Design and the Brain

[Blayz]

Again, this has to do with the fact that deleterious mutations are far more common (it's much easier to break something than improve it genetically) and the logistical factors involved in screening the population for beneficial mutations.

The second half of this sentence means the first half may not be true. We all know about deleterious mutations because they are easy (relatively speaking) to nail down, usually through some kind of genetic mapping in an animal model (Hands up those that think Mark knows all the early work done on his precious genes was done in animal models and only holds because common descent is true)

But how do you even begin to assay for a slight, or even major, benefit? What experiments do you perform to find the genetic factors for genius? or for something which makes you a 5% better sprinter? I have a colleague that was looking for super-fitness mutations in Australian athletes, but the work lost funding, because the research council is more interested in curing disease than finding out why athletes run faster.

 

[FishFace]

As usual you are utterly confused, if the comparison of the two genomes is any indication these are the changes:

35 million single base pairs (MB) and 5 million indels totaling 90 MB.

So where did the 68,000 figure come from in your last post? I'm only working with what you give me. Looks like these figures are correct, anyhow.

That comes to 40,000,000 differences and does not include the 8 chromosomal rearrangements from 2 MB to 4 MB totaling about 20 MB.

Chromosomal rearrangements are pretty rare, so I don't think the per-generation figure is going to be very relevant here, do you?

That means 1 indel and 7 single base substitutions permanently fixed per year of 5 million years. For an average population of 10,000 the mutation rate comes to 2.5 x 10^-8. For a population of 100,000 it's 1.5 x 10^-8. That's a 1.33% divergence and the mutation rate for all mutations are about 2.5 x 10^-8 now multiply that by 5x.

So we have 175 mutations per genome per generation. (In comparison to your "1 indel and 7 single b.p." that, by the way, is 8.75 mutations per year with a 20 year generation time) that's 4.3 million mutations over the course of 5 million years. Except both humans and chimpanzees have been evolving, which I forgot last post, so we expect 8.6 million mutation differences between humans and chimpanzees.

Where did your 5x come from? Looks like 0.5x to me.

Let's see if we can get this back on topic despite your constant efforts to derail it.

I take it you ain't gonna 'fess up to any of them mistakes then. Just carry on lecturing us all on how little we know of biology? At least you dropped that ridiculous frameshift argument!

You already have no clue how the highly conserved regulatory gene involved in the Cajal–Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. Now let's talk about what happens when highly conserved genes involved in neural functions change:

Let's not! Because all you're going to argue is that all mutations in conserved areas are deleterious, something you cannot back up. Citing examples of genetic diseases isn't an argument, except from ignorance. We know beneficial mutations happen. They might not be likely in conserved sequences, but not likely is different from not possible.

The examples of deleterious affects on neural functions are legion and not one example of a beneficial affect to be had.

Well, I guess beneficial effects don't tend to be quite so drastic, do they?

I'm not limiting myself to goddidit and goddidntdoit clutch phrases. I want to know what must have happened, the best way to know that is to learn how species are limited by the deleterious affects of mutations.

If you just want to know what must have happened, then why are you still here? Get out and do the research. Alternatively, sit tight and wait for someone else to do it. Quit telling us we're all wrong without good evidence, and lecturing us on our supposed deficits in biology when your credentials aren't exactly golden.

 

[Naraoia]

The regulatory gene HAR1f is one example among many of unique human genes involved in the development of the brain. I have no special interest in RNA non-coding genes but that was an extraordinary example of a region that would have had to undergo a massive overhaul.

You seem to want to focus on RNA, I think I can work with that.

Bravo, you deserve a round of applause for that. If memory serves it was you who brought up an RNA gene in the first place

Ok, you are wanting to talk about non-coding RNA genes and point mutations. That's pretty specific but intriguing.

In science you'd better be specific if you want to be meaningful. There's no statistics that can help you about vague questions.

There is nothing in scientific literature saying there are any affects other then deleterious. I research this regularly and I am not exaggerating when I say the examples of disease and disorder are legion while beneficial affects are non-existent.

Fair enough...

Honestly I don't know if you are just putting me on, running me in circles or simply wanting to focus on a narrow range of details. I would suggest we take a look at this:

All I want is that you support your arguments. By the way, the abstract doesn't say anything about the frequency of whatever type of mutations, so I don't know what point you want to make with it.

