Evolution's Brick Wall

[mark kennedy]

And again, without a predictive model for creation, the answer is no.

You don't need on so why should I? That's to say nothing of the 3:1 ratio of dominant to recessive traits being the vast majority of variation. Your not really saying much here, and clearly are oblivious to existing predictive models.

 

[Justatruthseeker]

And to clarify on what I mean when I say that cladistics are based on differences.

A fish has scales. A mammal does not. This is an observed differenceand it's used to classify what is a fish and what is not a fish. So by examining traits of fish, and differences between fish and not fish, we construct a fish clade.

Mutations create differences in DNA. It is these differences that are compared. How different is the HARf1 strand between people and chimps or chimps and chickens? That's what they were doing and talking about in the research. And by comparing what has changed and by comparing differences, they established rates of mutations.

X number of genes are different between animal A and animal B, therefore X amount of differences must have arisen in Y amount of time (the time since the last common ancestor).

So both paleontology and geneticists are looking at both similarities and differences when constructing the bush of life or tree of life or whatever you would like to call it.

No. Just because x amount of differences are observed now between Aand B, does not mean there were not always x amount of differences.

You are assuming they were once the same when no evidence exists that this was ever so..... No one was there to test the original similarities or differences at the claimed divergence points. The starting points are all assumed.....

 

[pitabread]

You don't need on so why should I?

If you want to argue for creation, you need to have something with which to argue for. Merely arguing against evolution doesn't cut it.

We already know how organisms reproduce and evolve over time. We don't know how organisms are created from scratch.

If you want to argue the latter, you can start by explaining how organisms would be created and what we would expect to observe if such a mechanism had been used in the past.

 

[Justatruthseeker]

If you want to argue for creation, you need to have something with which to argue for. Merely arguing against evolution doesn't cut it.

We already know how organisms reproduce and evolve over time. We don't know how organisms are created from scratch.

If you want to argue the latter, you can start by explaining how organisms would be created and what we would expect to observe if such a mechanism had been used in the past.

Similarities between creatures, yet differences as well. All fossils remaining the same across the assumed millions of years with new forms arising suddenly where they didn't exist before due to mating.

What else would you expect if you made everything from the same protons, electrons and neutrons?

So at the basic of levels all elements share similarities but are themselves vastly different, the same as life.

But isn’t it evolutionists themselves that argue abiogenesis is separate from evolution after genesis? So creation is separate from variation after genesis....

 

[pitabread]

But isn’t it evolutionists themselves that argue abiogenesis is separate from evolution after genesis? So creation is separate from variation after genesis....

Creationists are arguing that individual species were created in lieu of having evolved from earlier species. Therefore, if creationists want to argue that, they need to provide a predictive model (which would likely include having a mechanism from which to derive such a model).

So I'll ask you: if you believe human beings were created from scratch, how were they created (even hypothetically)? And from describing how it happened, what sort of predictive evidence could we look for that would confirm how this occurred?

 

[Job 33:6]

You totally missing the point, it comes down to cause and effect. Mutations in brain related genes result in disease and disorder, not adaptive evolution. That's not my opinion, it's a well established fact. The HAR 1f gene allows 2 substitutions in 300 million years and you know this f you actually read the paper, then there are 18 for no apparent reason with no conceivable cause. Functional constraint is only relaxed under very rare conditions and usually to preserve the Intigrity of the DNA, not to change it. One thing is sure, mutations are the worst possible explaination, because there is no such thing as a beneficial effect from a mutation in a brain related gene, let alone an adaptive trait on an evolutionary scale.

What? Are you suggesting that all mutations related to brain development cannot occur without it being degenerative?

And only in your own mind are their no conceivable reasons for accelerated rates of evolution. Stephen J Gould actually has a lot of talks about just this in relation to Cambrian fuana. If you would like, I can quote some of his material for you. And really punctuated equilibrium is all about varying rates of evolution.

 

[pitabread]

What? Are you suggesting that all mutations related to brain development cannot occur without it being degenerative?

Mark has been given examples to the contrary in the past. However this is just his schtick, regurgitating the same tired points over and over.

edited to add: IIRC, this was one of the examples:
https://www.news-medical.net/news/2...people-to-require-less-sleep-than-others.aspx

http://www.pnas.org/content/early/2018/03/06/1801693115

 

[Job 33:6]

Oh they established the rate of mutation, do tell.

