Posted on 06/08/2009 4:41:47 PM PDT by GodGunsGuts
Biomimicry: why the world is full of intelligent design
Forget human ingenuity - the best source of ideas for cutting-edge technology might be in nature, according to experts in 'biomimicry'
We humans like to think we're pretty good at design and technology – but we often forget that Mother Nature had a head start of 3.6 million years. Now, the way that geckoes climb walls, or hummingbirds hover, is at the centre of a burgeoning industry: biomimicry, the science of "reverse-engineering" clever ideas from the natural world....
(Excerpt) Read more at telegraph.co.uk ...
What is the “constraint” that would stop this change in DNA that is only one tenth the distance that you would freely allow a mouse DNA to change?
Is this a human specific “constraint” that you imagine?
If I run a DNA sequence with several hot spots for mutation through replication I will get every imaginable combination of mutations both in the “hot” spots and the rest of the sequence.
Damage creates variation, but so does DNA replication, especially DNA replication using error prone DNA polymerase, such as when a bacteria is under stress.
If all of cells were capable of changing their DNA specifically in response to selective pressure (”computing” rather than just following a molecular program), we would not observe selection, we would observe all the cells responding similarly by mutating their DNA in similar fashion.
This is not what is observed. What is observed in populations subjected to severe stress is the increase in genetic diversity initially and then a big drop off in numbers as only a few genetic varieties can survive the increasing stress, then the population that does emerge has changed DNA - not from a programmed response that any of the cells would have done; but from a process of selection from random generation
You are wrong on the subject. The micro-environment will be different for each cell. Each cell will respond in similar ways, yet constrained in the timing and sequence of their response. As an example every cell in the human body starts from one cell. If it did not compute then how do the different cell types and structures arise? By accident?
A body forms from a single cell by following a molecular program, not by “computing” solutions to problems.
A mistake in the program means developmental defects. An error is not correctable by a “computing” cell. The same defect will cause the same disability every time, not different disabilities depending on how the cell “computes”.
Did you not read the part about different micro-environments? The concentrations of different nutrients, poisons, etc. vary. That means the programs may not get to run to completion if at all.
A body forms from a single cell by following a molecular program, not by “computing” solutions to problems.
Then why is it that "identical" twins occur? BTW, programs compute.
This is NOT what is observed. What is observed is an increase in genetic variability as the stress response mutation increase is engaged in cell after cell, then a massive DIE OFF of all genetic variations that did not lead to heat resistance.
Identical twins followed an identical genetic program. How is it germane at all to whether the cell is following a set program or “computing” solutions?
When I say “molecular program” I mean there is a direct stimulus-response on a molecular level that is DETERMINISTIC. There is no “computing”. The cell itself has no ability to make decisions, responses are the direct result of molecular interactions.
http://www.genome.gov/15515096
New Genome Comparison Finds Chimps, Humans Very Similar at the DNA Level WASHINGTON, Wed., Aug. 31, 2005 - The first comprehensive comparison of the genetic blueprints of humans and chimpanzees shows our closest living relatives share perfect identity with 96 percent of our DNA sequence, an international research consortium reported today
At this point in time, a completely unbiased whole genome comparison between chimp and human has not been done and certainly should be. Despite this fact, several studies have been performed where targeted regions of the genomes were compared and overall similarity estimates as low as 86 percent were obtained.3 Once again, keep in mind that these regions were hand-picked because they already showed similarity at some level. The fact remains that there are large blocks of sequence anomalies between chimp and human that are not directly comparable and would actually give a similarity of 0 percent in some regions. In addition, the loss and addition of large DNA sequence blocks are present in humans and gorillas, but not in chimps and vice versa. This is difficult to explain in evolutionary terms since the gorilla is lower on the primate tree than the chimp and supposedly more distant to humans. How could these large blocks of DNA—from an evolutionary perspective—appear first in gorillas, disappear in chimps, and then reappear in humans?
