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Evolution via random mutations is impossible

pitabread

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No you're conflating issues. You said that we have observed DNA form naturally through reproduction. That is not what we have observed. We have observed it copied and recopied but not "formed" by any natural sources.

In this case I am referring to the replication of DNA as being part and parcel to its natural formation (via organic replication). And specifically that DNA is not an artificially manufactured human product.

If you're looking for the original origin of DNA, that is still being worked on. But there are known mechanisms about how things like DNA and RNA nucleotides could have originally formed.

I was pointing out that the Bible says that this is how it was created and that is what we do actually observe. Not assuming anything just pointing out the obvious observations and how they happen to agree with the book.

The Bible is completely silent on the subject of DNA. Which should be no surprise given that DNA wasn't discovered until centuries later.

Actually here's a video I did with SETI Astronomer Jill Tarter explaining exactly what it is they are looking for. To save time skip to 4:34 minutes in. Note how she says they are looking in the radio for frequency compression, or in the optical for time compression. These are either a radio burst or optical burst that would tell them that the signal likely had an intelligent source. If they observed such a signal it would NOT be human in origin. But the key here is that such a signal would be recognized by the observer from a previous experience that would tell them that the signal had an intent or purpose. That is the definition of specificity.

They aren't looking for "intent or purpose". Rather, they're looking for narrow-band signals whereby the only known source are artificially manufactured radio transmitters. IOW, they are making an inference about how the signal is generated. The actual purpose of the signal is completely irrelevant.

In the case of the code in DNA we don't have any known source. We have never observed DNA form artificially or naturally. But what we have observed is that the kind of structure found in the code of DNA has only been observed forming by intelligent sources...period.

You've just contradicted yourself. If per your claim we don't have a known source of DNA, then we can't assume anything about its origin being intelligent.
 
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BradB

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That still doesn’t change the fact that you creationists have arbitrarily decided that genetic similarities don’t show relatedness.

Actually we are not saying genetic similarity doesn't show any evidence of relationship. What we are saying is that it is only helpful in those cases where we have evidence that there is a possibility for relationship. Here's what I'm talking about. We know humans create humans. This has been a common observation since the beginning of humanity. We know that all other kinds reproduce after their kind. This also...observation. So when we look at the genetic code between two human siblings and find they are nearly a match, and then look at the codes between two very different cultural groups and see close similarity but much more distance, we can make the logical conclusion that the closer the similarity is between humans, the closer related they are.


On the other hand we have never observed a common ancestor produce two major and different forms over vast amounts of time. Therefore it is not anymore logical to say that similarity between genes in chimps and genes in humans means they are related, than it would be to claim that a scale that accurately weighs a sub atomic particle can accurately weigh a freight train.
 
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BradB

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In this case I am referring to the replication of DNA as being part and parcel to its natural formation (via organic replication). And specifically that DNA is not an artificially manufactured human product.

And this is why I carefully gave two examples of specificity observed that scientists infer intelligence...that were not a product of humans either. Dolphin language and alien space signals have nothing to do with human manufacture.

If you're looking for the original origin of DNA, that is still being worked on. But there are known mechanisms about how things like DNA and RNA nucleotides could have originally formed.

I agree. However we clearly observe the very specified nature of DNA. Since to date we have only ever observed specificity form by intelligent sources it is not unreasonable to conclude DNA code had an intelligent source.

The Bible is completely silent on the subject of DNA. Which should be no surprise given that DNA wasn't discovered until centuries later.

It is not surprising. What is surprising are many scientific principles that are mentioned in the Bible that authors of the time could have known nothing about. But that's for another discussion. The Bible does talk about reproduction quite a bit and clearly says that kinds will only reproduce after their own kind. Something we still observe today with no evidence to the contrary.


They aren't looking for "intent or purpose". Rather, they're looking for narrow-band signals whereby the only known source are artificially manufactured radio transmitters. IOW, they are making an inference about how the signal is generated. The actual purpose of the signal is completely irrelevant.