Well, if you have 18 mutations in 7 million years, that in and of itself is a rate. And if prior there were 2 mutations in 300 million years, that in and of itself is a rate of mutation as well.

 

[Justatruthseeker]

Well, if you have 18 mutations in 7 million years, that in and of itself is a rate. And if prior there were 2 mutations in 300 million years, that in and of itself is a rate of mutation as well.

But the vast majority of mutations are neutral, so there were differences to begin with, not similarities, the net change amounting to no change due to neutral mutations.

So they are in reality assuming change from similarity, even when they know the vast majority of mutation amount to no net change, so indicate original differences, not similarities.

 

[Justatruthseeker]

Creationists are arguing that individual species were created in lieu of having evolved from earlier species. Therefore, if creationists want to argue that, they need to provide a predictive model (which would likely include having a mechanism from which to derive such a model).

So I'll ask you: if you believe human beings were created from scratch, how were they created (even hypothetically)? And from describing how it happened, what sort of predictive evidence could we look for that would confirm how this occurred?

I already told you what evidence. Life showing no change at all. New forms appearing suddenly. Just as is observed in the fossil record.

Now evolution would predict constant change, the exact opposite of what we observe. And no, there is no cheating and proposing that on every single evolutionary tree where supposedly the splits took place to join one to the other, we are required to insert missing ancestors.

Unacceptable for every single claimed split, not just a few hundred or even thousands.

 

[Job 33:6]

.

Mark has been given examples to the contrary in the past. However this is just his schtick, regurgitating the same tired points over and over.

edited to add: IIRC, this was one of the examples:
https://www.news-medical.net/news/2...people-to-require-less-sleep-than-others.aspx

http://www.pnas.org/content/early/2018/03/06/1801693115

I thought the discussion on whether or not there were beneficial mutations was settled long ago.

 

[Justatruthseeker]

You have no idea what you're talking about. You didn't months ago when we first spoke (and when I first added you to the ignore list) and you still don't to this day (on the rare occasion that I actually look at your posts). But you are persistent. I'll give you that.

Blah, blah, blah is what I hear.

Every single person on this forum knows the truth of what I just said, that the vast majority of mutations are neutral.

Run and hide, ignore what you know to be true to protect your fragile ego’s......

And you all call yourself scientific when you can’t even admit to the truth that the majority of mutations are neutral.

But go ahead, defend your blabbering and show us all where the vast majority of mutations are not neutral....

Well, speak up..... show your evidence....

You are better off ignoring me before you look more the fool and propaganda machine....

 

[mark kennedy]

What? Are you suggesting that all mutations related to brain development cannot occur without it being degenerative?

Show me a single exception.

And only in your own mind are their no conceivable reasons for accelerated rates of evolution. Stephen J Gould actually has a lot of talks about just this in relation to Cambrian fuana. If you would like, I can quote some of his material for you. And really punctuated equilibrium is all about varying rates of evolution.

This isn't about fauna but I always enjoy Goulds stuff. Bow I don't know what you think but with punctuated equilibrium the hopefull monster would have his work cut out for him. This all happens two million years ago, without precursors, no more then a couple of hundred thousad years to facilitate and permenantly fix this extra ordinary giant leap.

 

[mark kennedy]

Double post.

 

[mark kennedy]

Blah, blah, blah is what I hear.

Every single person on this forum knows the truth of what I just said, that the vast majority of mutations are neutral.

Run and hide, ignore what you know to be true to protect your fragile ego’s......

And you all call yourself scientific when you can’t even admit to the truth that the majority of mutations are neutral.

But go ahead, defend your blabbering and show us all where the vast majority of mutations are not neutral....

Well, speak up..... show your evidence....

You are better off ignoring me before you look more the fool and propaganda machine....

Its not his fault, they have long regarded any change to be a mutation even if the modification of a DNA strain is through a presently unknown molecular process. Researchers identify this 'weird cluster of nucleotides' in bacteria. Come to find out it was capson 9, aka the krispur gene. It modified the bacteria immune system. Previously the cause had long been thought to be the result of mutations. The nylon eating bug had an adaptive trait allowing certain bacteria to digest nylon, it turns out an existing reading frame had neen swapped out.

