Is the Human Brain a Null Hypothesis for Darwinian Evolution?

[Loudmouth]

There is no dichotomy, the problem is that the only alternative to naturalistic evolution is God, as cause of anything, is rejected a priori (without prior).

It isn't rejected a priori. It just so happens that you have no evidence. There is nothing for science to investigate.

Obviously, an a priori assumption of universal common descent going all the way back to, and including, the Big Bang.

That is not assumed.

 

[Loudmouth]

Why is it the only alternative? Saying it's either A or B when you have no idea if there could be a C is a blatant false dichotomy. I admit that I haven't followed all your arguments but it seems that they are about specific mechanisms of evolution. Is it not possible that even if you managed to show that these mechanisms didn't work as we understand them to that there could be other naturalistic mechanisms that we haven't yet discovered or understood?

Why do you call common descent an assumption? It's a conclusion drawn from observations, your bias is showing.

Quite right. It's like saying that either fire is caused by phlogiston, or fire is caused by God. Phlogiston theory was refuted quite a while ago. Did this prove that fire was caused by God? Nope.

 

[Loudmouth]

Oh but you don't do null hypothesis or we would be talking about the human brain.

I showed you what the null hypothesis is.

Taxonomy is organized based on semantics and for the convenience of retrieving information. That is not an argument.

Phylogenies are not organized in such a manner. I am talking about phylogenies.

"Computational phylogenetics is the application of computational algorithms, methods, and programs to phylogenetic analyses. The goal is to assemble a phylogenetic tree representing a hypothesis about the evolutionary ancestry of a set of genes, species, or other taxa."
https://en.wikipedia.org/wiki/Computational_phylogenetics

That is not semantics.

Scientific method relies on directly observed or demonstrated facts, not a priori assumptions.

The morphology of extinct and extant species are directly observed and demonstrated facts.

The sequencing of a species genome is a directly observed and demonstrable fact.

This is what is used to test the theory of evolution.

Deleterious effects.

Please demonstrate that every single retroviral insertion will have a deleterious effect.

Again with the 'we', there is no one left LM. I'm going to tell you like I have Papias, they are all gone because the culture wars are over.

"We" is the larger scientific community. We have observed retroviruses inserting into genomes in the lab. Run away from this fact all you want, but there it remains.

Also, you are still fighting the culture war. You think that self enforced ignorance of the facts will allow you to attack knowledge gained through those facts. You are fighting the same war as book burners of the past.

Now as far as the lab work I'm aware of the Phoenix virus and it can't even be reconstructed. The ERVs are a dead issue and chasing it in circles is a waste of time.

They did reconstruct it.

" Here, we derived in silico the sequence of the putative ancestral “progenitor” element of one of the most recently amplified family—the HERV-K family—and constructed it. This element, Phoenix, produces viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665638/

They lined up a whole bunch of HERV-K insertions and derived the consensus sequence. They then built that DNA sequence and injected it into cells. Guess what? It started inserting into the genome, just as expected.

Nope, just bored to death with the circular fallacious logic.

You haven't been able to point to a single circular argument.

Again with the we, you are performing in an empty theater.

And yet here you are responding to it, the warrior of the culture war looking to burn down knowledge in the name of theologic purity.

You are rummaging a junk yard pretending to pass it off as a viable cause. Unless you are oblivious we are talking about adaptive evolution and I'm really tired of you trying to get me to chase a red herring.

Unless you are oblivious, I have already addressed that. I pointed to the 40 million mutations that separate chimps and humans. Those mutations include those that are responsible for the differences in brain size and intelligence.

They are a lame homology argument, nothing more.

Please stop lying about my argument.

I have said over and over and over . . . IT IS A PHYLOGENETIC ARGUMENT.

 

[mark kennedy]

I showed you what the null hypothesis is.

Unless you are oblivious, I have already addressed that. I pointed to the 40 million mutations that separate chimps and humans. Those mutations include those that are responsible for the differences in brain size and intelligence.

Please stop lying about my argument.

I have said over and over and over . . . IT IS A PHYLOGENETIC ARGUMENT.