Hehhh... I didn't say they were looking for intent AND purpose I said intent or purpose. In this case isn't a "manufactured" signal a signal with intention rather we know what it's intention is or not?
 
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Jjmcubbin

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Actually we are not saying genetic similarity doesn't show any evidence of relationship. What we are saying is that it is only helpful in those cases where we have evidence that there is a possibility for relationship. Here's what I'm talking about. We know humans create humans. This has been a common observation since the beginning of humanity. We know that all other kinds reproduce after their kind. This also...observation. So when we look at the genetic code between two human siblings and find they are nearly a match, and then look at the codes between two very different cultural groups and see close similarity but much more distance, we can make the logical conclusion that the closer the similarity is between humans, the closer related they are.


On the other hand we have never observed a common ancestor produce two major and different forms over vast amounts of time. Therefore it is not anymore logical to say that similarity between genes in chimps and genes in humans means they are related, than it would be to claim that a scale that accurately weighs a sub atomic particle can accurately weigh a freight train.
Do you see the contradiction?
You say since genomes of siblings are more closely related than two random persons, they are related.

Then you say that the same does not apply when the genomes of chimps and bonobos are more closely related to the human genome than any other species.
 
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BradB

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Do you see the contradiction?
You say since genomes of siblings are more closely related than two random persons, they are related.

Then you say that the same does not apply when the genomes of chimps and bonobos are more closely related to the human genome than any other species.

I thought I did a fairly good job of explaining why it is not a contradiction. If you have a bathroom scale that says you weigh 1000 lbs. You would suspect it was not working correctly. If you put a pencil on the scale and it read 0.015 pounds you could not say that the scale was working simply because it gave the correct weight of a pencil. But if you took a weight off of your bench press and set it on the scale you now have something of known weight to test the "test," so to speak. We know that humans produce humans (that's the known) so if our genetic "scale" between one human and another says they are closely related, we have good logical reasons to believe the scale is correct. But that logic doesn't hold up with the genetics between two different forms. We do not have the "known weight" principle to trust the test and are only assuming that because it holds true between two of the same form that it will hold true for two different forms. That is saying that because your bathroom scale weighs a pencil correctly it can weigh a bus correctly. We don't "know" this from a scientific stand point and we can't know this.
 
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Jimmy D

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I thought I did a fairly good job of explaining why it is not a contradiction. If you have a bathroom scale that says you weigh 1000 lbs. You would suspect it was not working correctly. If you put a pencil on the scale and it read 0.015 pounds you could not say that the scale was working simply because it gave the correct weight of a pencil. But if you took a weight off of your bench press and set it on the scale you now have something of known weight to test the "test," so to speak. We know that humans produce humans (that's the known) so if our genetic "scale" between one human and another says they are closely related, we have good logical reasons to believe the scale is correct. But that logic doesn't hold up with the genetics between two different forms. We do not have the "known weight" principle to trust the test and are only assuming that because it holds true between two of the same form that it will hold true for two different forms. That is saying that because your bathroom scale weighs a pencil correctly it can weigh a bus correctly. We don't "know" this from a scientific stand point and we can't know this.

If the field of genetics only dealt with vague generalities you might have a point.

Of course that isn’t the case.
 
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BradB

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If the field of genetics only dealt with vague generalities you might have a point.

Of course that isn’t the case.

So you are saying there is some other reason to believe similar genes between chimps and humans equates to relationship? Some "known weight" that demonstrates this to be the case? Please do go on.
 
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Jimmy D

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So you are saying there is some other reason to believe similar genes between chimps and humans equates to relationship? Some "known weight" that demonstrates this to be the case? Please do go on.

No, that’s not what I said, maybe I didn’t express my thoughts adequately.

My point was that tales about bathroom scale calibrations are meaningless (outside of a bathroom scale calibration forum of course) in a discussion about genetics.
 