Regardless, mutations are the worst explanation possible. Mutations are copy errors, in the G2 phase of cell explication the DNA is replicated. There is a quality control process and if mistakes cannot be repaired the cell is recycled through a process known as apostasis.

Most variation with regard to selective traits do not come from mutation, when they have an effect it is deleterious the vast majority of the time. The alleles (traits/alternate genes) are Mendelian processes that have little, if anything, to do with genetic mutations.

 

[mark kennedy]

Well, if you have 18 mutations in 7 million years, that in and of itself is a rate. And if prior there were 2 mutations in 300 million years, that in and of itself is a rate of mutation as well.

Thats based on comparisons, not mutation rate. There are no mutation rates because in this highly conserved gene there are no alternate gene sequences, diseased or othwise since a change, unless fully complte and functional, it would be lethal.

 

[Job 33:6]

Show me a single exception.



This isn't about fauna but I always enjoy Goulds stuff. Bow I don't know what you think but with punctuated equilibrium the hopefull monster would have his work cut out for him. This all happens two million years ago, without precursors, no more then a couple of hundred thousad years to facilitate and permenantly fix this extra ordinary giant leap.

https://www.nature.com/news/human-brain-shaped-by-duplicate-genes-1.10584

https://www.karger.com/Article/FullText/443947
Discussion
The result indicates that the SRGAP2 gene may have a significant role in the progression of overall brain size in mammals. These findings also provide strong evidence that the evolution of the SRGAP2 gene is intimately linked to the expansion of neuron numbers in the brain cortex of mammals. The brain mass and neuron number in the cortex are linearly correlated in mammals, and this finding is consistent with the earlier findings in primate brains [8]. The ancestral SRGAP2 gene in all mammalian lineages is subjected to a strong purifying selection in order to maintain the functional role of the gene. The deleterious mutations within a functional gene are amenable to a purifying selection and less likely to be fixed in a population. Thus, the signature of the purifying selection is imprinted on a gene in form of a substantial reduction in the amino acid substitution process. Moreover, the increase in the neuron number is negatively correlated with the substitution rates and nonsynonymous changes in different mammalian lineages. The stasis in terms of nonsynonymous changes indicates that the structure of the SRGAP2 protein was constrained in the last common ancestor of humans and chimpanzees. It seems that the natural selection has opted for an optimal protein structure of SRGAP2 that can carry out a specific function to maintain not only the maximal number of neurons but also the maximum size of the brain. However, the extraordinary increase in the brain size and neuron number in humans has been attributed to the novel copy (SRGAP2C) of the SRGAP2 gene [9]. It appears that SRGAP2Acontinues to maintain its ancestral function in humans, and the new duplicate, namely SRGAP2C,adopts a new function in humans and mediates the accelerated growth of the brain and the number of cortical neurons. This study clearly indicates that the ancestral SRGAP2 gene did play a very crucial role in the evolution of the brain size and the neuron number throughout the mammalian evolution. Therefore, the key role of the ancestral SRGAP2 gene in the manifestation of a large brain with a large number of neurons in the primate lineage cannot be ruled out before its duplication in the human lineage. In the human lineage, the novel SRGAP2C gene accumulated 7 amino acid substitutions within a short span of 4 million years after duplication from a highly constrained ancestral gene, SRGAP2A[10]. The relaxation of selective pressure on the SRGAP2Cgene might have played a crucial role in the manifestation of some of the human-specific high-level cognitive functions in the human lineage. The SRGAP2C protein is known to heteromerize with its ancestral protein SRGAP2A resulting in an antagonistic function equivalent to the knock-out of the ancestral gene [11]. It will be interesting to know whether any other brain-specific gene is interacting with this novel copy of SRGAP2C in a synergistic or antagonistic manner. It can be speculated that the human brain would not have reached this extraordinary level in terms of intelligence in the absence of this novel duplicated gene. Therefore, further evolutionary studies on the other novel duplicate genes in humans along with their ancestral paralogous genes in mammals will unveil the genomic basis of extraordinary human intelligence. The signature of local molecular clocks in ape and rodent lineages indicates that the constant rate of substitution in the SRGAP2 gene in two distantly related lineages is shaped by various selective forces.

