Darwin and Mendel

[bhsmte]

I imagine that the context was likely that he called it a universal acid in that it ate away at previously held ideas. Note however that I honestly didn't know who Dennet was, but I do recognize the book (never read it or any other book of that nature).

Correct, Dennett is stating the overwhelming objective evidence points away from long held religious beliefs, such as creation and this is not pleasant for those who hold onto that belief and is like an "acid".

Here is a little Dennett material. He is one smart dude.

Full Length Talk by Daniel Dennett - 'How To Tell You're An Atheist' - YouTube

 

[mark kennedy]

Just because an idea has been traditionally held for a long time doesn't make it better, but it doesn't make it bad either. What matters is whether or not it works for the present.

Got a little puzzle for you, Renaissance means 'rebirth', what is it a rebirth of? I'm not fishing here, it was classic Greek geometry and philosophy. There is a lot in the classics, traditional classics have revealed more every time they were explored.

 

[sfs]

As a rule mutations are not beneficial, so that's an argument from an exception.

No, it's not an argument from exception. It's a statement that a real process has been observed to occur many, many times.

It takes even more faith to believe an unprecedented duplication of SRGAP2a and stable mutations happened on the centromere to account for SRGAP2b,c and d.

What's unprecedented about it? Please be specific. Gene duplications happen all the time.

Most mutations are deleterious so I think his model is valid.

That doesn't address the problem with the Kondrashov's model. His model assumes that there is an abundance of sites in the human genome where ther are different possible bases, bases whose fitness differs by only a tiny amount. That part of the model is almost certainly right. It also assumes that most of those sites have the more fit base. That part is wrong in an evolutionary model: there is no mechanism for very slightly beneficial alleles to be preferred, since natural selection is too weak to act on these. So why do you think that assumption is correct?

Above, you extrapolated mutations account for most the benefits to an organism, even though most are neutral. Is extrapolation is only valid when it supports Darwinism?

Extrapolation that contradicts known facts about nature (like how unselected alleles behave) is not a good idea. I assume you agree.

You act as if it's common knowledge the modern synthesis has been replaced.

It's certainly common knowledge among evolutionary biologists that quite a lot has been added to evolutionary theory since the modern synthesis. So again, why did you cite the article?

Can you show us, not tell us, where genetic homeostasis is violated?

I already gave Mark several examples of positive selection; each of those is a violation of genetic homeostasis.

The genetic code being a language for example.
The origin of gene regulatory circuits in new species for another.

These would require a new thread -- this one is already crowded enough.

 

[TLK Valentine]

Got a little puzzle for you, Renaissance means 'rebirth', what is it a rebirth of? I'm not fishing here, it was classic Greek geometry and philosophy. There is a lot in the classics, traditional classics have revealed more every time they were explored.

Indeed -- and we owe a lot to the Arab world for preserving this material so that the Europeans could rediscover it.

 

[PsychoSarah]

Got a little puzzle for you, Renaissance means 'rebirth', what is it a rebirth of? I'm not fishing here, it was classic Greek geometry and philosophy. There is a lot in the classics, traditional classics have revealed more every time they were explored.

True, but remember the Dark Ages prior to that point was the height of religious power as far as Christianity was concerned. And one of the worst times to be alive in Europe.

 

[mark kennedy]

True, but remember the Dark Ages prior to that point was the height of religious power as far as Christianity was concerned. And one of the worst times to be alive in Europe.

The history of the Roman Catholic Church is bizarre, downright Shakespearean in it's political intrigue. Just watched 'Medici: Godfathers of the Renaissance', they installed three Popes and sponsored guys like Leonardo da Vinci and Michelangelo, Galileo Galilei.

I find it hard to believe that the Italian Renaissance was a bad time to be alive, at least if you lived someplace like Florence. It's called the Dark Ages because there is so little known about the period. That had a lot to do with Vikings, Visigods, Mongols and a bunch of other looting and pillaging in Europe during the period. The Renaissance was a time when the classics were revisited, that's what the word implies, the 'rebirth' of the classics. I'd say Italy developed a great deal of technology from the ancient Greeks.

 

[SLP]

You do know a condescending attitude only gets you so far.

How far do you think the Dunning-Kruger effect will get you?

 

[Loudmouth]

This isn't the first time I looked into this and as I recall it came down to regulation. If you see something significant there do tell but random links followed by begging the question of proof doesn't interest me.