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Brightmoon

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Actually we are not saying genetic similarity doesn't show any evidence of relationship. What we are saying is that it is only helpful in those cases where we have evidence that there is a possibility for relationship. Here's what I'm talking about. We know humans create humans. This has been a common observation since the beginning of humanity. We know that all other kinds reproduce after their kind. This also...observation. So when we look at the genetic code between two human siblings and find they are nearly a match, and then look at the codes between two very different cultural groups and see close similarity but much more distance, we can make the logical conclusion that the closer the similarity is between humans, the closer related they are.


On the other hand we have never observed a common ancestor produce two major and different forms over vast amounts of time. Therefore it is not anymore logical to say that similarity between genes in chimps and genes in humans means they are related, than it would be to claim that a scale that accurately weighs a sub atomic particle can accurately weigh a freight train.
https://migration.files.wordpress.com/2009/03/animalsevolution_lg.jpeg

Sorry it’s in German but German and English also share enough of a common ancestry that you should be able to understand it. ;)

Here’s how animals are related . You do have to look at juveniles or fetal forms to see common ancestry and this is something Darwin would have been aware of . DNA and genetics only confirm this . So stop spouting your favorite creationist lie about no evidence for common descent between major forms because this is animal life at its most basic
 
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tas8831

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Sorry to hear that. One cannot determine specificity of something without knowing what it does.

LOL!

So what good is the ID concept?

It cannot predict specificity? It has no means of finding specificity unless the IDist is told what it does?

GAME SHOW HOST: The question is xxx?

CONTESTANT: Um, I don't know - tell me the answer, and then I can tell you!

GAME SHOW HOST: You must be an Intelligent Design Advocate...

I already explained this in an earlier post. In order to recognize specificity the observer must make the connection from a previous experience. But just because he cannot make the connection doesn't negate its existence. We know the code in DNA does something and we know it does something very specific.

How specific and how do you know?

Your precision is lacking. You seem to be making an argument from analogy (...make the connection from a previous experience...). Analogies are not evidence.
Good for you. Perhaps you should save such questions for a geneticist who is also an IDist. I couldn't tell you what a line written in Spanish said. Does that mean Spanish language is not a specified language?

It means that you should not be telling people that you can speak Spanish - but only if others tell you what the words mean first.
 
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tas8831

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I know right? Most evolutionists hate discussing the topic of abiogenesis.
Hate it?

I will discuss it - like the amount of research that is being done on the subject in contrast to how much research creationists do on Creation.

I will discuss how creationist hate to admit that abiogenesis and evolution are separate topics, yet love to conflate them because they think they will have more leverage since there is less known about abiogenesis.

I will discuss that there is evidence for the abiotic synthesis of many of the precursor molecules for those utilized in the metabolism and 'construction' of living things, whereas creationists think that a deity speaking is a real mechanism for turning dust into these same molecules.
 
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tas8831

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That's because every experiment performed to date which produces proteins, is totally incompatible with every other process, and you need them all to start at the same time. Sort of leaves them with a bunch of goo that does nothing.

LOL!

Citation please.
 
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tas8831

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I wrote to you before that I had read several of the previous threads in which you pull out your repetitive arguments and just re-post them no matter what the previous attempts had accomplished (nothing - your claims appeared to have been demolished each time). I have no intention of re-hashing the same arguments you've tried before, so I am not going to respond to this right now.
Thought I had better respond to this one before it drifted too far into the stacks.



I'm not entirely sure what you mean here but no, I'm not the first Creationist to take an interest in the evidencial approach to the subject of origins.



Yes I know, there are many such papers out there.

Among the mutations that affect a typical gene, different kinds produce different impacts. A very few are at least momentarily adaptive on an evolutionary scale. Many are deleterious. (Rates of Spontaneous Mutation. Genetics, 1998)
If we are going to consider mutations (copy errors) as driving adaptive evolution we do well to consider their effects.



It seems to me there are more mechanisms preventing and repairing mutations from having an effect, then there are benefits from mutations in adaptive evolution.

