Design and the Brain

[mark kennedy]

That's cool. It means you actually understand something about evolution.

I know what the word means as defined in a scientific context and how it's different from a priori assumptions but thanks...I think...

Perhaps the vast majority of mutations are synonymous or deleterious, but advantageous mutations aren't nonexistant. And once they appear, they are fixed much more easily than a neutral mutation, not to mention a harmful one.

When did I say they were nonexistent? I am saying they simply don't account for a series of adaptations that triple the brain in size and complexity. Researchers have no problem with this, why should we?

I advise you to play with the free evolution simulator Populus. Quite cool; I've just done a few sims with it (single autosomal locus diallelic simulations, fyi). I gave the advantageous allele an initial frequency of 10^-5 (one copy in a population of 50 000), and tried selective advantages of 1%, 2%, 3%, 4%, 5% and 10%. For all but the 1% case the allele increased in frequency within 1000 generations, the maximum Populus can display (and from 4% upwards the allele tended to get fixed before 1000 generations). And that happened consistently in more than five runs per parameter value. With an initial frequency of 10^-6 (and I would think that implies a huge population size for an early hominid), the results were much the same, though I didn't do as many sims with that setting.

The frequency would have to be considerably higher but then again I have no idea where you coming from with this.

You see, it would seem that a mutation with only 2-3% of a selective advantage could conquer a population of 50 000 in a few hundred or thousand generations. And in a population of 50 000 there will be many mutations in each generation, some of which will probably be beneficial. (How long is that gene in question? It would be nice to actually calculate how many mutations are likely to arise within it per generation. Of course there will be fewer mutations in a smaller population, but they will also be quicker to get fixed if beneficial)

If memory serves the ASPM gene is 1300 base pairs long. The HARf is 118 with 18 substitutions, the ones in human lineages being unique. Again I'm not sure where you are coming from with this.

Besides, two million years is 80 000 human generations if we calculate with a 25-year generation time, which is probably a very conservative estimate for earlier humans. I mean, we didn't really start postponing children until Bridgetjonesian ages before the twentieth century, did we?

From 2 million years to roughly 1.5 million years the cranial capacity double. The stats have to be adjusted accordingly. Bear in mind that the Neanderthals had a cranial capacity 10% greater then our own. The thing is, this is not going to allow itself to be stretched over the many generations making a nice linear progression.

An interesting post though, I just think you are giving random mutations too much credit. There would have to be a molecular mechanism for an adaptation of this magnitude. Rest assured, it would in no way be mistaken for a spontaneous mutation.

 

[Chalnoth]

An interesting post though, I just think you are giving random mutations too much credit. There would have to be a molecular mechanism for an adaptation of this magnitude. Rest assured, it would in no way be mistaken for a spontaneous mutation.

How, pray tell? You've been shown the math that it's entirely plausible for the random mutations to have been fixed in the ~1.5-2 million years that the brain size of our ancestors doubled.

Furthermore, remember that the HAR1 gene you are citing has 18 substitutions that are different compared to other descendants from the same common ancestor some ~7 million years ago. How many of those 18 substitutions are actually substitutions in the chimpanzee line? How many happened before the massive increase in brain size? That all 18 mutations had to happen in the ~1.5-2 million years is a worst case scenario for evolution, and yet the numbers turn out that it was entirely possible for 18 consecutive mutations to have been fixed in the human population in that time.

 

[FishFace]

That's absurd, the brain can only increase in size, density and complexity when protein coding genes are altered at an amino acid sequence level.

No, your brain exhibits some similarities to muscle. You can grow more muscle tissue by exercise and you can alter your brain by practice. If what gamespotter said is true, then we could also have increased its size by eating more protein.

No it's not, this is one of the things that would have had to occur and there is no known molecular mechanism to facilitate such a major overhaul of such a highly conserved gene.

You beg the question. It's a circular argument to say that the gene could not have changed because it is highly conserved.

 

[mark kennedy]

Just two things, the HARf gene couldn't have been changed at random or in piecemeal fashion. Also if a protein diet could account for it then why does the body increase by 10% while the brain triples in size. All a change in diet is going to do is provide more protein, not change the amino acid sequence of the protein coding gene.

