I already did that work in a post above that one. A substitution mutation changes a single amino acid but does not cause a frame shift mutation.
If I do the same thing with human mRNA, will you accept it?
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Still playing the semantics game I see, let's work on the effect of mutations then we can tweek the terminology. Not really into the semantic hair splitting.
Not interested in E. coli, the subject is brain evolution and comparative genomics. Mutation rates might be of interest but it never gets that far, just gets dragged off on tangents like this one.
I already did that work in a post above that one. A substitution mutation changes a single amino acid but does not cause a frame shift mutation.
If I do the same thing with human mRNA, will you accept it?
Still not seeing a relevant point emerging from this.
I have no reason to dismiss a well developed argument. It's not really fair to ask if I will accept something I haven't seen yet but I will make every effort to thoughtfully consider it.
You claimed that substitution mutations could not occur in brain related genes because they would result in frame shift mutations.
"In other words, 70% of the genes in each species would have to experience mutations. If you know anything about mutations it's that most of the are deleterious (harmful), almost 98%. This requires an impossible number of changes in highly conservative genes resulting in fully functional reading frames which almost never happens."--mark kennedy, post #5
If substitution mutations do not result in frame shifts, then your argument isn't supported.
If I am able to show that substitution mutations in human genes will not produce a frame shift just as I did for the E. coli gene, will you accept it as evidence that substitution mutations do not cause frame shifts?
Your still splitting semantical hairs.
The only way it's going to be functional is if the substitution results in a viable protein which has to get past functional constraints. Sure it happens, even in human protein coding genes but the deleterious effects far outweigh any
possible, let alone imagined, adaptive evolutionary giant leaps.
So far I have just laid a little groundwork with comparisons and the likelihood of these presumed adaptive changes.
No, that is what you are doing. You are trying to argue that the similarity between chimps and humans is not 98% simply because 70% of proteins differ by 1-2%. Do you understand how bad that argument is?
Let's look at cytochrome c as an example. Here is a comparison of the human and yeast proteins at the amino acid level:
They differ by 36%, yet both proteins are still fully functional.
You still haven't answered the most basic question. What do you think is the cause for the physical differences between the human and chimp brain, if it isn't the sequence differences between their respective genomes?
In addition to the myosin gene duplications and subsequent mutations in SRGAP2 and ARHGAP11 fostered brain evolution and development in humans.
SRGAP2C - helped our brains grow larger.
http://www.nature.com/news/human-brain-shaped-by-duplicate-genes-1.10584
ARHGAP11B - fostered folds and evolution of human cerebrum.
http://www.sciencemag.org/content/347/6229/1465.abstract
You say it isn't the answer, but the scientists obviously disagree. Can you explain why?Do you understand that 20% of those differences would require gross structural changes? That's some 40,000 amino acids that diverge in just over 20,000 genes. I understand the argument is going to be dismissed no matter what it is but I'm still aware of the fact that mutations on this scale, especially in a short space of time isn't an answer.
Interesting example but not the same thing as brain related genes. You could make similar arguments from immune systems, perhaps not as dramatic.
I've not only answered that there are a couple of dynamite images in the thread showing it in full color. Now we will get to HAR1f eventually but that usually ends these discussions so I'll hold off on it for a while. The differences are obvious, the human brain is nearly three times bigger and well, apes don't send men into space, men sent one chimpanzee though.
Have a nice day
Mark
Do you understand that 20% of those differences would require gross structural changes?
That's some 40,000 amino acids that diverge in just over 20,000 genes.
I understand the argument is going to be dismissed no matter what it is but I'm still aware of the fact that mutations on this scale, especially in a short space of time isn't an answer.
Interesting example but not the same thing as brain related genes.
I've not only answered that there are a couple of dynamite images in the thread showing it in full color.
Now we will get to HAR1f eventually but that usually ends these discussions so I'll hold off on it for a while. The differences are obvious, the human brain is nearly three times bigger and well, apes don't send men into space, men sent one chimpanzee though.
Have a nice day
Mark
About 2mya the nearly threefold expansion of the human brain from that of apes happens almost over night.
After all these years, I still get a chuckle out of a YEC saying stuff like this.
After all these years, I still get a chuckle out of a YEC saying stuff like this.
Indeed.
No magical doubling overnight. Slow steady increases over 3 million years. The "misrepresentation" that mark tries to con people into accepting is cherry picked data. I could do the same for modern humans by selecting someone from 100 years ago with a cranium much smaller than the average, and then someone from 50 years with a cranium much larger than the average. I bet I could demonstrate a doubling in human brain size in just 50 years using the mark kennedy method of cherry picked data.