230px-DNA_Repair.jpg

DNA ligase, shown above repairing chromosomal damage, is an enzyme that joins broken nucleotides together by catalyzing the formation of an internucleotide ester bond between the phosphate backbone and the deoxyribose nucleotides. (DNA Repair. Wikipedia)
There is also this from the Rates of Spontaneous Mutation paper quoted and cited above:

Organisms limit their mutation rates by diverse mechanisms. These include metabolic controls over concentrations of endogenous and exogenous mutagens, pre-replication DNA repair systems, the insertion accuracy of polymerases, 3′-exonucleolytic proofreading, and several post-replication systems for repairing mismatches. Different organisms apply different sets of these mechanisms, and the efficiency of a particular mechanism varies among organisms. Sometimes an organism's mutation rate is considered to be “determined” by the particular set of mechanisms it applies. (Rates of Spontaneous Mutation. Genetics, 1998)​



Just think it's one of evolutionary biology's head twisters is all.



Not really a big interest of mine, just a passing remark really.



That's simple enough, the role of mutations in the evolution of the human brain from that of apes is well qualified:

One of the study's major surprises is the relatively large number of genes that have contributed to human brain evolution. “For a long time, people have debated about the genetic underpinning of human brain evolution,” said Lahn. “Is it a few mutations in a few genes, a lot of mutations in a few genes, or a lot of mutations in a lot of genes? The answer appears to be a lot of mutations in a lot of genes. We've done a rough calculation that the evolution of the human brain probably involves hundreds if not thousands of mutations in perhaps hundreds or thousands of genes—and even that is a conservative estimate.” (Human Brain Evolution Was a 'Special Event')
The burden of proof was and is, how do you get the requiste changes required for the evolution of the human brain 2mya ago:

Since then they have discovered at least two dramatic giant leaps that would have had to occur in order of the human brain to have emerged from ape like ancestors SRGAP2, HAR1F. In addition genes involved with the development of language (FOXP2), changes in the musculature of the jaw (MYH16) , and limb and digit specializations (HACNS1).

The ancestral SRGAP2 protein sequence is highly constrained based on our analysis of 10 mammalian lineages. We find only a single amino-acid change between human and mouse and no changes among nonhuman primates within the first nine exons of the SRGAP2 orthologs. This is in stark contrast to the duplicate copies, which diverged from ancestral SRGAP2A less than 4 mya, but have accumulated as many as seven amino-acid replacements compared to one synonymous change. (Human-specific evolution of novel SRGAP2 genes by incomplete segmental duplication Cell May 2012)​

What is the problem with 7 amino acid replacements in a highly conserved brain related gene? The only observed effects of changes in this gene in humans is disease and disorder:
  • 15,767 individuals reported by Cooper et al. (2011)] for potential copy-number variation. We identified six large (>1 Mbp) copy-number variants (CNVs), including three deletions of the ancestral 1q32.1 region…
  • A ten year old child with a history of seizures, attention deficit disorder, and learning disabilities. An MRI of this patient also indicates several brain malformations, including hypoplasia of the posterior body of the corpus callosum…
  • Translocation breaking within intron 6 of SRGAP2A was reported in a five-year-old girl diagnosed with West syndrome and exhibiting epileptic seizures, intellectual disability, cortical atrophy, and a thin corpus callosum. (Human-specific evolution of novel SRGAP2 genes by incomplete segmental duplication Cell May 2012)
The search for variation with regard to this vital gene yielded no beneficial effect upon which selection could have acted. The only conceivable way the changes happen is relaxed functional constraint which, unless it emerged from the initial mutation perfectly functional it surly would have killed the host. Mutations are found in children with 'developmental delay and brain malformations, including West Syndrome, agenesis of the corpus callosum, and epileptic encephalopathies'.(cited above)

Of course Creationists have their opinions about this gene:

SRGAP2A, SRGAP2B, SRGAP2C, and SRGAP2D, which are located in three completely separate regions on chromosome number 1.1 They appear to play an important role in brain development.2 Perhaps the most striking discovery is that three of the four genes (SRGAP2B, SRGAP2C, and SRGAP2D) are completely unique to humans and found in no other mammal species, not even apes…Unique in their protein coding arrangement and structure. The genes do not look duplicated at all… (Newly Discovered Human Brain Genes Are Bad News for Evolution by Jeffrey P. Tomkins, Ph.D)​

