Therefore, one of the major limitations is that when two different bacterial species share almost the same 16S rRNA gene sequence; this technique alone would not be useful for distinguishing them confidently.
For species identification, 16S rRNA gene sequence results of aerobic Gram-positive bacteria should be interpreted cautiously with basic phenotypic tests results, and additional biochemical tests or sequencing of additional gene loci are often required for definitive identification.
http://jmm.sgmjournals.org/content/58/8/1030.full
Shall I continue?
KBCid wrote: Yup there certainly are "ways to test for distinctive variations in DNA", Variations are one thing and relatedness is another. Now tell me how many genetic markers are used to define relatedness?
Pierson5 wrote:A genetic marker is a gene or DNA sequence with a known location on a chromosome that can be used to identify individuals or species. It can be described as a variation (which may arise due to mutation or alteration in the genomic loci) that can be observed. A genetic marker may be a short DNA sequence, such as a sequence surrounding a single base-pair change (single nucleotide polymorphism, SNP), or a long one, like (as I mentioned before) minisatellites.
How exactly does a genetic marker define an individual or specie? How do you know that 2 separate species which have a very similar marker in a similar place were not designed that way?
KBCid wrote:Comparing two peoples genetic markers... 16 of them determines heredity.
Yup your missing something; The problem posed by phylogenetics is that genetic data are only available for living taxa, and the fossil records (osteometric data) contains less data and more-ambiguous morphological characters.[6] A phylogenetic tree represents a hypothesis of the order in which evolutionary events are assumed to have occurred.
http://en.wikipedia.org/wiki/Phylogenetics
Pierson5 wrote:I was addressing your claim that I made a false analogy. It appears there isn't one and you now move onto an issue with phylogenetics.
You have made a false analogy. I was just showing how limited the test actually is besides what I just posted above. You have yet to show how the 16S rRNA method is equivalent to a paternity test.
Pierson5 wrote:Analyzed protein sequences extracted from Mastodon and Tyrannosaurus rex fossil fragments. As expected, when these sequences were compared with those of modern organisms, Mastodons were found to be most closely related to modern elephants, while T-rex was genetically similar to modern birds. This confirmed scientists' hypotheses that the taxa were evolutionarily related.
What do you know, a scientific hypothesis confirmed with experimentation. Scientific method you say?
So how did the scientific method absolutely define relatedness? I think I'll refer you to a creationist site here as I tire of performing the research to keep knocking down your conceptual truths;
Dinosaur Protein Sequences and the Dino-to-Bird Model
by Jeffrey Tomkins, Ph.D.
Those sequences of high enough quality to be usable were then analyzed using dino-to-bird evolution as a filter.10 Interestingly, an external laboratory re-analyzed the data using a computational technique called Neighbor-Net analysis that was better suited to the type of data collected.8 Their results showed that the T. rex protein grouped more closely with amphibians and did not show a close relationship with either chicken or ostrich--two birds that evolutionists like Jack Horner claim actually have dinosaur genomes with just a few minor differences to make them birds.
http://www.icr.org/article/4949/