I find it significant that a mutation results in a new phenotype that is then selected for. Why don't you find it significant, especially given the fact that you claim that such things don't exist?

Ok, so you should have no trouble characterizing the mutations. Are they substitutions, indels, or inversions?

It's right there in the paper.

"Second, all four nonsynonymous substitutions that show an association with coat color cause a change in amino acid charge. At the first three amino acid sites (18, 109, 160), the change is from a positively charged arginine to an uncharged amino acid. At the fourth site (233), an uncharged glutamine is replaced with a positively charged histidine. Additionally, all four mutations are located in functionally important regions of the receptor that are likely to be involved in interactions with other proteins. Two of the substitutions are located in extracellular regions (amino acid sites 18 and 109) and two are located in intracellular regions (sites 160 and 233); none are located in transmembrane domains of the receptor (Fig. 3). A number of previously described dark phenotypes at the extension locus in the mouse (16) and other organisms (21–25) are due to single amino acid mutations in MC1R, although none of the mutations described here have been previously reported."
The genetic basis of adaptive melanism in pocket mice

Why are these mutations not screened and more importantly, what caused the change in the first place? Any change in the gene is considered a mutation so don't bother trying to lure me into an argument against mutations. I know you are equivocating mutations, variations and epigentic adaptations, even if you don't. I do have to wonder if you are aware of the differences.

Screened? What do you even mean? All offspring in vertebrate species are born with mutations, as far as I am aware. Humans are born with 20 to 50 mutations. I am talking about a change in DNA sequence in a gene for a protein that changes the way it reacts with its ligand. In this case, the mutations in the murine Mc1r gene produced a cell membrane bound protein that is more senstive to melacortinin, resulting in higher expression of melanin.

Would you just stop using 'evolution' as a slogan and a clutch phrase, no one else cares and I think it's lame. Evolution is defined as the change of alleles, any change is a mutation, so a mutation is an example of evolution.

I will keep using the appropriate scientific term, which is evolution.

Why does it bother you so much?

Begging the question of proof again...

Baloney.

That's nice that you mapped fruit flies, that was cutting edge stuff fifty years ago. What I know about Mendelian genetics is that adaptations are not the result of random mutations.

Talk about 50 year old science . . .

Luria–Delbrück experiment - Wikipedia, the free encyclopedia

http://jb.asm.org/content/63/3/399.full.pdf

It was shown 50 years ago that adaptations were the result of random mutations. Luria and Delbruck won the Nobel for demonstrating this.

They rejected neodarwinism because it included Medelian genetics, why do you deny the obvious in circles?

You are the one drawing the circle, not I.

Marx and Engels loved Darwinism but Darwin couldn't have cared less about communism. Darwinism has falling out of favor with the intellectual elite and almost utterly disproven by scientists. The Synthesis brought Darwinism back in to the mix by piggy backing it on genetics, a new up and coming science that had great promise. It's a scam, genetics never needed Darwinism and Darwinism would have died of it's own inadequacies had it not been able to leach off of genetics.

More nonsense. When will you admit that Soviet Russia rejected Darwinism? Why continue with the denial?

Yea actually you are the one getting it wrong, did you ever find a single germline cell invasion into the human genome documented anywhere?

It's documented in the human genome paper:

Table 11 : Initial sequencing and analysis of the human genome : Nature

You still won't admit that there are over 200,000 ERV's in the human genome? You are still in denial?

You mean why won't I chase your pedantic chants in circles, because it goes nowhere, that's why.

Denial denial denial. That's all you have.

Yet again, you have been proven wrong and it won't change your argument one bit. You just going to repeat your error and no one on here will correct you because Creationists will have nothing to do with these forums and none of your cohorts care about the actual facts.

I have been proven wrong? Lysenkoism is more than just the rejection of Mendelian genetics. They embraced Lamarckism which is the exact opposite of Darwinian evolution. Why do you insist on being wrong on this one?

You've never argued from or for science, you have always trolled the forum for creationists and taunted them till they left. It's called trolling and as far as I can tell the only ones left are the trollers.

Who is the one citing multiple peer reviewed scientific articles in this thread? That would be me.