In one of the areas of the human genome that would have had to change the most, Human Accelerated Region (HAR), we find a gene that has changed the least over just under 400 million years HAR1F. Just after the Cambrian is would have had to emerge de novo, fully formed, fully functional and permanently fixed along broad taxonomic categories. In all the time since it would allow only two substitutions, then, while the DNA around it is being completely overhauled it allows 18 substitutions in a regulatory gene only 118 nucleotides long. The vital function of this gene cannot be overstated:

The most dramatic of these ‘human accelerated regions’, HAR1, is part of a novel RNA gene (HAR1F) that is expressed specifically in Cajal– Retzius neurons in the developing human neocortex from 7 to 19 gestational weeks, a crucial period for cortical neuron specification and migration. HAR1F is co-expressed with reelin, a product of Cajal–Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. (An RNA gene expressed during cortical development evolved rapidly in humans, Nature 16 August 2006)​

This all has to occur after the chimpanzee human split, while our ancestors were contemporaries in equatorial Africa, with none of the selective pressures effecting our ancestral cousins. This is in addition to no less then 60 de novo (brand new) brain related genes with no known molecular mechanism to produce them. Selection can explain the survival of the fittest but the arrival of the fittest requires a cause:

The de novo origin of a new protein-coding gene from non-coding DNA is considered to be a very rare occurrence in genomes. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee. The functionality of these genes is supported by both transcriptional and proteomic evidence. RNA– seq data indicate that these genes have their highest expression levels in the cerebral cortex and testes, which might suggest that these genes contribute to phenotypic traits that are unique to humans, such as improved cognitive ability. Our results are inconsistent with the traditional view that the de novo origin of new genes is very rare, thus there should be greater appreciation of the importance of the de novo origination of genes…(De Novo Origin of Human Protein-Coding Genes PLoS 2011)
Whatever you think happened one thing is for sure, random mutations are the worst explanation possible. They cannot produce de novo genes and invariably disrupt functional genes.



God created humans and apes originally and they have separate lineages.



Currently I'm a warehouse worker, my bachelors is in Bible and Theology. I'm more like a liberal arts student and life science buff then a scientist. My interest has been in fossils and comparative genomics, what I've been most focused on the the genetic basis of the evolution of the human brain from that of apes. It's always nice to encounter a professional educator or real world scientist on here. You always learn something.

Grace and peace,
Mark
 
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tas8831

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You may think that the Miller experiment offered a ray of hope for the evolutionist, because he was able to create a few amino acids in an array that supposedly simulated the early primitive earth atmosphere. At the time it was commonly believed that the early atmosphere consisted of Methane, Ammonia, Hydrogen, and water vapor, which is precisely what Miller used in his array. He then shot electrical arcs through the apparatus to simulate lightning and eventually collected some amino acids at the bottom of the mixture. Amino acids are of course the building blocks for proteins which are the building blocks for cells. Many believed that Miller had proven that life could have spontaneously formed under early atmosphere conditions, given enough time for chance to put the components all together. However many other scientists have questioned the validity of the experiment pointing out that it didn't accurately represent what the early atmosphere would have been like. They argued that Hydrogen would have escaped into the outer atmosphere and therefore the early earth's atmosphere consisted of a Nitrogen, Carbon dioxide, and water vapor composition. Numerous experiments were done with this mixture, including by Miller, and had negative results.

So for the sake of argument let's say Miller had the atmosphere right. What did he actually create? A few amino acids? But those are not proteins.

Snipped the ridiculous attempts at 'probability calculations' -

I suggest that you read this:

EXOBIOLOGY: An Interview with Stanley L. Miller

In it, Miller actually explains why he did his experiments.

Creationist have misrepresented him, his motives, his claims and conclusions, etc. It has to be purposeful, IMO.


After you read that and correct your missive, perhaps you can impress us with all of the great creation-related research creation scientists have done.