Wrong way around, mark. 20% of the proteins have gross structural changes due to mutations. The gross structural changes come after the mutation.
How many amino acids per gene are there? If there are 300 amino acids per gene, that is 6,000,000 amino acids. If there are only 40,000 differences in 6,000,000 amino acids, that's just a 0.67% difference.
What is it about this math that is such a problem for you?
Added in edit:
Found a reference that has the median protein length at 375 amino acids for the human genome, which is in the same ball park as other mammals. Median is not the same as average, so we can't simply multiply to get the absolute numbers. However, for what we are comparing the median is close enough to the average for our purposes. All the median does is reduce the effects of outliers, as compared to the average.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1150220/
The only thing we are rejecting is your faulty math.
When you say that the the chimp and human genomes can't be 98% similar because genes differ by 2% on average, how are we not supposed to laugh at that?
Then how do you explain the physical differences between the human and chimp brain if it is not due to the genetic differences between humans and chimps?
Showing what? You never explain the mechanisms that results in different sized brains between chimps and humans.
If it isn't due to the genetic differences between our species, then how do you explain it?
So why is the brain bigger if it isn't due to genetic differences?
After all these years I would have expected better then that from you.
How does any of this point to your God being real?We have been told for decades that we are nearly identical to Chimpanzees in our DNA, it's simply not true. That is vitally important when it comes to the human brain since the genes involved in the development of the brain do not respond well to changes of any kind, especially mutations. The human brain is almost three times bigger then the Chimpanzee and there are dramatic differences in the brain related genes. With that in mind consider whether or not the evolution of the human brain from that of apes has any known molecular basis. If not, do you think this creates a logical and scientific disproof of the Darwinian doctrine that men and apes share a common ancestor?
Only 29% of the genes in the comparison of the Chimpanzee Genome and the Human Genome sequences are the same. More importantly, with brain related genes I have yet to see one that had a beneficial effect. These are the effects most often seen:
CharcotMarieTooth (CMT) sensorimotor neuropathy
Infantile spasms, dystonia, and other X-linked phenotypes
Schizophrenia
Brain tumors
Alzheimer's disease
Parkinson's disease
Pick a chromosome, any chromosome and you will find a disease or disorder effecting the human brain as the result of a mutation.
Human Genome Project Landmark Poster
FIGURE 2. Comparative neuroanatomy of humans and chimpanzees. (Genetics and the making of Homo sapiens. Nature April 2003)
Charles Darwin in the preface to On the Origin of Species credits Jean-Baptiste Lamarck with being the first man to propose that the doctrine that species, including man, are descended from other species. This, Darwin argues, being the result of law, and not of miraculous interposition. One of Darwins contemporaries, Gregor Johann Mendel, was doing a series of experiments with pea plants that yielded the laws of inheritance that would become the cornerstone of modern genetics. Darwins book popularized the idea of common decent while Mendels only surviving paper would not be rediscovered for nearly half a century later. Mendelian laws of inheritance became inextricably linked to waves of discovery starting with chromosome theory and culminating in the molecular basis of heredity: The DNA double helix. Darwinism contributed nothing to the waves of discovery but was philosophically commingled with genetics in what has become known as the modern synthesis.
In order to examine the scientific basis for common descent I propose to examine the genetic basis for the common descent of humans from that of apes. The most dramatic and crucial adaptation being the evolution of the human brain. Charles Darwin proposed a null hypothesis for his theory of common descent :
If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. (Darwin, On the Origin of Species)
With a cranial capacity nearly three times that of the chimpanzee the molecular basis for this giant leap in evolutionary history is still almost, completely unknown. Changes in brain related genes are characterized by debilitating disease and disorder and yet our decent from a common ancestor with the chimpanzee would have had to be marked by a massive overhaul of brain related genes. I propose that a critical examination of common descent in the light of modern insights into molecular mechanisms of inheritance is the single strongest argument against human/ape common ancestry.
Darwin discussed what he called the 'bane of horticulture', this was infertility. Haldane in 'The Cost of Natural Selection indicated "genetic deaths," which is either deaths or it's equivalents in reduced fertility. He said that it would take 300 generations for a beneficial mutation to become fixed with 1667 accrued in 10 million years.