Cells are the fundamental working units of every living system. All the instructions needed to direct their activities are contained within the chemical DNA (deoxyribonucleic acid). DNA from all organisms is made up of the same chemical and physical components. The DNA sequence is the particular side-by-side arrangement of bases along the DNA strand (e.g., ATTCCGGA). This order spells out the exact instructions required to create a particular organism with its own unique traits. The genome is an organism’s complete set of DNA. Genomes vary widely in size: the smallest known genome for a free-living organism (a bacterium) contains about 600,000 DNA base pairs, while human and mouse genomes have some 3 billion. Except for mature red blood cells, all human cells contain a complete genome. DNA in the human genome is arranged into 24 distinct chromosomes--physically separate molecules that range in length from about 50 million to 250 million base pairs. A few types of major chromosomal abnormalities, including missing or extra copies or gross breaks and rejoinings (translocations), can be detected by microscopic examination. Most changes in DNA, however, are more subtle and require a closer analysis of the DNA molecule to find perhaps single-base differences. From the Genome to the Proteome: Human Genome Project​

​

Two fundamental errors in as many posts, why am I not surprised. Why don't you guys learn a little about basic biology before you start pontificating about it. You have this whole thing backwards, you don't start with the protein product, you have to have a change in the amino acid sequence. That's what happens when you don't learn basic biology before becoming on of these psuedoscientific apologists, you end up making fundamental errors that conflate and distort real scientific reasoning.

 

[TheBear]

When I look at the human brain, I see workmanship and intelligent design. How did Evolution design male and female brains? How could Evolution differeniate between lots of testosterone in one brain and estrogen in another?

I do not see how Evolution could design a human brain. Especially when you examine the difference between male and female brain chemicals.

I can't figure it out. Therefore, God did it.

 

[Naraoia]

Just two things, the HARf gene couldn't have been changed at random or in piecemeal fashion.

Why?

Also if a protein diet could account for it then why does the body increase by 10% while the brain triples in size. All a change in diet is going to do is provide more protein, not change the amino acid sequence of the protein coding gene.

I think one way a protein-rich diet could boost brain evolution is positive feedback. Such a diet is part of a more predatory lifestyle. Heaven knows why humans' ancestors first started to eat more meat, but suppose they did (which certainly happened at some point). Now, if you are better at planning and coordinating a hunt (and, well, humans don't have any particular predatory adaptations - so they must rely on their wits to hunt successfully), you get more energy- and protein-rich meat stuff to eat. You can sustain a larger brain, so a brain size increasing mutation isn't so likely to be selected against - and then your mutant offspring are even better at planning and coordinating hunts. And making weapons and whatever. So they get even better nutrition. And so on.

I'm not saying this was the selective force that tripled human brain size - it would be pretty dishonest of me to say anything certain, because I don't know much about this field -, but it certainly could have been one of those forces.

Why don't you guys learn a little about basic biology before you start pontificating about it. You have this whole thing backwards, you don't start with the protein product, you have to have a change in the amino acid sequence. That's what happens when you don't learn basic biology before becoming on of these psuedoscientific apologists, you end up making fundamental errors that conflate and distort real scientific reasoning.

I just hope you didn't aim that at me. I dearly dearly hope.

 

[mark kennedy]

I can't figure it out. Therefore, God did it.

Yea right, it makes more sense to say God didn't do it.

 

[Naraoia]

Yea right, it makes more sense to say God didn't do it.

What makes more sense to say is we have no positive evidence to believe God did it. Not knowing the mechanism for something, even if you really really don't know and can't even imagine, is no reason to assert a mechanism can't be found.

 

[mark kennedy]

Why? I think one way a protein-rich diet could boost brain evolution is positive feedback. Such a diet is part of a more predatory lifestyle. Heaven knows why humans' ancestors first started to eat more meat, but suppose they did (which certainly happened at some point). Now, if you are better at planning and coordinating a hunt (and, well, humans don't have any particular predatory adaptations - so they must rely on their wits to hunt successfully), you get more energy- and protein-rich meat stuff to eat. You can sustain a larger brain, so a brain size increasing mutation isn't so likely to be selected against - and then your mutant offspring are even better at planning and coordinating hunts. And making weapons and whatever. So they get even better nutrition. And so on.

