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That is a real question for now, the ancient pre flood world is another thing. I do not live 1000 years now, doesn't work that way now. If all you want to determine is how things now work, we can leave the creation evolution origins debate out of it.The real question is how it works and what are the limits.
Yea you did, it's 96% at best and you have absolutely nothing to say about the molecular basis for the three fold expansion from the human brain from that of apes. Yea, we have been round and around about this and nothing substantive about this so far. It's telling.I conceded nothing. I just don't feel like getting into a tit-for-tat with you about the relative divergence of human and chimp genomes. Especially since this would hardly be the first time that people have had a go-round with you about that.
It's boring.
Yea you did, it's 96% at best and you have absolutely nothing to say about the molecular basis for the three fold expansion from the human brain from that of apes. Yea, we have been round and around about this and nothing substantive about this so far. It's telling.
-_- the cause is mutations in genes. While the current understanding of genes related to intelligence is not particularly expansive, it's not as if we know of NONE related to it.Yea not surprising at all except there is no cause, just an assumed effect.
-_- that's just straight up incorrect. The HAR regions are named such BECAUSE they change so much, and if you bothered to look up HAR1F, you'd find it is no different in this regard. Not shocking, considering that it wouldn't be labeled as an HAR if it had been highly conserved. Many of the HARs are related to neurodevelopment, did you do no research? Even mentioning them weakens every aspect of your argument, since they demonstrate that many of the genes related to human brain development are highly prone to mutation.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.
At least you got its function right. Yet, a highly variable gene sequence in our species.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)
-_- mutation. Genes can be produced via mutation. I suppose you don't realize that chimps have many analogous genes that are slightly different, so there is no reason that mutations on genes which already existed couldn't be responsible for human intelligence. But hey, let's assume your incorrect assertion has merit and that 60 entirely new genes had to appear in the human evolutionary line after the split between human and chimp evolutionary lines. That gives about 12 million years for mutations to produce these genes, and mutations can be as small as 1 base pair change and as large as the duplication of entire chromosomes. So, I'll be generous and assume all mutations are just 1 base pair. I'll also be generous and assume that the population of organisms ancestral to modern humans had an average of 10,000 individuals born every year, and each individual born had only 10 mutations (compared to what we observe in humans; 40-60). That would mean that after human and chimp evolutionary lines had split, 1200000000000 mutations the size of single base pairs had occurred. Now, I will be generous and assume only 1% of those mutations are additions, and account for the fact that genes are generally around 27,000 base pairs long in humans. That would mean that, within this time period, about 444,444 new genes could be produced just through addition mutations alone. Even if only 1% of these mutations impacted genes at all, that would result in 4444 genes altered. And this is a worst case scenario that doesn't even represent the much more favorable reality. About 9% of the genome is genes, with 8% being regulatory genes and 1% producing proteins with non-regulatory functions. And you are going to throw a fit over a measly 60 genes?This is in addition to no less then 60 de novo (brand new) brain related genes with no known molecular mechanism to produce them.
Which is mutation. Mutations that cause catastrophic failure result in miscarriages or death in early childhood, so those just weed themselves out regardless of the environment.Selection can explain the survival of the fittest but the arrival of the fittest requires a cause:
Your own source suggests that genes which arise "de novo" are more common than traditionally thought. In no way does it support your position that there is NO mechanism by which these genes arose. It's mutation.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)
Demonstrably wrong, as in bacteria, de novo genes are the reason why some can digest nylon now. Beneficial mutations make up about 5% of mutations, with neutral mutations making up a majority and malignant mutations being about 30%. Of course, the worst of that 30% results in organisms that will die before they are able to reproduce, so they are weeded out of the population quite quickly.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.
Clearly wrong, since most HARs, the regions of the human genome most prone to change, are related to neurodevelopment.Brain related genes do not respond well to changes.
-_- the only effects that would overtly stand out and give reason to check a person's genes would be ones that cause disorder. Do you think we pull aside geniuses to have their genomes sequenced just for their intelligence? Because we don't do that. The vast majority of people that have their genomes sequenced are going to be sick, one way or another.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)
Why? Incomplete genes are generally broken and don't do anything at all, and their presence allows for a later mutation to hit them and jump start functionality. Heck, humans are full of genes that, if left active, would do survivable amounts of harm. Hence why the majority of genes are regulatory and many exist just to keep other genes from ever being active.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.