The major increase in the brain size and neuron number in two distant lineages, namely humans and elephants, is an example of parallel and convergent patterns of adaptive phenotypic evolution. This hypothesis can be supported by the fact that aerobic energy metabolism genes in the brain evolved adaptively in human and elephant lineages in addition to the presence of other common traits, such as large brain, high intelligence, social bond, long gestation period and long life span [24]. The elephant has a large brain size with a maximum number of neurons (257 billions); nevertheless, the cerebral cortex of elephants contains only about one third of the number of cortical neurons present in humans [25]. Although elephants have a lower number of cortical neurons, they exhibited many advanced cognitive abilities which they share with humans, such as insightful problem solving and tool use [26]. The evolution of shared neural traits in humans and elephants might be due to regular interactions and frequent conflicts between two distantly related species in a common ecological niche throughout their evolutionary history. The drastic difference in the brain size and the number of cortical neurons between humans and chimpanzees, despite maintaining an identical sequence structure by the SRGAP2 gene and encoded protein, may be attributed to the altered gene expression or expression of the duplicated SRGAP2C gene in humans.

The presence of a large brain in the human-chimpanzee common ancestor and a reduction in the brain size and neuron numbers in the derived early hominids and the recent chimpanzee lineages is not consistent with available fossil evidences. It clearly indicates that the brain size and neuron numbers were considerably reduced in the ancestral human lineage (320-380 cm3 in Sahelanthropus) [27] as well as in the chimpanzee lineage. The fossil evidences suggested that there was a substantial decrease in endocranial volume in recent human populations in different parts of the world during the last 10,000 years [28]. It has been argued that the reduction in body size may be the primary cause for this decrease in the brain size [29]. Therefore, the human-chimpanzee common ancestor might have a larger body size with a comparable brain size and number of cortical neurons. However, this study indicates that a considerable decrease in the brain size and body size in both human and chimpanzee lineages occurred after the split, probably due to existing environmental conditions and other genetic factors. The molecular findings of the brain size are not consistent with fossil records due to the fact that the brain size reported from fossil records may not be accurate estimates of the brain size in the common ancestor of human and chimpanzee. The estimates from crushed or incomplete fragments of fossil records are prone to inaccuracy in measurement with a large margin of error.

The rate of amino acid substitution during protein evolution is guided by the stringency of functional constraint. Proteins with a rigorous function are likely to accumulate a less number of amino acid changes during their evolutionary history and consequently evolve slower than proteins with a weaker functional constraint. There are many examples of evolutionary constraints on genes linked with the stringency of their function. Essential genes of bacteria evolve slower than nonessential genes [30] and house-keeping genes are known to be under stronger selective constraint than tissue-specific genes [31]. Similarly, the genes coding for proteins involved in a common physiological function are likely to evolve in a correlated manner [32]. Therefore, the correlation between the evolution of a phenotypic trait and the evolution of a gene suggests a key role of the SRGAP2 gene in the manifestation of a phenotypic trait (i.e. number of neurons in the cortex) in mammals. Further studies on this gene and the interaction partners with a more elaborate neural trait dataset will give us new insights into the mechanistic role of the gene in the rapid increase in intelligence in mammals.

http://www.pnas.org/content/109/Supplement_1/10709

https://www.nature.com/articles/nature02358

And the one posted above.
http://www.pnas.org/content/early/2018/03/06/1801693115.short?rss=1

I cant tell if you are suggesting that no beneficial mutations occur at all, anywhere. Or if you are simply suggesting that you dont think any occur strictly with respect to the evolution of the brain.

Also, as Ive said before, the human chimpanzee ancestor was closer to 7 million years ago, so we are talking about 2 mutations over the span of about 6-7 million years.

 

[Job 33:6]

This isn't about fauna but I always enjoy Goulds stuff. Bow I don't know what you think but with punctuated equilibrium the hopefull monster would have his work cut out for him. This all happens two million years ago, without precursors, no more then a couple of hundred thousad years to facilitate and permenantly fix this extra ordinary giant leap.