Again, you need the genes to be altered at an amino acid sequence level. Proteins are not just raw building material they are molecular machines like this one:

The developmental and evolutionary mechanisms behind the emergence of human-specific brain features remain largely unknown. However, the recent ability to compare our genome to that of our closest relative, the chimpanzee, provides new avenues to link genetic and phenotypic changes in the evolution of the human brain. We devised a ranking of regions in the human genome that show significant evolutionary acceleration. Here we report that 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. HAR1 and the other human accelerated regions provide new candidates in the search for uniquely human biology. (An RNA gene expressed during cortical development evolved rapidly in humans Nature 443, 167-172, 14 September 2006)​

This is a regulatory gene involved in a crucial developmental period for the Cajal–Retzius neurons in the human cortex from the 7th to the 17th week of development. This regulatory gene has not been significantly changed since the Cambrian Explosion but all of the sudden accumulates 18 substitutions. There is a reason I think this is important, primarily, I'm interested in molecular mechanisms that are involved in adaptive evolution.

I'm not saying this was the selective force that tripled human brain size - it would be pretty dishonest of me to say anything certain, because I don't know much about this field -, but it certainly could have been one of those forces. I just hope you didn't aim that at me. I dearly dearly hope.

My focus has not changed in some time, my interest is in Genetics and Molecular Biology. I am sometimes a little course so in the interests of an open exchange I would suggest some open course software might be of interest to you.

The quantitative aspects of biology - including molecular biology, biochemistry, genetics, and cell biology - represent the core of the academic program. Courses are designed to provide a solid background in the physical sciences and to develop an integrated scientific perspective.​

MIT Department of Biology Open Course Software

Enjoy!

What makes more sense to say is we have no positive evidence to believe God did it. Not knowing the mechanism for something, even if you really really don't know and can't even imagine, is no reason to assert a mechanism can't be found.

I'm not saying it can't be found, just that it should not be assumed without direct observation or demonstrated evidence. It is a fatal flaw to assume that random mutations are capable of producing anything other then disease and disorder except in the rarest of circumstances.

 

[Naraoia]

Again, you need the genes to be altered at an amino acid sequence level. Proteins are not just raw building material they are molecular machines like this one:

Who on earth do you think said that proteins are raw material for a genetic sequence??? Proteins are raw material for... well, our own proteins. And animal proteins are better for that purpose than most plant ones. Meat/fat/etc is also far easier to digest than plant material (no cellulose), so you don't need to eat so much to get the same amount of nutrition, and you don't need to have a large and complex digestive system to house all those symbiotic bacteria. Eating more meat is saving energy and resources that can then be turned to other purposes. Such as building and maintaining a large brain, if a large brain is otherwise advantageous.

I'm not saying that a more meaty diet caused the mutations, I'm only saying that it might have made it possible to retain those mutations that increased brain size.

Here we report that 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

Novel? Compared to chimps, that is? So are they saying HAR1F is a duplicate gene? Don't gene duplicates experience relaxed selection because of functional redundancy? Then a mutation doesn't even need to be strictly beneficial to get fixed...
​

There is a reason I think this is important, primarily, I'm interested in molecular mechanisms that are involved in adaptive evolution.

That's one thing I'm getting more and more interested in. Especially the evo-devo aspects.

MIT Department of Biology Open Course Software

Enjoy!

What am I to do with that?

I'm not saying it can't be found, just that it should not be assumed without direct observation or demonstrated evidence. It is a fatal flaw to assume that random mutations are capable of producing anything other then disease and disorder except in the rarest of circumstances.

What should be assumed, then? God certainly isn't a good alternative because, if omnipotent, he cannot be tested, and if not, he cannot be tested either - not until someone comes up with an acceptable set of properties and predictions of a God model.

 

[mark kennedy]

Eating more meat is saving energy and resources that can then be turned to other purposes. Such as building and maintaining a large brain, if a large brain is otherwise advantageous.

If and only if the adaptive trait is already being expressed, the requisite changes in the amino acid sequence are in place and the deleterious effects have been eliminated. In short, you have the cart before the horse.

I'm not saying that a more meaty diet caused the mutations, I'm only saying that it might have made it possible to retain those mutations that increased brain size.

Mutations are either selected against or they are adaptive evolutionary changes.

Novel? Compared to chimps, that is? So are they saying HAR1F is a duplicate gene?​

As compared to the chimpanzee, Gorilla, Orangatan...dog platypus...etc. See the comparison in the top left had corner. I don't see any explanation at all for the unprecedented change of a regulatory gene. No explanation is offered, it's just a difference found by researchers that they identified and characterized.

​

Don't gene duplicates experience relaxed selection because of functional redundancy? Then a mutation doesn't even need to be strictly beneficial to get fixed...
​

When it comes to a regulatory gene involved in the development of the human cortex it must be strictly beneficial.