They are also found in normal, healthy people. There's just no reason to dedicate huge amounts of money to variations in the human genome that result in minimal differences. Since there are so many genes which contribute to our intelligence, notable variations in intelligence are due to combinations of different alleles, not just 1. Hence why humans have brain size ranges, brain structure ranges, etc.Mutations are found in children with 'developmental delay and brain malformations, including West Syndrome, agenesis of the corpus callosum, and epileptic encephalopathies'.
Oh, a child head contained a smaller than average brain? Shocker. Brain size ranges for children are much wider than for adults, due to hormonal cues that impact brain growth happening later in some children than others. Furthermore, you missed the point I made entirely, or that the upper level of Lucy's species, 550 cc, EXCEEDS that of the upper end of the chimp range (500 cc). This means that at least 1 of Lucy's species had a brain demonstrably bigger than chimps. But again, it was never her brain that made her a transitional.Lucy had a chimpanzee size brain, as did the Taung child, in fact she was kind of smaller then average.
420-520 cc for that species. They are distant cousins to the evolutionary line relevant to humans, so there was no reason to bring them up. They aren't considered transitional to humans at all.Speaking of transitionals I noticed you don't have much of a taste for Paranthropos right where you would expect a hominid fossil, a period covering a million years and it's just an ape transitional.
They didn't live in as good of places for producing fossils as human ancestors did, but they do exist.Curious, very curious indeed, especially considering our primate cousins are virtually unrepresented in the fossil record.
It's not missing, it's mutation. I've run out of time, however, and will have to address the rest of your post later.Ok I'm not buying that scientists know as much about the weather 800,000 years ago. I'm really not going to buy the proposition that you can just insert natural selection every time you are missing an actual molecular cause.
-_- that's just straight up incorrect. The HAR regions are named such BECAUSE they change so much, and if you bothered to look up HAR1F, you'd find it is no different in this regard. Not shocking, considering that it wouldn't be labeled as an HAR if it had been highly conserved. Many of the HARs are related to neurodevelopment, did you do no research? Even mentioning them weakens every aspect of your argument, since they demonstrate that many of the genes related to human brain development are highly prone to mutation.
HAR1A even has a secondary structure unique to humans, though chimpanzees have one very similar to it. You unintentionally pointed out one of the main mutations that could have contributed to human intelligence. Nice job, I couldn't have done it better myself. I'm just going to cut out the rest of your post that tries to argue that this brain region is highly conserved and not prone to mutation, because that is factually incorrect.
At least you got its function right. Yet, a highly variable gene sequence in our species.
-_- that latter half would only be true if this was the sole gene responsible for human intelligence, and it demonstrably is not. You are right in that the form of the gene present in humans is not present in chimps, so it must have appeared in the evolutionary timeline after the evolutionary lines of human and chimp had already split. If you can find any articles on whether or not it is present in Neanderthals, I would be very interested.
-_- mutation. Genes can be produced via mutation. I suppose you don't realize that chimps have many analogous genes that are slightly different, so there is no reason that mutations on genes which already existed couldn't be responsible for human intelligence. But hey, let's assume your incorrect assertion has merit and that 60 entirely new genes had to appear in the human evolutionary line after the split between human and chimp evolutionary lines.
That gives about 12 million years for mutations to produce these genes, and mutations can be as small as 1 base pair change and as large as the duplication of entire chromosomes.
So, I'll be generous and assume all mutations are just 1 base pair. I'll also be generous and assume that the population of organisms ancestral to modern humans had an average of 10,000 individuals born every year, and each individual born had only 10 mutations (compared to what we observe in humans; 40-60). That would mean that after human and chimp evolutionary lines had split, 1200000000000 mutations the size of single base pairs had occurred. Now, I will be generous and assume only 1% of those mutations are additions, and account for the fact that genes are generally around 27,000 base pairs long in humans. That would mean that, within this time period, about 444,444 new genes could be produced just through addition mutations alone. Even if only 1% of these mutations impacted genes at all, that would result in 4444 genes altered. And this is a worst case scenario that doesn't even represent the much more favorable reality. About 9% of the genome is genes, with 8% being regulatory genes and 1% producing proteins with non-regulatory functions. And you are going to throw a fit over a measly 60 genes?
Which is mutation. Mutations that cause catastrophic failure result in miscarriages or death in early childhood, so those just weed themselves out regardless of the environment.
Your own source suggests that genes which arise "de novo" are more common than traditionally thought. In no way does it support your position that there is NO mechanism by which these genes arose. It's mutation.