We are fauna, so yes, it is a discussion about fauna.

 

[mark kennedy]

https://www.nature.com/news/human-brain-shaped-by-duplicate-genes-1.10584

https://www.karger.com/Article/FullText/443947
Discussion
The result indicates that the SRGAP2 gene may have a significant role in the progression of overall brain size in mammals. These findings also provide strong evidence that the evolution of the SRGAP2 gene is intimately linked to the expansion of neuron numbers in the brain cortex of mammals. The brain mass and neuron number in the cortex are linearly correlated in mammals, and this finding is consistent with the earlier findings in primate brains [8]. The ancestral SRGAP2 gene in all mammalian lineages is subjected to a strong purifying selection in order to maintain the functional role of the gene. The deleterious mutations within a functional gene are amenable to a purifying selection and less likely to be fixed in a population. Thus, the signature of the purifying selection is imprinted on a gene in form of a substantial reduction in the amino acid substitution process. Moreover, the increase in the neuron number is negatively correlated with the substitution rates and nonsynonymous changes in different mammalian lineages. The stasis in terms of nonsynonymous changes indicates that the structure of the SRGAP2 protein was constrained in the last common ancestor of humans and chimpanzees. It seems that the natural selection has opted for an optimal protein structure of SRGAP2 that can carry out a specific function to maintain not only the maximal number of neurons but also the maximum size of the brain. However, the extraordinary increase in the brain size and neuron number in humans has been attributed to the novel copy (SRGAP2C) of the SRGAP2 gene [9]. It appears that SRGAP2Acontinues to maintain its ancestral function in humans, and the new duplicate, namely SRGAP2C,adopts a new function in humans and mediates the accelerated growth of the brain and the number of cortical neurons. This study clearly indicates that the ancestral SRGAP2 gene did play a very crucial role in the evolution of the brain size and the neuron number throughout the mammalian evolution. Therefore, the key role of the ancestral SRGAP2 gene in the manifestation of a large brain with a large number of neurons in the primate lineage cannot be ruled out before its duplication in the human lineage. In the human lineage, the novel SRGAP2C gene accumulated 7 amino acid substitutions within a short span of 4 million years after duplication from a highly constrained ancestral gene, SRGAP2A[10]. The relaxation of selective pressure on the SRGAP2Cgene might have played a crucial role in the manifestation of some of the human-specific high-level cognitive functions in the human lineage. The SRGAP2C protein is known to heteromerize with its ancestral protein SRGAP2A resulting in an antagonistic function equivalent to the knock-out of the ancestral gene [11]. It will be interesting to know whether any other brain-specific gene is interacting with this novel copy of SRGAP2C in a synergistic or antagonistic manner. It can be speculated that the human brain would not have reached this extraordinary level in terms of intelligence in the absence of this novel duplicated gene. Therefore, further evolutionary studies on the other novel duplicate genes in humans along with their ancestral paralogous genes in mammals will unveil the genomic basis of extraordinary human intelligence. The signature of local molecular clocks in ape and rodent lineages indicates that the constant rate of substitution in the SRGAP2 gene in two distantly related lineages is shaped by various selective forces.

The major increase in the brain size and neuron number in two distant lineages, namely humans and elephants, is an example of parallel and convergent patterns of adaptive phenotypic evolution. This hypothesis can be supported by the fact that aerobic energy metabolism genes in the brain evolved adaptively in human and elephant lineages in addition to the presence of other common traits, such as large brain, high intelligence, social bond, long gestation period and long life span [24]. The elephant has a large brain size with a maximum number of neurons (257 billions); nevertheless, the cerebral cortex of elephants contains only about one third of the number of cortical neurons present in humans [25]. Although elephants have a lower number of cortical neurons, they exhibited many advanced cognitive abilities which they share with humans, such as insightful problem solving and tool use [26]. The evolution of shared neural traits in humans and elephants might be due to regular interactions and frequent conflicts between two distantly related species in a common ecological niche throughout their evolutionary history. The drastic difference in the brain size and the number of cortical neurons between humans and chimpanzees, despite maintaining an identical sequence structure by the SRGAP2 gene and encoded protein, may be attributed to the altered gene expression or expression of the duplicated SRGAP2C gene in humans.