That's one thing I'm getting more and more interested in. Especially the evo-devo aspects.

That's good because its the whole evolution/creation controversy in a nutshell (see my signature) .

What am I to do with that?

Learn more on the subject you are getting more and more interested in.

What should be assumed, then? God certainly isn't a good alternative because, if omnipotent, he cannot be tested, and if not, he cannot be tested either - not until someone comes up with an acceptable set of properties and predictions of a God model.

I do not invoke God except as the primary source or the unmoved mover. The issue here is history and either there is credible supporting evidence for events or there isn't. Genetics and Molecular Biology are about living systems not natural history. TOE is more then science because as science it is perfectly compatible with a Christian (evangelical/fundamentalist) worldview and philosophy of history. What Darwinism has done has blended atheistic/agnostic philosophy with the genuine article of science used as bait and I'm not biting.

 

[Naraoia]

If and only if the adaptive trait is already being expressed, the requisite changes in the amino acid sequence are in place and the deleterious effects have been eliminated. In short, you have the cart before the horse.

What exactly is your problem here? (Deleterious effects can be eliminated at any time. Organism dies, no sex no kids no problem.)

Mutations are either selected against or they are adaptive evolutionary changes.

Or they are synonymous and don't make any copulating difference.

As compared to the chimpanzee, Gorilla, Orangatan...dog platypus...etc. See the comparison in the top left had corner. I don't see any explanation at all for the unprecedented change of a regulatory gene. No explanation is offered, it's just a difference found by researchers that they identified and characterized.

Sigh. Try once more. Is this HAR something a newly duplicated gene?

When it comes to a regulatory gene involved in the development of the human cortex it must be strictly beneficial.

Umm... I wouldn't think so. Or, I'd think so in a slightly different sense.

(again, supposing HARwhatever was newly duplicated). Duplication of a single gene can upset gene dosage balance. In that case loss of function may be beneficial, until the combined functions of the ancestral and the new copy are restored to the original level. And even if there isn't a serious dosage issue, both copies are still relatively free to accumulate otherwise harmful mutations so long as something fulfils all the necessary functions. That means more mutations can get into the gene than otherwise.

Learn more on the subject you are getting more and more interested in.

That's okay... but *confused* I scrolled through the courses, picked a developmental biology one and went to see what it's all about... and among the notes, all the pdf titled "introduction" had was a list of technical terms. If the whole thing is like that I'd be better off spending a few dozen pounds in Blackwells.

I do not invoke God except as the primary source or the unmoved mover. The issue here is history and either there is credible supporting evidence for events or there isn't. Genetics and Molecular Biology are about living systems not natural history.

Waddaf***?

TOE is more then science because as science it is perfectly compatible with a Christian (evangelical/fundamentalist) worldview and philosophy of history. What Darwinism has done has blended atheistic/agnostic philosophy with the genuine article of science used as bait and I'm not biting.

How has Darwinism done that?

 

[FishFace]

Just two things, the HARf gene couldn't have been changed at random or in piecemeal fashion.

Well colour me con-- wait, you didn't provide any evidence.

Also if a protein diet could account for it then why does the body increase by 10% while the brain triples in size. All a change in diet is going to do is provide more protein, not change the amino acid sequence of the protein coding gene.

You didn't read what he said, did you. He didn't provide a source (which he should) but, if he's correct, then the brain would grow disproportionately because the brain is sacrificed over the rest of our body if there's a protein shortage.
Like I say, he needs to provide a source.

The rest of your post implies we think that eating protein will cause mutations. That's obviously wrong.

 

[Pete Harcoff]

What makes more sense to say is we have no positive evidence to believe God did it. Not knowing the mechanism for something, even if you really really don't know and can't even imagine, is no reason to assert a mechanism can't be found.

Not to mention it doesn't in any way invalidate the other evidence that exists for human/chimp common ancestry.

 

[Pete Harcoff]

What Darwinism has done has blended atheistic/agnostic philosophy with the genuine article of science used as bait and I'm not biting.

Reading this you'd think On the Origin of Species was a treatise on atheism.

 

[Naraoia]

Reading this you'd think On the Origin of the Species was a treatise on atheism.

Why, maybe it is... I haven't managed to read it yet, though it's been sitting on my bookshelf for nigh on two months now

 

[mark kennedy]

Well colour me con-- wait, you didn't provide any evidence.