Demonstrably wrong, as in bacteria, de novo genes are the reason why some can digest nylon now.
Beneficial mutations make up about 5% of mutations, with neutral mutations making up a majority and malignant mutations being about 30%. Of course, the worst of that 30% results in organisms that will die before they are able to reproduce, so they are weeded out of the population quite quickly.
Clearly wrong, since most HARs, the regions of the human genome most prone to change, are related to neurodevelopment.
-_- the only effects that would overtly stand out and give reason to check a person's genes would be ones that cause disorder. Do you think we pull aside geniuses to have their genomes sequenced just for their intelligence? Because we don't do that. The vast majority of people that have their genomes sequenced are going to be sick, one way or another.
Where's the supposed disorder associated with this one?
Ok, we have a mutation and a disorder. Fabulous. So, how does this demonstrate that all mutations related to genes that deal with the brain are negative, or, at a minimum, none are beneficial? Because there are very few genes so highly conserved in humans that everyone has them the same (mostly HOX genes). We all have variations in genes related to brain development and function. So, what's the "original, ideal gene"?
Why? Incomplete genes are generally broken and don't do anything at all, and their presence allows for a later mutation to hit them and jump start functionality. Heck, humans are full of genes that, if left active, would do survivable amounts of harm. Hence why the majority of genes are regulatory and many exist just to keep other genes from ever being active.
They are also found in normal, healthy people. There's just no reason to dedicate huge amounts of money to variations in the human genome that result in minimal differences. Since there are so many genes which contribute to our intelligence, notable variations in intelligence are due to combinations of different alleles, not just 1. Hence why humans have brain size ranges, brain structure ranges, etc.
Oh, a child head contained a smaller than average brain? Shocker. Brain size ranges for children are much wider than for adults, due to hormonal cues that impact brain growth happening later in some children than others. Furthermore, you missed the point I made entirely, or that the upper level of Lucy's species, 550 cc, EXCEEDS that of the upper end of the chimp range (500 cc). This means that at least 1 of Lucy's species had a brain demonstrably bigger than chimps. But again, it was never her brain that made her a transitional.
420-520 cc for that species. They are distant cousins to the evolutionary line relevant to humans, so there was no reason to bring them up. They aren't considered transitional to humans at all.
They didn't live in as good of places for producing fossils as human ancestors did, but they do exist.
https://www.outlookindia.com/public/uploads/articles/2017/4/27/5_630_630.jpg
https://wolvesonceroamed.files.wordpress.com/2013/03/sivapithecus.jpg
These also don't get as much press as human transitionals, since we're kinda a self-centered species.
It's not missing, it's mutation. I've run out of time, however, and will have to address the rest of your post later.
Secondly, brain related genes do not respond well to mutations, in fact, they invariably result in disease and disorder of not death
Ever notice that there are no Chimpanzee ancestors in the fossil record?
There are a few, but ever notice that there are no Giant Philistines in the fossil record? Or fish big enough to house a human inside, unscathed?
Funny.
I know of two, the Taung Child and Lucy based on the cranial capacity and timeline. There is also Paranthropus, these creatures are dated between 2mya and 3mya with no human ancestors found from that period.And this has to do with the topic how? Have you bothered to read the posts? Is this just another attempt to derail the thread? What's next false accusations and name calling?
There are a few chimpanzee ancestors in the fossil record? Show us...(photos of the fossils will do but no artistic contrivances please)....also no ancestor of the gaps arguments if you can avoid them, just show us this actually led to a Chimpanzee....
How things work then was the living systems would have nearly pristine genomes. Since then they have accumulated mutations and bottleneck effects from adaptive evolution. There are adaptive mechanisms science is only beginning to understand:That is a real question for now, the ancient pre flood world is another thing. I do not live 1000 years now, doesn't work that way now. If all you want to determine is how things now work, we can leave the creation evolution origins debate out of it.
The question of human brain evolution remains unaddressed, much less answered.
That added to the fact that the fossil record if you really look at it isn't showing a viable human ancestor before the Homo Erectus fossils where the cranial capacity would have doubled over night with no known molecular mechanism capable of producing this giant leap.
There are adaptive mechanisms science is only beginning to understand:
My whole argument in this thread really comes down to mutations are the worst possible explanation for human brain evolution. Arguments to the contrary have not yet presented themselves.
Where is CRISPR found in any eukaryotic genome?
Then how do you explain the difference in brain size between chimps and humans? Is it due to the DNA differences between the human and chimp genomes?