The presence of a large brain in the human-chimpanzee common ancestor and a reduction in the brain size and neuron numbers in the derived early hominids and the recent chimpanzee lineages is not consistent with available fossil evidences. It clearly indicates that the brain size and neuron numbers were considerably reduced in the ancestral human lineage (320-380 cm3 in Sahelanthropus) [27] as well as in the chimpanzee lineage. The fossil evidences suggested that there was a substantial decrease in endocranial volume in recent human populations in different parts of the world during the last 10,000 years [28]. It has been argued that the reduction in body size may be the primary cause for this decrease in the brain size [29]. Therefore, the human-chimpanzee common ancestor might have a larger body size with a comparable brain size and number of cortical neurons. However, this study indicates that a considerable decrease in the brain size and body size in both human and chimpanzee lineages occurred after the split, probably due to existing environmental conditions and other genetic factors. The molecular findings of the brain size are not consistent with fossil records due to the fact that the brain size reported from fossil records may not be accurate estimates of the brain size in the common ancestor of human and chimpanzee. The estimates from crushed or incomplete fragments of fossil records are prone to inaccuracy in measurement with a large margin of error.

The rate of amino acid substitution during protein evolution is guided by the stringency of functional constraint. Proteins with a rigorous function are likely to accumulate a less number of amino acid changes during their evolutionary history and consequently evolve slower than proteins with a weaker functional constraint. There are many examples of evolutionary constraints on genes linked with the stringency of their function. Essential genes of bacteria evolve slower than nonessential genes [30] and house-keeping genes are known to be under stronger selective constraint than tissue-specific genes [31]. Similarly, the genes coding for proteins involved in a common physiological function are likely to evolve in a correlated manner [32]. Therefore, the correlation between the evolution of a phenotypic trait and the evolution of a gene suggests a key role of the SRGAP2 gene in the manifestation of a phenotypic trait (i.e. number of neurons in the cortex) in mammals. Further studies on this gene and the interaction partners with a more elaborate neural trait dataset will give us new insights into the mechanistic role of the gene in the rapid increase in intelligence in mammals.

http://www.pnas.org/content/109/Supplement_1/10709

https://www.nature.com/articles/nature02358

And the one posted above.
http://www.pnas.org/content/early/2018/03/06/1801693115.short?rss=1

I cant tell if you are suggesting that no beneficial mutations occur at all, anywhere. Or if you are simply suggesting that you dont think any occur strictly with respect to the evolution of the brain.

Also, as Ive said before, the human chimpanzee ancestor was closer to 7 million years ago, so we are talking about 2 mutations over the span of about 6-7 million years.

The SRGAP 2 gene is another comparison requiring a giant leap of adaptive evolution. Repeated gene duplications and none of the daughter genes have any of the marks of gene duplication. Major amino acid substitions that would have to be done with clockwork precision and like I keep telling you, this never happens in human brain related genes. You just showed another devastating burden of proof to add to an astronomically improbable 18 nucleotide substitution. In both example it's extensive substitutions, not point mutations or indels which are far more common. No hint of a cause just the assumption that it must be the result of mutations. Then the fact that it shows four versions of the gene and not only must the amino acid sequence have no frameshift or deleterious effects it must fold seamlessly into its three dimensional structure. Then like I keep reminding you, this all happens 2 mya without precursors, there are no members of the genus Homo prior to Homo habilis who had a chimpanzee size brain

According to one research group they compared 10 mammalian lineages, finding only one single amino acid change between the human and mouse and no changes amount nonhuman primates within the first 9 exons of SRGAP2 orthotics. In stark contrast to the duplicate copies that show as many as 7 amino acid replacements.

They search 15,767 individuals and found 6 CVN, which are variant allele. The effects of these changes were seizures, attention deficit, brain malformation, cortical atrophy etc. No known beneficial or neutral effects noted which is exactly what you would expect from such a highly constrained gene. (Human Specific evolution of novel SRGAP2 gene by incomplete segmental duplication. Cell 2012)

 

[mark kennedy]

We are fauna, so yes, it is a discussion about fauna.

Now we are fauna, I don't think animalia cells are even in the same kingdom classification.