There's no reason for a flame war unless your ready to concede an argument that you have already lost. This would be a really good time to take an interest in genetics and some of the research that has been so important to us over the years. The problem is that you do little more then post links and chant slogans and it's a shame. There is so much to be learned here.

Grace and peace,
Mark

The flame war started when you lied about Nazis and Russians in order to cast blame on a theory you don't even understand. That would be the very first post, by you.

 

[Loudmouth]

Sounds like some proselytizing for the belief in common ancestry. You're pushing mutation rates beyond and reasonable rate to think that explains 40 million indel and substitution mutations. Another mistake is assuming those mutations are the only differences between humans and chimps.
How about you SHOW us not tell us how mutations created new genes? Specifically the SRGAP2B, SRGAP2C, and SRGAP2D genes flanking the centromere?

You are the one claiming that the observed processes of mutation can not produce those changes. You going to step up and prove it?

 

[Loudmouth]

As a rule mutations are not beneficial, so that's an argument from an exception. Takes faith to believe those arguments. It takes even more faith to believe an unprecedented duplication of SRGAP2a and stable mutations happened on the centromere to account for SRGAP2b,c and d.



Most mutations are deleterious so I think his model is valid.
Above, you extrapolated mutations account for most the benefits to an organism, even though most are neutral. Is extrapolation is only valid when it supports Darwinism?

I see a lot of claims, but zero peer reviewed references to back them up. Why is that?

The genetic code being a language for example.

If genetics is a code, then so too is the rest of chemistry. The code for oxygen can be spelled like this

The origin of gene regulatory circuits in new species for another.

That's exactly what the pocket mouse example deals with. It is a change in a protein which changes the regulation of a gene.

The genetic basis of adaptive melanism in pocket mice

 

[sfs]

Interesting.

"Interesting" meaning "I agree that I got exactly what I asked for, a specific beneficial mutation", or meaning "I'm going to ignore this answer"?

It's just something that makes no sense to me, the ERVs are the result of highly unlikely viral invasions in the Germline. This happens about 25 million years ago so it's right when the primates were separating along broad taxonomic lines. I can't believe I'm the only one who ever had a problem with that.

It's also something that had nothing to do with the conversation. If someone remarks that the weather is nice today, do you respond, "No, they account for 8% of the genome"? Kind of a bonkers response, no?

But specifically white fur, which of course has the advantage of camouflage. You missed the question, why white?

How did we come to be talking about white fur? Regardless, in cases where white fur has been selected fur, it's white fur because that's what the mutation produces, and that trait is beneficial so it spreads.

Let's not put the cause before the effect, there has to be a reason for the coat to change white. What's more I don't think a northern migration of various species that adapted on an evolutionary scale qualifies as a made up story. We know of some pretty dramatic evolutionary adaptations resulting from populations moving further and further north. This is one of my favorites:

Thr-Ala-Ala coding element, and de novo amplification of the coding element gave rise to an entirely new coding region that encodes the repetitive tripeptide backbone of AFGP. The deletion, recruitment, and amplification events did not need to occur in the order given. Indeed, an AFGP/trypsinogen hybrid protein coding region formed by some amount of duplication of the 9-nt Thr-Ala-Ala coding element before bulk deletion of trypsinogen sequence might in fact be a more stable structure for the evolving gene than large deletion first and amplification later. Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish​

I'm just saying, arctic wildlife had to evolve with one very important trait that is vital, the white coat and skin. There is also the issue of this enigmatic protein coding sequence apparently built from a simple repeat. Surely this interests you, making comparisons to populations of other climates.

I have no idea why any of this is relevant. You asked for beneficial mutations, and you've been given them. Do you agree or not?

That's putting the effect before the cause and not all changes in the genome are random. I'm sure there are adaptive mechanisms and I suspect they can be found by comparing arctic wildlife to populations that live in warmer climates. White is a very specific color and some wildlife is only white at birth like the seals, that doesn't sound random to me.

I'll be honest, I haven't a clue where to look for a mechanism like this. I just think random copy errors is the worst possible answer.

Try to hear what people are saying to you. Yes, we can identify the mechanism of adaptation by comparing arctic populations to temperate ones, just as we can find the mechanism for similar adaptations by comparing humans from northern latitudes to those from the tropics, and those from high altitudes to those in the lowlands, and so on. Not only can we make these comparisons, we have done so. In fact, that's precisely the kind of comparison I've spent a good deal of my career on. And when we make those comparisons, we do indeed find the mechanism: random mutations filtered by natural selection.