Your all over the road and it's been a while since I took any of the convoluted mess seriously. Let's start with the fact that the OP and the proposal of the thread has been left unaddressed. See (ERVs put chimp/human common ancestry beyond any reasonable doubt.) The ERVs are a dead issue, I have not the slightest intention of chasing this around the mulberry bush with you. This is the null hypothesis I proposed, more importantly, the one Darwin suggested:

If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. (On the Origin of Species, Chapter 6 - Difficulties on Theory)
​

The Phylogentic Argument is a waste of time it's already been dealt with at length. Taxonomy is a highly subjective means of organizing details, nothing more.

What we really know about ERVs:

• Most retroviruses infect somatic cells, but might infect of germline cells on rare occasions.
• ERVs have been inactivated by mutation for the most part and do nothing.
• ERVs have been proposed to be involved in multiple sclerosis (MS) and HERVs were found in greater frequency in the sera of people with schizophrenia.
• 98,000 human ERV elements and fragments making up nearly 8% of our genome and no HERVs capable of replication had been identified.

Endogenous retrovirus

The inverse logic is intuitively obvious, if the homology argument for things in common can prove common ancestry then differences can prove independent lineage, thus creation. Failure to accept the inverse logic is tantamount to an open admission of predicating all arguments on assumptions made before the evidence is considered.

One of the HERVs (Human ERVs) was reconstructed.

This family, termed HERV-K (HML2), makes up less than 1% of HERV elements but is one of the most studied (Human endogenous retroviruses)​

What makes this such a lackluster argument is that the Darwinian will just keep repeating that ERVs are the result of germline invasions, something that has simply been assumed as far as I can tell. Long technical discussions about how ERVs work are tedious so most Creationists won't bother with them. The researchers got the 'Phoenix Virus' to work, it had 20 amino acids and just one frameshift. In order to understand why this is important you would need to know how protein coding works on a molecular level.

Phoenix Virus research:

the characterization of the insertion sites of 11 (nearly) full-length HERV-K(HML2) endogenous elements gave a rather different result, with five of them found far from known human genes (>100 kb on each side), four being in the vicinity (<20 kb) of genes, and only two inserted within genes (M. Dewannieux, unpubl.). This discrepancy is probably due to the strong counter-selection that should operate in vivo against insertions within genes, which are most probably deleterious for the proper expression of the targeted genes. (Identification of an infectious progenitor for the multiple-copy HERV-K human endogenous retroelements (Genome Research, Oct. 31,2006)​

The HERV-K (HML2) is less then 1% of the human genome and yet it is the most studied. When they revive this sequence they actually manage to reconstruct it but with one frameshift. What is interesting about the results is that only two are within genes. The explanation being that they are probably deleterious so their are defenses that prevent this. Doesn't it make sense that the germline cells would be protected as well?

The amino acids need an open reading frame. When they got it working they they wanted to see how it would interact with living cells and it was introduced to live T cells. Guess what, it really can get into the DNA but I'm still waiting for the part where it's demonstrated that massive germline invasions are possible.

Let's take a look at a little Darwinian mythology and try to picture what they believe happened here. Our supposed ancestors from about 25 million years ago would have been inundated with a massive dose of these pathological ERV viruses. As a result the ERVs would replicate at random in the genomes until random mutations disrupted the reading frame, leaving fragments like the HERV K. Getting this far into the ancestry of apes in Darwinian evolution leaves you following a lot of long 'ghost lineages' but geographically always go back to the East African Rift valley. (Nature, 30 May 2013)

This is an area that has made a number of paleontologists famous, especially the Leaky family who found so many of the Homo habilis and Homo erectus fossils in and around this area. So in case you were wondering when this supposed ERV onslaught of germline invasions would have happened it would have been right around there. What the Darwinian desperately wants to prove is a correlation between the molecular evidence and the fossil record. What they are doing is taking this highly technical ERV research, molecular clock age estimates and reconcile it with the fossil record. My positive argument here will simply be this, no matter how many ways it's reconstructed ERVs are just another homology argument.

You are trying to use an old statistical argument, specifically, the odds of mutations occurring at a specific loci. It's become one of the main stays of the Talk Origins arguments and since Creationists tend to ignore it they think it means it's irrefutable. It's not, it's just so obscure Creationists are bored to death with it.