You have a real gift for ignoring obvious facts while raising irrelevant questions.It was found in bacteria immune systems but it can be used with any DNA sequence.
'Increases in brain size and complexity are evident in the evolution of many primate lineages…However, this increase is far more dramatic in the lineage leading to humans than in other primate lineages…accelerated protein evolution in a large cohort of nervous system genes, which is particularly pronounced for genes involved in nervous system development, represents a salient genetic correlate to the profound changes in brain size and complexity during primate evolution,'(Molecular Evolution of the Human Nervous System. Bruce T. Lahn et al. Cell 2004)
What is your analysis of the genetic identity between and pair of 'kinds'? By that I mean, have you compared any 2 species that creationists accept as being derived from a common kind? And if not, why not? and if not, of what value is your analysis of the chimp-human question?Yea you did, it's 96% at best
and you have absolutely nothing to say about the molecular basis for the three fold expansion from the human brain from that of apes.
We have big brains (1100 cc to 1500 cc) they have small brains (300 cc to 600 cc)…
We are bi-pedal and they are knuckle walkers,
We have pronounced chins they have small receded chins,
We have a big toe in line with our other toes and they have opposable or separated big toes, ours for balance and walking, theirs for grasping and other forms of manipulation…
We have very different skeletal structures…
We have rounded craniums and a flatter face, they have a flatter cranium with a pronounced sagittal crest and protruding lower face (better for biting adversaries)…they have a distinctly protruding brow ridge (which varies to a small degree) and we have a far less protruding brow ridge (which varies to a small degree)
The difference in the orbital socket allows us to see laterally for more than any ape but definitely more than chimps (their skull hinders viewing freely to the sides). Our eye sockets are allegedly wider relative to our height than a chimps and in humans the outer margin is recessed much further back.
Chimp teeth demonstrate a need as a weapon and a show of dominance as well as for eating, where humans teeth are smaller, more regular, for eating (and sometimes part of attracting mates)
Our pelvis is properly designed for our distinctly bi-pedal gait, the chimps is longer and narrower for knuckle walking, Humans by nature are bi-pedal except for short bursts of walking on all fours, chimps are arboreal knuckle walkers with short bursts of standing or walking upright.
Our spines are long and straight for energy efficiency and support, the chimps is bent differently and positioned so their heads can jutt forward for walking on all fours,
We exhibit 3 main morphological types (Neanderthal Sapiens, Denisovan Sapiens, and Sapien sapiens) chimps do not demonstrate different morphological types,
Chimp-kind is only found in Africa, while human-kind is found everywhere in the world,
Chimp intelligence is dwarfed compared to even the lowest examples of human intelligence,
Humans live long compared to chimps,
Humans demonstrate things like uniqueness of culture, religion, philosophy, abstract thinking, art, intricate application of symbolic thought, and more, where chimps exhibit none of these things,
We have a covering of fine hairs and theirs are thick, course, fur.
The best of signing chimps only know objects wanted or not wanted, and learn specific phrases taught by conditioning in order to get food, petting, sex, and so on.
Human communication (language) utilizes vocabulary but also syntax. For chimps "give orange me," can mean something totally different than "give me orange" even among different signing chimps. We can condition them to sign “give orange me” to ask for an apple and “give me orange” to say they are tired now….they do not get confused or associate the difference…On the other hand, from a very young age, humans understand this. If your two or three year old asks for some orange and you gave them apple, they would protest or say “No! Orange not apple”…or at least exhibit confusion
We have an innate ability to create new meanings by combining and ordering words in diverse ways. Chimps studied, taught, and even conditioned for years, show no such capacity.
Human children demonstrate the ability (on their own) to vary syntax and express related ideas and concepts (sometimes vert abstract) while even the most mature chimps, trained from birth show no propensity of being able to produce this variance to either communicate with others or even to get their own way.
Cognition scientists have concluded after half a century of research that “chimps” are unable to infer the mental state of another, whether they are happy, sad, angry, interested in some goal, in love, jealous or otherwise, while even 1 and 2 year old humans can do this (see the Project Nim documentary). In addition, even trained “chimps” do not conversate with other individuals though as individuals they do demonstrate some basic emotions (anger, rage, happiness, grief, depression, etc.)
Just more to consider from a Homo Cognitarus
You're a wee bit behind the times. The chimpanzee genome was sequenced and compared to the human genome in 2005. A total of 2.7 billion base pairs of chimpanzee sequence could be compared.
Please give me a reference for this so I can check it out, thanks.
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