Now do you have an actual objection to that mechanism, or do you just reject it because you have a fuzzy feeling that it isn't plausible?

 

[Loudmouth]

It's just something that makes no sense to me, the ERVs are the result of highly unlikely viral invasions in the Germline. This happens about 25 million years ago so it's right when the primates were separating along broad taxonomic lines. I can't believe I'm the only one who ever had a problem with that.

You are aware that our lineage has accumulated ERV's since it split from the rest of the primates, right? In fact, we have about 100 ERV's from the time since our split from chimps.

Are you also aware that an argument from incredulity is not going to fly? Do you really think "Well, I just can't believe it" is a valid argument?

But specifically white fur, which of course has the advantage of camouflage. You missed the question, why white? Let's not put the cause before the effect, there has to be a reason for the coat to change white.

Why not white? Mutations in the same genes which increase melanin in response to environmental cues can also reduce melanin production.

That's putting the effect before the cause and not all changes in the genome are random. I'm sure there are adaptive mechanisms and I suspect they can be found by comparing arctic wildlife to populations that live in warmer climates. White is a very specific color and some wildlife is only white at birth like the seals, that doesn't sound random to me.

What are these adaptive mechanisms that mutate specific genes at specifc bases in response to specific stimuli?

I'll be honest, I haven't a clue where to look for a mechanism like this. I just think random copy errors is the worst possible answer.

That would be the opposite of science.

 

[sfs]

He's going to say a beneficial allele of course, just doesn't know or want to talk about how it got there.

It got there by mutation, of course. Just like the other 500 billion mutations that have occurred just in the current generation of humans.

 

[Loudmouth]

Just to nip this in the bud, we already know that humans are born with mutations. They have sequenced mom and dad's DNA, and then compared it to baby's DNA. Guess what? Baby has mutations not found in Mommy and Daddy.

"Here we present, to our knowledge, the first direct comparative analysis of male and female germline mutation rates from the complete genome sequences of two parent-offspring trios. Through extensive validation, we identified 49 and 35 germline de novo mutations (DNMs) in two trio offspring, . . ."
http://www.nature.com/ng/journal/v43/n7/full/ng.862.html

We also know from work 50 years ago (Luria, Delburck, and the Lederbergs) that the mutations are random with respect to fitness.

 

[sfs]

Just to nip this in the bud, we already know that humans are born with mutations. They have sequenced mom and dad's DNA, and then compared it to baby's DNA. Guess what? Baby has mutations not found in Mommy and Daddy.

"Here we present, to our knowledge, the first direct comparative analysis of male and female germline mutation rates from the complete genome sequences of two parent-offspring trios. Through extensive validation, we identified 49 and 35 germline de novo mutations (DNMs) in two trio offspring, . . ."
http://www.nature.com/ng/journal/v43/n7/full/ng.862.html

We also know from work 50 years ago (Luria, Delburck, and the Lederbergs) that the mutations are random with respect to fitness.

Yeah, but they didn't watch in real time as the mutations actually occurred. So all we have is guesswork and supposition. Or something like that.

 

[Loudmouth]

Yeah, but they didn't watch in real time as the mutations actually occurred. So all we have is guesswork and supposition. Or something like that.

I have always liked this article.

"We describe the use of a series of gradually expanded thymine nucleobase analogs in probing steric effects in DNA polymerase efficiency and fidelity. In these nonpolar compounds, the base size was increased incrementally over a 1.0-A range by use of variably sized atoms (H, F, Cl, Br, and I) to replace the oxygen molecules of thymine. Kinetics studies with DNA Pol I (Klenow fragment, exonuclease-deficient) in vitro showed that replication efficiency opposite adenine increased through the series, reaching a peak at the chlorinated compound. Efficiency then dropped markedly as a steric tightness limit was apparently reached. Importantly, fidelity also followed this trend, with the fidelity maximum at dichlorotoluene, the largest compound that fits without apparent repulsion."
Probing the active site tightness o... [Proc Natl Acad Sci U S A. 2005] - PubMed - NCBI

Just to pull it full circle, they used the tonB gene to measure mutation rates which happens to be the same gene that results in bacteriophage resistance seen in the Luria-Delbruck fluctuation assay. They saw that mutation rates declined as you increased the size of the incoming nucleotide up to the point that the nucleotide could no longer fit into the active site of the polymerase. This demonstrates that there is a loose fit between the polymerase and incoming nucleotide which results in the wrong base being incorporated at random times.