Figure 4.4.1. Human endogenous retrovirus K (HERV-K) insertions in identical chromosomal locations in various primates

There are at least seven different known instances of common retrogene insertions between chimps and humans, and this number is sure to grow as both these organism's genomes are sequenced (see Prediction 4.5: Molecular evidence - Endogenous retroviruses)

That's about it, Talk Origins wants you to accept the assumption that ERVs are the result of germline invasions then drop a probability argument in your lap. The essence of the argument is the strongest argument against germline invasions in the first place. They are rare and they are pretty much random. Once they hook you with the assumption that they must be the result of a germline invasion they use the probability argument for common ancestry. The only way it would be possible for mutations and insertions to be in the same place is a common ancestor. It's just another homology argument buried in highly technical viral research but it really comes down to a false assumption and some anecdotal comparisons.

You got nothing, you are way off topic and you are arguing from an outdated and ridiculous Talk Origins argument. It's pretty obvious what is going on here. You can't look at the actual fossils and comparative genomics in adaptive evolution so you pick the most convoluted argument available. If you lose the debate it's ok because nothing substantive is at stake and if you make a point no one will ever know the difference.

The ERVs are a dead issue, I refuse to chase this red herring with you. Why don't you at least try to honestly focus on the actual topic under consideration or start another thread on these pointless ERVs.

It isn't rejected a priori. It just so happens that you have no evidence. There is nothing for science to investigate....

That is not assumed.

Nonsense, the a priori assumption of universal common descent by exclusively naturalistic means is the very epicenter of Darwinian logic:

Lamarck was the first man whose conclusions on the subject excited much attention. This justly-celebrated naturalist first published his views in 1801; he much enlarged them in 1809 in his "Philosophie Zoologique,' and subsequently, in 1815, in the Introduction to his "Hist. Nat. des Animaux sans Vertébres.' In these works he upholds the doctrine that species, including man, are descended from other species. He first did the eminent service of arousing attention to the probability of all change in the organic, as well as in the inorganic world, being the result of law, and not of miraculous interposition. (Darwin, On the Origin of Species)
​

This should be in your signature, it's what you are arguing for and from. Instead of standing on the courage of your convictions you are denying the essential tenants of this driving force in modern evolutionary biology. My guess is you are simply unaware, otherwise you simply don't care about the subject matter and enjoy baiting serious debate without substance.

The unifying principle of modern evolutionary biology being categorically denied by an avid defender. That is what has done the most to convince me that you will not honestly admit to the actual evidence. You deny your own foundational premise. Sad really...

Have a nice day
Mark

 

[Bugeyedcreepy]

Nonsense, the a priori assumption of universal common descent by exclusively naturalistic means is the very epicenter of Darwinian logic:

so, how is the scientific method going to explore something that isn't naturalistic? Is there a testable, falsifiable hypothesis for the supernatural?

 

[mark kennedy]

so, how is the scientific method going to explore something that isn't naturalistic? Is there a testable, falsifiable hypothesis for the supernatural?

The same way it explores anything, is deals with the actual evidence. Impossible is still impossible and the origin of life is still impossible by naturalistic mens.

The wrath of God is being revealed from heaven against all the godlessness and wickedness of people, who suppress the truth by their wickedness, since what may be known about God is plain to them, because God has made it plain to them. For since the creation of the world God’s invisible qualities—his eternal power and divine nature—have been clearly seen, being understood from what has been made, so that people are without excuse. (Rom. 1:18-20)
​

That's kind of the point, the evidence follows.

Grace and peace,
Mark

 

[Bugeyedcreepy]

The same way it explores anything, is deals with the actual evidence. Impossible is still impossible and the origin of life is still impossible by naturalistic mens.

The wrath of God is being revealed from heaven against all the godlessness and wickedness of people, who suppress the truth by their wickedness, since what may be known about God is plain to them, because God has made it plain to them. For since the creation of the world God’s invisible qualities—his eternal power and divine nature—have been clearly seen, being understood from what has been made, so that people are without excuse. (Rom. 1:18-20)
​

That's kind of the point, the evidence follows.

Grace and peace,
Mark

...I've obviously missed something. Could you give an example of the evidence please? and it is scientific evidence, right?

 

[VirOptimus]

The same way it explores anything, is deals with the actual evidence. Impossible is still impossible and the origin of life is still impossible by naturalistic mens.