And by creation-related research, I do not mean pathetic and dishonest attempts to poke holes in evolution, I mean actual research into creation.
 
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mark kennedy

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I wrote to you before that I had read several of the previous threads in which you pull out your repetitive arguments and just re-post them no matter what the previous attempts had accomplished (nothing - your claims appeared to have been demolished each time). I have no intention of re-hashing the same arguments you've tried before, so I am not going to respond to this right now.
Well then don't but what your ignoring is the burden of proof, particularly with regards to brain related genes. Generalizations about mutation plus selection doesn't change what the fossil evidence and genomic comparisons are telling us. Brain related genes had to undergo a massive overhaul requiring hundreds, if not thousands of mutations in hundreds if not thousands of genes. That's not my conclusion, that's from Bruce Lahn. There are also 60 de novo genes that are unique to the human genome inextricably linked to the size and complexity of the human brain as compared to apes. 2 1/2 million years ago our hominid ancestors would have had a cranial capacity would have been under 600 cc, then about 1.9 million years ago with Turkana Boy and the Homo erectus fossils they are approaching modern human proportions.

Dismiss it, ignore it if you please, it's a typical response. I repeat those facts because as of right now they have went unanswered and calling them 'demolished' is begging the question of proof on your hands and knees.
 
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tas8831

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I thought I did a fairly good job of explaining why it is not a contradiction. If you have a bathroom scale that says you weigh 1000 lbs. You would suspect it was not working correctly. If you put a pencil on the scale and it read 0.015 pounds you could not say that the scale was working simply because it gave the correct weight of a pencil. But if you took a weight off of your bench press and set it on the scale you now have something of known weight to test the "test," so to speak. We know that humans produce humans (that's the known) so if our genetic "scale" between one human and another says they are closely related, we have good logical reasons to believe the scale is correct. But that logic doesn't hold up with the genetics between two different forms. We do not have the "known weight" principle to trust the test and are only assuming that because it holds true between two of the same form that it will hold true for two different forms. That is saying that because your bathroom scale weighs a pencil correctly it can weigh a bus correctly. We don't "know" this from a scientific stand point and we can't know this.

Always analogies.


Here is why you analogies fail (I will probably get dinged from spam, as I have felt the need to re-post this a dozen times - but creationists keep ignoring it):

I forget now who originally posted these on this forum, but I keep it in my archives because it offers a nice 'linear' progression of testing a methodology and then applying it:

The tested methodology:

Science 25 October 1991:
Vol. 254. no. 5031, pp. 554 - 558

Gene trees and the origins of inbred strains of mice

WR Atchley and WM Fitch

Extensive data on genetic divergence among 24 inbred strains of mice provide an opportunity to examine the concordance of gene trees and species trees, especially whether structured subsamples of loci give congruent estimates of phylogenetic relationships. Phylogenetic analyses of 144 separate loci reproduce almost exactly the known genealogical relationships among these 24 strains. Partitioning these loci into structured subsets representing loci coding for proteins, the immune system and endogenous viruses give incongruent phylogenetic results. The gene tree based on protein loci provides an accurate picture of the genealogical relationships among strains; however, gene trees based upon immune and viral data show significant deviations from known genealogical affinities.

======================

Science, Vol 255, Issue 5044, 589-592

Experimental phylogenetics: generation of a known phylogeny

DM Hillis, JJ Bull, ME White, MR Badgett, and IJ Molineux
Department of Zoology, University of Texas, Austin 78712.

Although methods of phylogenetic estimation are used routinely in comparative biology, direct tests of these methods are hampered by the lack of known phylogenies. Here a system based on serial propagation of bacteriophage T7 in the presence of a mutagen was used to create the first completely known phylogeny. Restriction-site maps of the terminal lineages were used to infer the evolutionary history of the experimental lines for comparison to the known history and actual ancestors. The five methods used to reconstruct branching pattern all predicted the correct topology but varied in their predictions of branch lengths; one method also predicts ancestral restriction maps and was found to be greater than 98 percent accurate.