Like Darwin, he used artificial selection to illustrate what would have had to happen in natural settings:
"especially in slowly breeding animals such as cattle, one cannot cull even half the females, even though only one in a hundred of them combines the various qualities desired." (Haldane, The Cost of Natural Selection)
For us to have evolved from apes it would have required an accelerated evolution of brain related genes. The evolution of the human brain would have had to start it's accelerated evolution on a molecular basis some 2 million years ago and within Homo Erectus (considered human by most creationists) would have had a brain size twice that of the Austropihicene and early Hominids:
Early Ancestors:
A. Afarensis with a cranial capacity of ~430cc lived about 3.5 mya.
A. Africanus with a cranial capacity of ~480cc lived 3.3-2.5 mya.
P. aethiopicus with a cranial capacity of 410cc lived about 2.5 mya.
P. boisei with a cranial capacity of 490-530cc lived between 2.3-1.2 mya.
OH 5 'Zinj" with a cranial capacity of 530cc lived 1.8 mya.
KNM ER 406 with a cranial capacity of 510cc lived 1.7 million years ago.
(See Smithsonian Human Family Tree)
Homo Erectus Skulls:
Hexian 412,000 years old had a cranial capacity of 1,025cc.
ZKD III (Skull E I) 423,000 years old had a cranial capacity of 915cc.
ZKD II (Skull D I) 585,000 years old had a cranial capacity of 1,020cc
ZKD X (Skull L I) 423,000 years ago had a cranial capacity of 1,225cc
ZKD XI (Skull L II) 423,000 years ago had a cranial capacity of 1,015cc
ZKD XII (Skull L III) 423,000 years ago had a cranial capacity of 1,030cc
Sm 3 >100,000 years ago had a cranial 917cc
KNM-WT 15000 (Turkana Boy) 1.5 million years ago had a cranial capacity of 880cc
(Source: Endocranial Cast of Hexian Homo erectus from South China, AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 2006)
Homo habilis that would have lived. 2.51.5 mya with a cranial capacity of ~600 cc. The next link would have been Homo erectus with a cranial capacity of ~1000cc. KNM-WT 15000 (Turkana Boy) would have lived 1.5 mya and the skeleton structure shows no real difference between anatomically modern humans. The skull while smaller then the average cranial capacity of humans but close to twice that of his ancestors of 2 mya.
That means for our ancestors to have evolved it would have required a dramatic adaptive evolution of the size just under 2 mya sandwiched between two long periods of relative stasis. One such gene would have been the HARf regulatory gene involved in the early development of the human neocortex from 7 to 19 gestational weeks. With only two substitutions allowed since the common ancestor of the of 310 mya the divergence between humans and chimpanzees indicates 18 substitutions as early as 2 mya. (Nature, vol. 443, no. 7108, pp. 167-172 September 14, 2006)The ASPM gene while 99.3% the same for the humanchimpanzee comparison is marked by ten insertions/deletions equal to or longer than 50 bp, all of them located within introns. Primary microcephaly (MCPH) is a neurodevelopmental disorder characterized by global reduction in cerebral cortical volume.(Genetics, Vol. 165, 2063-2070, December 2003) In addition, a total of 2014 genes or ~10% of brain related genes analyzed differed in expression between humans and chimpanzees brains.(Genome Res. 14:1462-1473, 2004 ).
Evolutionists used to be able to use a 10 million year timeline, then it was 5 million years but when it comes to the most important adaptation you are looking at less then 1 million years and realistically it's only half that.
Darwin's null hypothesis for common descent is not unanswerable:
If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. (Darwin, On the Origin of Species)
If you take the road less traveled and choose to question common descent popularized by Darwin I submit that human brain evolution is prime topic. Darwin's theory is supposed to absolutely break down if a complex organ by decent with modification. My proposal is simply this, the human brain had neither the time nor the means to have evolved from that of apes.
Grace and peace,
Mark
A scattergram, if I know anything about science it's that specificity is the key, not blurry charts and rhetoric.
No it means they are fundamentally different, the mutations are assumed.
It's nice that you like math, it will be helpful when we get to mutation rates.
So says the person who thinks that a 1-2% difference in genes means that chimps and humans can't share 98% of their genomes.The part where you guys stop using it.
We haven't gotten to the math yet, still determining the divergence.
You would have to appreciate the effect of mutations on genes, that requires an actual understanding of the overwhelmingly negative effects.
Special creation explains it, the genetic differences are there by design not the result of mutations.
You really don't get it do you? 2mya the average brain size is comparable to modern apes, then it doubles almost over night.
You do know I'm a creationist right?
I'm a little dumbfounded but I will assume the question is just awkwardly worded. Of course the divergence would have to be the result of requisite changes in genes. The problem is that brain related genes do not respond to changes. They simply don't.
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