 

[mark kennedy]

It got there by mutation, of course. Just like the other 500 billion mutations that have occurred just in the current generation of humans.

But when do they become permanently fixed, that is, what are their odds of fixation?

Most mutations, even those that are favorable, are accidentally lost when rare (The population genetics of adaptation, Orr HA.)​

Generally they are more likely to happen somewhere other then a protein coding gene, so yea it would be neutral as most are. However, single substitution can be devastating, causes frameshifts, disease and disorder more often then not in protein coding genes. The fact is that there are a host of DNA repair mechanisms:

DNA Repair​

Where are the adaptation mechanisms? That's what I would like to know.

 

[Loudmouth]

But when do they become permanently fixed, that is, what are their odds of fixation?

The odds of fixation are 1/n where n is the population size. However, I'm guessing that you aren't asking the odds of a mutation going from one person in one generation to 99% of the population in a future generation.

If you are asking when a mutation becomes a permanent part of a genome, then the answer is anywhere in the replication of the genome during the process of producing gametes. Most mutations come from men due to the fact that we are continually making new gametes which means more replications. Women produce all of their eggs while still in the womb, so there are only a few generation of cells between early progenitor cells and fully mature eggs.

Most mutations, even those that are favorable, are accidentally lost when rare (The population genetics of adaptation, Orr HA.)​

Every single person is born with 20 to 50 mutations. It is the same thing as saying that a winning lottery ticket is rare, yet people win the lottery all of the time. Unless a lineage goes extinct, you will continue to have winners as rare mutations have to be passed on just by the fact that people keep reproducing.

Generally they are more likely to happen somewhere other then a protein coding gene, so yea it would be neutral as most are. However, single substitution can be devastating, causes frameshifts, disease and disorder. The fact is that there are a host of DNA repair mechanisms:

A single substitution can also be nearly neutral, or beneficial. You always forget to mention that.

What about the hundreds of thousands of differences between the proteins of humans and chimps. Are all of those devastatingly detrimental?

Where are the adaptation mechanisms? That's what I would like to know.

You are the one who claims they exist. You show us.

 

[sfs]

So were our examples beneficial mutations or not, Mark?

 

[Vaccine]

No, it's not an argument from exception. It's a statement that a real process has been observed to occur many, many times.

Talk origins has a list of so-called "beneficial" mutations but beneficial and gain of function mutations are not the same thing. Got any examples of mutations causing a completely new function that didn't exist before? You don't find a lighting strike that made a X and infer enough lightning strikes could write a poem. You're telling me SRGAP2a was duplicated and stabilized 3x in humans because you can point to a beneficial mutation elsewhere? That's fine if you believe it, but I don't have enough faith in mutations and selections creative power.

What's unprecedented about it? Please be specific. Gene duplications happen all the time.

"There is no precedent for duplicated genes even being able to jump into these super-stable sequences, much less reorganizing themselves afterwards. "
So, why are the human and chimpanzee/bonobo genomes so similar? A reply to Professor Larry Moran | Uncommon Descent

That doesn't address the problem with the Kondrashov's model. His model assumes that there is an abundance of sites in the human genome where ther are different possible bases, bases whose fitness differs by only a tiny amount. That part of the model is almost certainly right. It also assumes that most of those sites have the more fit base. That part is wrong in an evolutionary model: there is no mechanism for very slightly beneficial alleles to be preferred, since natural selection is too weak to act on these. So why do you think that assumption is correct?

I didn't see where he made that assumption:
"all nucleotide sites have selection coefficients within this range"

I think it comes down to whether you believe beneficial mutations outnumber deleterious mutations or not. I think his model is correct because there are more deleterious mutations then beneficial mutations.

Extrapolation that contradicts known facts about nature (like how unselected alleles behave) is not a good idea. I assume you agree.

You use the term "facts" very generously.

I already gave Mark several examples of positive selection; each of those is a violation of genetic homeostasis.

Another example of using the micro- to infer the macro-. We can jump a foot so given enough time we can jump 30 foot. Those positive selections did not produce a new species so there was no violation of genetic homeostasis.