The supposed fact that human DNA is 98 to 99 percent similar to chimpanzee DNA is actually misleading.
The availability of the chimp genome sequence in 2005 has provided a more realistic comparison. It should be noted that the chimp genome was sequenced to a much less stringent level than the human genome, and when completed it initially consisted of a large set of small un-oriented and random fragments. To assemble these DNA fragments into contiguous sections that represented large regions of chromosomes, the human genome was used as a guide or framework to anchor and orient the chimp sequence. Thus, the evolutionary assumption of a supposed ape to human transition was used to assemble the otherwise random chimp genome.
Analyzing the Source of Similarity
So how exactly did scientists come up with the highly-touted 98 to 99 percent similarity estimates?
First, they used only human and chimp DNA sequence fragments that already exhibited a high level of similarity. Sections that didn’t line up were tossed out of the mix. Next, they only used the protein coding portions of genes for their comparison. Most of the DNA sequence across the chromosomal region encompassing a gene is not used for protein coding, but rather for gene regulation, like the instructions in a recipe that specify what to do with the raw ingredients.3 The genetic information that is functional and regulatory is stored in “non-coding regions,” which are essential for the proper functioning of all cells, ensuring that the right genes are turned on or off at the right time in concert with other genes. When these regions of the gene are included in a similarity estimate between human and chimp, the values can drop markedly and will vary widely according to the types of genes being compared.
The diagram in Figure 1 illustrates how a gene is typically represented as a portion of a chromosome. As indicated, there is considerably more non-coding sequence ahead of the gene, within it (”introns”), and behind it. The 98 to 99 percent sequence similarity estimates are often derived from the small pieces of coding sequence (”exons”). Other non-coding sequences, including the introns and sequences flanking the gene region, are often omitted in a “gene for gene” comparative analysis. The critical importance of the non-coding sequences in the function of the genome was not well understood until recently, but this does not excuse the bias of the “98 to 99 percent similarity” claim. [LINK]
You post this to back up your less than 2% post and you want me to retract? Get a life!
What the heck are you talking about. Show me the precise examples. I have been talking about the paper I presented to you concerning ebgA targeted mutations. I have no idea what subject you are talking about. You have provided nothing to back up what you are asserting. "Tending towards" and "being the same" are none theless different environments.
Identical twins followed an identical genetic program. How is it germane at all to whether the cell is following a set program or “computing” solutions?
Because you claim a monotonic response. It is evident that some cells become a part of another body at some juncture of the program being run. It is therefore evident that a computation was made with inputs from the immediate environment which resulted in different development.
I mean there is a direct stimulus-response on a molecular level that is DETERMINISTIC. There is no “computing”.
Well, then you have no idea what computing is. You might start here ...Finite-state machine
Computers are deterministic. Otherwise, it's garbage in garbage out.
the percentage of ‘98%’ is only 98% similarity out of the 2 percent of the entire genome that is compared to humans and even that 98% is an overestimation. Coding dna comprises only 2% of the genome while the non coding region comprises the remaining 98%- are ya folloowing along?
First, they used only human and chimp DNA sequence fragments that already exhibited a high level of similarity. Sections that didn’t line up were tossed out of the mix. Next, they only used the protein coding portions of genes for their comparison. Most of the DNA sequence across the chromosomal region encompassing a gene is not used for protein coding, but rather for gene regulation, like the instructions in a recipe that specify what to do with the raw ingredients.3 The genetic information that is functional and regulatory is stored in “non-coding regions,” which are essential for the proper functioning of all cells, ensuring that the right genes are turned on or off at the right time in concert with other genes. When these regions of the gene are included in a similarity estimate between human and chimp, the values can drop markedly and will vary widely according to the types of genes being compared.”
http://www.icr.org/article/4624/
“It appears that only about 1.5% of the human genome consists of genes, which code for proteins. These genes are clustered in small regions that contain sizable amounts of “non-coding” DNA (frequently referred to as “junk DNA”) between the clusters. “
http://www.apologeticspress.org/articles/2070
and just for good measure:
“Despite this fact, several studies have been performed where targeted regions of the genomes were compared and overall similarity estimates as low as 86 percent were obtained.3 Once again, keep in mind that these regions were hand-picked because they already showed similarity at some level. The fact remains that there are large blocks of sequence anomalies between chimp and human that are not directly comparable and would actually give a similarity of 0 percent in some regions.”