And then you continue with the article...

[...article...]Isn't that what you asked for when you said:

Do they say a word about beneficial mutations (or the lack thereof)? No. Therefore, irrelevant. If they have anything relevant to say I'd rather see that.

If you think I have a long list of diseases and disorders try scanning that article. They will tell you that, 'these programs and mechanisms are perturbed in disease' and proceed to give you a long list of them.

That 'these programs and mechanisms are perturbed in disease' doesn't tell us anything about what may happen without disease.

 

[Loudmouth]

The regulatory gene HAR1f is one example among many of unique human genes involved in the development of the brain. I have no special interest in RNA non-coding genes but that was an extraordinary example of a region that would have had to undergo a massive overhaul.

I still don't understand your choice of words here. What does "massive overhaul" mean in this context?

There is nothing in scientific literature saying there are any affects other then deleterious. I research this regularly and I am not exaggerating when I say the examples of disease and disorder are legion while beneficial affects are non-existent.

Then surely you have heard of the Human Haplotype project. I urge you to visit www.hapmap.com. You can search for brain specific genes and you will find that there are many different alleles (i.e. mutations) for these genes that are not disease related.

 

[Pete Harcoff]

The second half of this sentence means the first half may not be true.

Based on the literature I've read on mutation rates (particularly derived from experiments), beneficial mutations do appear to be rare on the order of at least several magnitudes. Mind you, I've seen nothing to suggest they are rare enough to be a problem for evolution, particularly human->chimp evolution. I'd leave it up to mark to show why, but he never has and probably never will.

 

[Naraoia]

Based on the literature I've read on mutation rates (particularly derived from experiments), beneficial mutations do appear to be rare on the order of at least several magnitudes.

Can you give me one or two good and understandable papers on that? It's way too late for my evolution essay but learning isn't just for essays

 

[Blayz]

Based on the literature I've read on mutation rates (particularly derived from experiments), beneficial mutations do appear to be rare on the order of at least several magnitudes. Mind you, I've seen nothing to suggest they are rare enough to be a problem for evolution, particularly human->chimp evolution. I'd leave it up to mark to show why, but he never has and probably never will.

It has to depend on your definition of beneficial, doesn't it? Every cell in your body differs by every other by 120 bases, and every human differs from every other by 3 million. Finding beneficial mutations is hard because you have to
a) define bebeficial
b) develop a suitable animal model
c) perform the genetic mapping
d) get money for a thru c.

 

[AlHailThePowerOfJesusName]

The Brain Refutes Evolution

 

[Pete Harcoff]

Can you give me one or two good and understandable papers on that? It's way too late for my evolution essay but learning isn't just for essays

Sure: Fitness effects of advantageous mutations in evolving Escherichia coli populations

 

[mark kennedy]

Can you give me one or two good and understandable papers on that? It's way too late for my evolution essay but learning isn't just for essays

You might find this interesting:

If RNA's only job were making proteins, then nearly all the RNAs produced in cells should be transcripts of protein-coding genes. (A small fraction of RNAs serve in the protein-transcription machinery.) But in 2005, Jill Cheng and her colleagues at Affymetrix, a genomics company in Santa Clara, Calif., showed that less than half of the RNA produced by 10 of the chromosomes in human cells represented transcripts of traditional genes. In the team's experiments, 57 percent of the RNA was transcribed from noncoding, "junk" regions.

The results from ENCODE were even more striking. In the slice of DNA studied in that project, between 74 percent and 93 percent of the genome produced RNA transcripts. What becomes of this tremendous output is uncertain. John M. Greally of the Albert Einstein College of Medicine in New York says it's likely that some portion of it is made accidentally and simply discarded. But the discovery that so much of the genome is being transcribed into RNA underscores how out-of-date the central dogma has become.

Indeed, the closer researchers look, the more functions they find that RNA transcripts perform. An alphabet soup of new acronyms describes the newfound roles of RNAs.... In mice, about 34,000 of the RNA transcripts produced by the genome are nonprotein-coding, outnumbering the roughly 32,000 transcripts that code for proteins, according to a 2005 study by an international group of scientists called the Functional Annotation of Mouse Consortium.​

​

Genome 2.0 Mountains of new data are challenging old views by Patrick Barry. Science News Online.