==================================

Science, Vol 264, Issue 5159, 671-677

Application and accuracy of molecular phylogenies

DM Hillis, JP Huelsenbeck, and CW Cunningham
Department of Zoology, University of Texas, Austin 78712.

Molecular investigations of evolutionary history are being used to study subjects as diverse as the epidemiology of acquired immune deficiency syndrome and the origin of life. These studies depend on accurate estimates of phylogeny. The performance of methods of phylogenetic analysis can be assessed by numerical simulation studies and by the experimental evolution of organisms in controlled laboratory situations. Both kinds of assessment indicate that existing methods are effective at estimating phylogenies over a wide range of evolutionary conditions, especially if information about substitution bias is used to provide differential weightings for character transformations.



We can ASSUME that the results of an application of those methods have merit.


Application of the tested methodology:

Implications of natural selection in shaping 99.4% nonsynonymous DNA identity between humans and chimpanzees: Enlarging genus Homo

"Here we compare ≈90 kb of coding DNA nucleotide sequence from 97 human genes to their sequenced chimpanzee counterparts and to available sequenced gorilla, orangutan, and Old World monkey counterparts, and, on a more limited basis, to mouse. The nonsynonymous changes (functionally important), like synonymous changes (functionally much less important), show chimpanzees and humans to be most closely related, sharing 99.4% identity at nonsynonymous sites and 98.4% at synonymous sites. "



Mitochondrial Insertions into Primate Nuclear Genomes Suggest the Use of numts as a Tool for Phylogeny

"Moreover, numts identified in gorilla Supercontigs were used to test the human–chimp–gorilla trichotomy, yielding a high level of support for the sister relationship of human and chimpanzee."



A Molecular Phylogeny of Living Primates

"Once contentiously debated, the closest human relative of chimpanzee (Pan) within subfamily Homininae (Gorilla, Pan, Homo) is now generally undisputed. The branch forming the Homo andPanlineage apart from Gorilla is relatively short (node 73, 27 steps MP, 0 indels) compared with that of thePan genus (node 72, 91 steps MP, 2 indels) and suggests rapid speciation into the 3 genera occurred early in Homininae evolution. Based on 54 gene regions, Homo-Pan genetic distance range from 6.92 to 7.90×10−3 substitutions/site (P. paniscus and P. troglodytes, respectively), which is less than previous estimates based on large scale sequencing of specific regions such as chromosome 7[50]. "




Catarrhine phylogeny: noncoding DNA evidence for a diphyletic origin of the mangabeys and for a human-chimpanzee clade.

"The Superfamily Hominoidea for apes and humans is reduced to family Hominidae within Superfamily Cercopithecoidea, with all living hominids placed in subfamily Homininae; and (4) chimpanzees and humans are members of a single genus, Homo, with common and bonobo chimpanzees placed in subgenus H. (Pan) and humans placed in subgenus H. (Homo). It may be noted that humans and chimpanzees are more than 98.3% identical in their typical nuclear noncoding DNA and probably more than 99.5% identical in the active coding nucleotide sequences of their functional nuclear genes (Goodman et al., 1989, 1990). In mammals such high genetic correspondence is commonly found between sibling species below the generic level but not between species in different genera."
 
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tas8831

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Dismiss it, ignore it if you please, it's a typical response. I repeat those facts because as of right now they have went unanswered and calling them 'demolished' is begging the question of proof on your hands and knees.

Rather than re-hash, I simply searched:

mark, did you forget all the other times you posted this same stuff about your "3 fold expansion from earlier apes to humans" only to be shown all the intermediate transitional fossils that fill in your imagined "gap"? We could go through that all again, in addition to the genes themselves and all the over evidence - but after person after person has shown you the obvious and clear evidence time after time, year after year, I have to suspect that you'll ignore it yet again.

Then, it seems likely your responses will again be filled with empty, evidence free trash talk about shooting ghosts in a barrel on their hand and knees.

I'm just hoping you don't hide relevant data again.......