The wrath of God is being revealed from heaven against all the godlessness and wickedness of people, who suppress the truth by their wickedness, since what may be known about God is plain to them, because God has made it plain to them. For since the creation of the world God’s invisible qualities—his eternal power and divine nature—have been clearly seen, being understood from what has been made, so that people are without excuse. (Rom. 1:18-20)
​

That's kind of the point, the evidence follows.

Grace and peace,
Mark

Firstly, if you could prove that origin of life is impossibel by natural means then you would surely win the Nobel prize, as you cant, its just an empty assertion.

Secondly, biblical verses are not scientific evidence, its just preaching and should not be used in a scientific debate. But it do show that the only reason you argue the science is because of your religios belief.

 

[mark kennedy]

...I've obviously missed something. Could you give an example of the evidence please? and it is scientific evidence, right?

Firstly, if you could prove that origin of life is impossibel by natural means then you would surely win the Nobel prize, as you cant, its just an empty assertion.

Secondly, biblical verses are not scientific evidence, its just preaching and should not be used in a scientific debate. But it do show that the only reason you argue the science is because of your religios belief.

The verse I quoted is natural revelation, it's why no one ever asks for a definition of God. That aside, if you are interested in scientific evidence start with the OP, it's loaded with it. In fact, through out the thread I have quoted, cited and linked from fairly extensive research across broad lines of scientific literature.

You get various mutation rates depending on ancestral population sizes and time. The thing is this is based on 1.33% divergence and because of the deleterious effects on fitness it's hard to reconcile such a high mutation rate.

Using conservative calculations of the proportion of the genome subject to purifying selection, we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common...Calculations are based on a generation length of 20 years and average autosomal sequence divergence of 1.33% (Table 1). (Estimate of the Mutation Rate per Nucleotide in Humans)
​

With the inclusion of the indels the divergence jumps from 1.23% to almost 5%.

human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions. (Initial sequence of the chimpanzee genome and comparison with the human genome Nature 437, 69-87 1 September 2005)
​

That means that about 5mya the common ancestors would have had a wave of mutations that would have simply been too deleterious to be sustainable. That's why evolutionists will never openly discuss the indels, the divergence is simply too great. Mainly because of what would have to change in order to get a brain three times bigger then apes:

The 118-bp HAR1 region showed the most dramatically accelerated change, with an estimated 18 substitutions in the human lineage since the human;chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes. Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (Myr) ago. No orthologue of HAR1 was detected in the frog (Xenopus tropicalis), any of the available fish genomes (zebrafish, Takifugu and Tetraodon), or in any invertebrate lineage, indicating that it originated no more than about 400 Myr ago

See FIGURE 2 from An RNA gene expressed during cortical development evolved rapidly in humans. (Nature 443, 167-172 14 September 2006)
​

Now if you really want to get into this I strongly suggest you learn something about fossils, that's when it get real interesting.

Have a nice day
Mark

 

[VirOptimus]

Mark, I both know and understand the science perfectly fine, thats why I disniss your posts out of hand. You do neither.

Try to write a peer reviewed science article on the subject and see how that goes.

 

[mark kennedy]

Mark, I both know and understand the science perfectly fine, thats why I disniss your posts out of hand. You do neither.

Try to write a peer reviewed science article on the subject and see how that goes.

When you get done with your peer reviewed article let me know. What I never quite understand is how a person can think themselves the voice of science without even so much as reading the literature, let alone thinking about the details. If you know and understand so much about science then why have you managed to say nothing substantive, let alone scientific. The approach you are using is about all evolutionists have, it's called an ad hominem fallacy, it's an argument that never happened.

You understand science perfectly? I don't think you know what the word means

Have a nice day
Mark

 

[Loudmouth]

/

You get various mutation rates depending on ancestral population sizes and time. The thing is this is based on 1.33% divergence and because of the deleterious effects on fitness it's hard to reconcile such a high mutation rate.

Using conservative calculations of the proportion of the genome subject to purifying selection, we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common...Calculations are based on a generation length of 20 years and average autosomal sequence divergence of 1.33% (Table 1). (Estimate of the Mutation Rate per Nucleotide in Humans)
​

They seemed to have reconciled it just fine: "suggests that synergistic epistasis among harmful mutations may be common". What they are saying is that individuals with two or more mutations are strongly selected against which increases the rate at which deleterious mutations are removed from the population.