You have that backwards, I have focused almost exclusively on the evidence while you have talked in short pedantic quips.

You didn't read what he said, did you. He didn't provide a source (which he should) but, if he's correct, then the brain would grow disproportionately because the brain is sacrificed over the rest of our body if there's a protein shortage.

A statement supported exclusively upon the credibility of the poster which remains to be established.

Like I say, he needs to provide a source.

You don't even define the problem and I have ample source material.

The rest of your post implies we think that eating protein will cause mutations. That's obviously wrong.

That is an obvious distortion, I said that mutations are no explanation at all. Eating protein has absolutely nothing to do with it. At best eating meat could be an effect of an adaptive trait being expressed but can in no way be considered a cause of adaptive evolution. The amino acid sequence of the protein coding genes determines the protein product, not the other way around.

The absurdity of your statements are not only evident, they are obvious.

 

[mark kennedy]

Pete,

How does this change when the divergence goes from 1.33% to 6%?

"Rates and patterns of molecular evolution:
We observed a total of 199 differences between the human and chimpanzee sequences: 131 transitions (66%), 52 transversions (26%), and 16 insertion-deletion variants (8%). Insertion-deletion variants were less than one-tenth as common as nucleotide substitutions and consisted of changes of 1 bp (8 mutations), 2 bp (5 mutations), 3 bp (1 mutation), and 4 bp (2 mutations). Thus, 15/16 of these insertion-deletion variants would have resulted in frameshift mutations in coding regions. Approximately one-fifth of all single nucleotide mutations were transitions at CpG dinucleotides...

Table 3. Estimates of mutation rate assuming different divergence times and different ancestral population sizes

4.5 mya, pop.= 10,000 mutation rate is 2.7 x 10^-8
4.5 mya, pop.= 100,000 mutation rate is 1.6 x 10^-8
5.0 mya, pop.= 10,000 mutation rate is 2.5 x 10^-8
5.0 mya, pop.= 10,0000 mutation rate is 1.5 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 2.3 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 1.4 x 10^-8
6.0 mya, pop.= 10,000 mutation rate is 2.1 x 10^-8
6.0 mya, pop.= 100,000 mutation rate is 1.3 x 10^-8

Table 4. Estimates of mutation rate for different sites and different classes of mutation

Transition at CpG mutation rate 1.6 x 10^-7
Transversion at CpG mutation rate 4.4 x 10^-8
Transition at non-CpG mutation rate 4.4 x 10^-8
Transversion at non-CpG mutation rate 5.5 x 10^-9
All nucleotide subs mutation rate 2.3 x 10^-8
Length mutations mutation rate 2.3 x 10^-9
All mutations mutation rate 2.5 x 10^-8

Rates calculated on the basis of a divergence time of 5 mya, ancestral population size of 10,000, generation length of 20 yr, and rates of molecular evolution given in Table 1.


Calculations are based on a generation length of 20 years and average autosomal sequence divergence of 1.33%
-----------------------------------------------------

Estimate of the Mutation Rate per Nucleotide in Humans (Michael W. Nachmana and Susan L. Crowella
Genetics, 297-304, September 2000) "​

Since this was published the known divergence has grown by 5X:

 

[mark kennedy]

Why, maybe it is... I haven't managed to read it yet, though it's been sitting on my bookshelf for nigh on two months now

Oh you totally should read it, the guy was a great writer. When it comes to how favorable traits are passed on to the next generation he was so clueless that he married his cousin. Still, On the Origin of Species was remarkably well written and I would recommend it to Creationist and Evolutionist alike.

 

[Naraoia]

You have that backwards, I have focused almost exclusively on the evidence while you have talked in short pedantic quips.

Why, then, did I get the impression that the gist of your argument, no matter the actual evidence you've presented, was "I can't believe it happened this way"?

That is an obvious distortion, I said that mutations are no explanation at all. Eating protein has absolutely nothing to do with it.

Then we've missed something horribly.

At best eating meat could be an effect of an adaptive trait being expressed but can in no way be considered a cause of adaptive evolution.

Why on earth can't it be both? Why can't the acquisition of a new ability open the door to even more new traits?

The amino acid sequence of the protein coding genes determines the protein product, not the other way around.

Why the heck do you keep stressing this to people who understand it? And anyway, what exactly are you trying to say with it?

The absurdity of your statements are not only evident, they are obvious.

*raises eyebrows* How? (And aren't "evident" and "obvious" kinda synonyms?)