I have been looking for molecular machines involved in adaptations but I thought they would be enzymes or something. I'm starting to wonder if it's not the non-coding RNA behind it.

 

[Blayz]

I have been looking for molecular machines involved in adaptations but I thought they would be enzymes or something. I'm starting to wonder if it's not the non-coding RNA behind it.

You should read the work of one of my erstwhile profs, John Mattick at UQ. He is the champion of the RNA computer.

here's a starter
http://www.imb.uq.edu.au/index.html?id=11681

 

[MoonLancer]

The Brain Refutes Evolution

only yours, and its more of a stubborn denial.

 

[mark kennedy]

Bravo, you deserve a round of applause for that. If memory serves it was you who brought up an RNA gene in the first place

Actually I am glad you brought it up and insisted on me pursuing these non-coding RNA genes. By the way, the Science News Online article I recommended mentions the RNA regulatory gene I brought up:

The researchers found that one of these sequences is a noncoding region of DNA that's related to brain function, they reported in the Sept. 14, 2006 Nature. Pollard and her colleagues speculate that this region produces a regulatory RNA and that changes in this RNA contributed to the evolution of the human brain.

With regulatory RNAs appearing to play such an instrumental role in animal development, it's no surprise that scientists are finding disease-associated mutations in regions of the genome formerly regarded as junk.

David Altshuler of the Broad Institute in Cambridge, Mass., and his colleagues looked for DNA mutations in 1,464 patients with type 2 diabetes. Three of the mutations that correlated with the disease were in DNA segments that don't code for proteins, the team reported in the June 1 Science. Other scientists have found mutations in noncoding DNA that link to diseases such as autism, breast cancer, lung cancer, prostate cancer, and schizophrenia.​

In science you'd better be specific if you want to be meaningful. There's no statistics that can help you about vague questions.

Well yea and Google search engines can be a little unforgiving as well.

Fair enough...

Just hang on, I really don't have a handle on it but I keep running into talk about splice sites. Mostly it's disease and disorder but RNA genes can splice other RNA genes. I realize I am talking in generalities here but it's just a germ of an idea I'm catching out of the corner of my eye.

All I want is that you support your arguments. By the way, the abstract doesn't say anything about the frequency of whatever type of mutations, so I don't know what point you want to make with it.

Generally discussions about mutations are anecdotal, particularly when they are discovering so many new things. I don't know if it was accidental but you actually hit on some pretty interesting stuff.

Mutations mostly do nothing at all, then the ones that have an affect are usually deleterious. Beneficial affects will be rare in the extreme and then usually only for a time. When your looking for adaptations I'm thinking random mutations are a dead end, can't really prove it yet but it still seems to be the case.

And then you continue with the article...

Do they say a word about beneficial mutations (or the lack thereof)? No. Therefore, irrelevant. If they have anything relevant to say I'd rather see that.

That 'these programs and mechanisms are perturbed in disease' doesn't tell us anything about what may happen without disease.

Like I said, they are not going to speculate about what might happen. What they will elaborate on at length is known affects and more importantly, what these non-coding RNA genes actually do.

At any rate, just wanted to tell you that what I thought was a wild goose chase turned out to be pretty interesting.

Thanks a bunch
Mark

 

[mark kennedy]

You should read the work of one of my erstwhile profs, John Mattick at UQ. He is the champion of the RNA computer.

here's a starter
http://www.imb.uq.edu.au/index.html?id=11681

Thanks, I've seen some of his work. He was one of the authors of the, 'Non-coding RNAs in the nervous system' I quoted from earlier. At any rate, I'm tried and I've been staring at this thing so long I'm seeing spots.

Catch you on the flip flop.

 

[RealityCheck]

Uh, since when have advertising trolls been spamming these boards?

 

[AlHailThePowerOfJesusName]

Kill the troll!

 

[Blayz]

Kill the troll!

My irony meter just broke.

 

[Chalnoth]

My irony meter just broke.

How often do you get that thing repaired these days?

 

[TheOutsider]

How often do you get that thing repaired these days?

Around here, you have to buy them in bulk.

 

[Naraoia]

You might find this interesting:

Very interesting but I wasn't asking for that