Well, since you’ve accused me of lying, perhaps you can back up your accusation, and perhaps you can help me with my math here CW- I never was good at math, and might be mistaken (and just for hte record- a mistake is NOT the same thing as a lie- just htought you’d like to know).
Let’s simplify this a bit, so it’s easier to understand. Let’s take just one gene from a human, and one from a chimp, and compare them, as this is representative of the entire genome of both species-
IF a gene’s coding region comprises only 1.5% of hte entire gene, while hte non coding region comprises 98.5%, and the similarities between chimp and human genes is only 86% similar in the actual coding region of hte gene, which again, is only 1.5% of hte entire gene, then how on earth does that equate to our genes being 98% similar to a chimps? IF we only compare the coding region, which again, is only 1.5% of hte entire gene, and if the remaining 98.5% is NOT similar, again, how is it not a fact that our entire genes are less than 2% similar to a chimps?
If I took two cups, filled one with 98.5 green peas and one pea which was 86% green, and 14% blue- then filled the other cup with 98.5 tiny purple marshmallos, and one pea that was 86% green, and 14% blue, then I ask you- how would that make both cup’s contents 98% similar? Am I missing something here? The contents of the cup are only 1.5% similar- less than 2% of hte entire cup’s contents is similar to the other in my world- not sure about in your world?
I sure would like to live in your world, where math doesn’t matter, where chemical laws don’t apply, where the second law of thermodynamics doesn’t play a role in macroevolutionary processes, where biological laws don’t matter, and where macroevolution miraculously overcomes any and all impossibilities, and where 1.5% similarities actually mean 98% similar (which is really only 86% similar when you compare ALL the areas of the coding portion of hte gene, and not just the area of hte coding region that matches, while htrowing out or ignoring the areas that don’t match, and only comparing the coding area, and not hte non coding area, which as we know, is NOT junk dna as previously claimed, and hwich DOES play a critical role in seperating species one from another).
The SOS response in bacteria increases the mutation rate throughout the entire bacterial genome, and the variation produced is random.
The majority of the variations produced are not viable in the context of the increasing stress leading to MASSIVE DIE OFF.
If your hypothesis of the “computing” cell was correct, why did the vast majority of cells and the vast majority of genetic variations all get eliminated?
A biological program is not making decisions or thinking(what I would call ‘computing’); each molecular response is directly the result of a molecular stimulus.
The cell is not thinking, it is responding.
And its response is to increase its evolution rate during stress, which produces genetic variation which the stress acts upon selectively such that only those variations amenable to the stress survive.
And I am talking about, also having presented the paper, is the SOS response where the mutations are directed to two specific locations in the ebgA gene. This is under conditions where the environment is not lethal. This is repeatable. The authors cite other experiments and show that no other locations are involved.
If your hypothesis of the “computing” cell was correct, why did the vast majority of cells and the vast majority of genetic variations all get eliminated?
It is not my hypothesis. It is promoted by Dr. James Shapiro among other people. And in the experiment I am mentioning the MASSIVE DIEOFF that you mention does not occur.
Mutation assays were as described previously (27), including that cell viability measurements for all experiments reported showed no net growth or death of the frameshift-bearing cells. Some variability is seen in absolute values from experiment to experiment, but relative values between strains remained the same within a minimum of three repeats.
...