In Christ-





And one thing regarding your quote of Tomkins - he was once a decent researcher, now he appears to be little more than a carnival barker.

His claim "Perhaps the most striking discovery is that three of the four genes (SRGAP2B, SRGAP2C, and SRGAP2D) are completely unique to humans and found in no other mammal species, not even apes…" is laughably incorrect:

Gene: SRGAP2B (ENSG00000196369) - Orthologues - Homo sapiens - Ensembl genome browser 92

"The genes do not look duplicated at all…"

He says no paralogs? Also wrong:

Gene: SRGAP2B (ENSG00000196369) - Paralogue alignment - Homo sapiens - Ensembl genome browser 92

And of course he wants to pretend 'creation', right?

Human-specific evolution of novel SRGAP2 genes by incomplete segmental duplication
Human-specific evolution of novel SRGAP2 genes by incomplete segmental duplication

SUMMARY

Gene duplication is an important source of phenotypic change and adaptive evolution. We use a novel genomic approach to identify highly identical sequence missing from the reference genome, confirming the cortical development gene Slit-Robo Rho GTPase activating protein 2 (SRGAP2) duplicated three times in humans. We show that the promoter and first nine exons of SRGAP2 duplicated from 1q32.1 (SRGAP2A) to 1q21.1 (SRGAP2B) ~3.4 million years ago (mya). Two larger duplications later copied SRGAP2B to chromosome 1p12 (SRGAP2C) and to proximal 1q21.1 (SRGAP2D), ~2.4 and ~1 mya, respectively. Sequence and expression analysis shows SRGAP2C is the most likely duplicate to encode a functional protein and among the most fixed human-specific duplicate genes. Our data suggest a mechanism where incomplete duplication created a novel function —at birth, antagonizing parental SRGAP2 function 2–3 mya a time corresponding to the transition from Australopithecus to Homo and the beginning of neocortex expansion.
 
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tas8831

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In further support, I offer this debate:

mark kennedy v. Loudmouth: Do chimps and humans share a common ancestor?

These threads started by you:

Is the Human Brain a Null Hypothesis for Darwinian Evolution?

Darwinian Theator of the Mind: AKA Human Brain Evolution

And this very telling post - from a fellow Christian:



You write that, mark, when you just cut and pasted the whole OP, from the last time you posted the exact same thread, from years ago, right here: Is the Human Brain the Null Hypothesis for Darwin's Theory? ???

Wow.

Remember that time, your "misunderstanding" was fully explained to you - did you forget all that?

I see you even again hid a bunch of skulls so as to misrepresent the data. Remember, that the last several times you hid data that way, it's been pointed out?

One example where you cut and pasted the same false "gap", and were corrected, is here, from 2011:

You post the "gap" Post #32:
Why are there gaps in the fossil record?

Your misrepresentation is corrected, post #34.

Want more? A simple search using the search engine in the upper right shows plenty of times you've cut and pasted the same misrepresentations, and been corrected.

And now we have yet another of mark's cut and past misleading threads.

In Christ-

Papias

P.S. I see that you've also started another identical cut & paste thread in the Christians only section, at this link: Is the Human Brain a Null Hypothesis for Darwinian Evolution? mark, how many times have you cut and pasted this same misrepresentation? I've lost count, so could you help me out with a number?



Same basic arguments - not once ignored, but multiple times refuted.
 
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Justatruthseeker

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tas8831

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You know it as well. but then that's why you didnt provide any sources that contradict what I said.

We can start with RNA if you would like, the now claim to fame.

The RNA world hypothesis: the worst theory of the early evolution of life (except for all the others)a


Allow me to point out that what I was asking you to provide citations for was this claim of yours:

"That's because every experiment performed to date which produces proteins, is totally incompatible with every other process, and you need them all to start at the same time. Sort of leaves them with a bunch of goo that does nothing."

Bashing the RNA world hypothesis, I am pretty sure, does not encompass "EVERY EXPERIMENT PERFORMED" which produces proteins.

Tell me again where the original Asian came from?
 
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