Recombination-dependent adaptive mutation occurs in a hypermutable subpopulation of the stressed cells (10-4 to 10-5) (28, 59). We suggest that SOS induction may be the event that differentiates subpopulation cells from the main population. Although no net cell death was observed during the experiments with the dinI psiB strain (see Materials and Methods), death of only the subpopulation would have been undetectable.
A biological program is not making decisions or thinking(what I would call ‘computing’); each molecular response is directly the result of a molecular stimulus.
Thinking is not the term I used. Computing is. And the cell computes. A computer computes based on input same as the cell.
They were only LOOKING at those two particular locations.
When people use error prone DNA polymerase to produce genetic variability, the ENTIRE sequence is subject to mutational change.
Are you suggesting that error prone DNA polymerase was somehow directed to specific genetic locations while the rest of the genome was replicated using high fidelity DNA polymerase?
Error prone DNA polymerase used to replicate the entire genome will create RANDOM variation over the entire genome.
If all you are saying by claiming a “computing” cell is that it has a programmed response to stimulus, then you would be hard pressed to find anyone to disagree with you.
If you are trying to claim that the “computing” cell is making decisions and somehow “knows” which mutations to produce in which gene regions to increase its survivability, that is simply not supported by the evidence.
What would drive them to do that if it was just luck that these locations mutated? That said there are probably mutations elsewhere outside of the particular ebgA gene, but within the ebgA gene there were only two.
When people use error prone DNA polymerase to produce genetic variability, the ENTIRE sequence is subject to mutational change.
Yes, people would do that since they don't know how to control its expression like the cell does. This paper was to evaluate what controlled the SOS response. If you read the paper you can see the some control products were necessary to evoke the hypermutability while others had little effect on that part of the response. It still remains that only two mutations were discovered in the populations able to regain the ability to metabolize lactose.
If you are trying to claim that the “computing” cell is making decisions and somehow “knows” which mutations to produce in which gene regions to increase its survivability, that is simply not supported by the evidence.
I can't address your "knows" since that implies conciousness, but the cell computes.
We find that SOS-induced levels of proteins other than RecA are needed for adaptive mutation. We report a requirement of RecF for efficient adaptive mutation and provide evidence that the role of RecF in mutation is to allow SOS induction. We also report the discovery of an SOS-controlled inhibitor of adaptive mutation, PsiB. These results indicate that adaptive mutation is a tightly regulated response, controlled both positively and negatively by the SOS system.
Evolution is based upon the notion of adaptive mutations being subject to natural selection.
Once you admit the existence of adaptive mutations and the ability of natural selection to act upon them, you have accepted the entire premise of the theory of evolution through natural selection of genetic variation.
No, I'm not surprised, but you should be. Because along with those mutations there should have been others within that group. There were none. The gene involved did not have the lactose metabolitic activity prior to the experiment. It just looked a bit like the lac gene.
Evolution is based upon the notion of adaptive mutations being subject to natural selection.
No it isn't. Neo-Darwinism cannot use the word "adaptive" before the fact. Only the word "mutations" can be used. Natural selection is supposedly what defines the adaptation.
Once you admit the existence of adaptive mutations and the ability of natural selection to act upon them, you have accepted the entire premise of the theory of evolution through natural selection of genetic variation.
Nope. There are recent papers that try to explain away the adaptive mutations, because it is a "stain" upon Neo-Darwinism. They attack the adaptive part by concluding that the mutation rate would decimate the population under study and thus the mutation rates evidenced by the mutations in the ebgA gene were impossible burdens on the bacteria.
Within the group that restored lactose activity? Why do you insist there should have been more than two mutations that restored the ability?
Mutations that are adaptive are not at all a “stain” upon the theory of evolution through natural selection.
The only point you seem to differ on is the meaning of adaptive. By calling the cell “computing” and talking about the mutations being “adaptive” you seem to be under the impression that somehow specific mutations are being specifically directed.
You have repeatedly failed to show that the mutations brought about by using error prone DNA polymerase to replicate the genome produce anything other than genome wide genetic variability.
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