With the inclusion of the indels the divergence jumps from 1.23% to almost 5%.

human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions. (Initial sequence of the chimpanzee genome and comparison with the human genome Nature 437, 69-87 1 September 2005)
​

Why is that a problem?

That means that about 5mya the common ancestors would have had a wave of mutations that would have simply been too deleterious to be sustainable.

No, that isn't true at all. The mutations would have occurred continuously over the last 5 million years, not all at once.

That's why evolutionists will never openly discuss the indels, the divergence is simply too great.

You haven't shown that it is too great. You have simply asserted it. Why would we need to consider your claims when you have no evidence to back them?

Mainly because of what would have to change in order to get a brain three times bigger then apes:

The 118-bp HAR1 region showed the most dramatically accelerated change, with an estimated 18 substitutions in the human lineage since the human;chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes. Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (Myr) ago. No orthologue of HAR1 was detected in the frog (Xenopus tropicalis), any of the available fish genomes (zebrafish, Takifugu and Tetraodon), or in any invertebrate lineage, indicating that it originated no more than about 400 Myr ago

See FIGURE 2 from An RNA gene expressed during cortical development evolved rapidly in humans. (Nature 443, 167-172 14 September 2006)
​

Why is that a problem?

Now if you really want to get into this I strongly suggest you learn something about fossils, that's when it get real interesting.

Have a nice day
Mark

Sometimes it is rather sad that you lack a sense of irony.

 

[Loudmouth]

Your all over the road and it's been a while since I took any of the convoluted mess seriously. Let's start with the fact that the OP and the proposal of the thread has been left unaddressed.

I already addressed it. The differences between the human and chimp brain is due to the mutations that separate the two species.

Will you address my response or not?

See (ERVs put chimp/human common ancestry beyond any reasonable doubt.) The ERVs are a dead issue, I have not the slightest intention of chasing this around the mulberry bush with you.

Then don't question common ancestry between humans and chimps unless you are willing to address the evidence that supports it. Also, if you have to deny the direct observation of retroviruses producing ERVs, what does that say about your argument?

If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. (On the Origin of Species, Chapter 6 - Difficulties on Theory)

So where have you been shown that the human brain could not have been produced by numerous, successive, and slight modifications?

The Phylogentic Argument is a waste of time it's already been dealt with at length. Taxonomy is a highly subjective means of organizing details, nothing more.

That is simply untrue. Phylogenies are objective.

"The degree to which a given phylogeny displays a unique, well-supported, objective nested hierarchy can be rigorously quantified. Several different statistical tests have been developed for determining whether a phylogeny has a subjective or objective nested hierarchy, or whether a given nested hierarchy could have been generated by a chance process instead of a genealogical process (Swofford 1996, p. 504). These tests measure the degree of "cladistic hierarchical structure" (also known as the "phylogenetic signal") in a phylogeny, and phylogenies based upon true genealogical processes give high values of hierarchical structure, whereas subjective phylogenies that have only apparent hierarchical structure (like a phylogeny of cars, for example) give low values (Archie 1989; Faith and Cranston 1991; Farris 1989; Felsenstein 1985; Hillis 1991; Hillis and Huelsenbeck 1992; Huelsenbeck et al. 2001; Klassen et al. 1991)."
http://www.talkorigins.org/faqs/comdesc/section1.html#nested_hierarchy

You can't simply ignore the evidence.

The inverse logic is intuitively obvious, if the homology argument for things in common can prove common ancestry then . . .

We are using a phylogenetic argument. Please stop misrepresenting our argument.

How many times do we need to go over this?

What makes this such a lackluster argument is that the Darwinian will just keep repeating that ERVs are the result of germline invasions, something that has simply been assumed as far as I can tell.

Do you have to assume a suspect is guilty in order to get a DNA match from a blood sample at a crime scene? Do we have to witness a suspect leaving his DNA at a crime scene in order to use it in court?

The evidence that germline invasions occurred are heritable ERVs. ERVs are the evidence that germline invasions leave, just as the DNA at a crime scene is what a criminal leaves.

. The researchers got the 'Phoenix Virus' to work, it had 20 amino acids and just one frameshift. In order to understand why this is important you would need to know how protein coding works on a molecular level.

I have forgotten more about protein translation than you have ever known. I am not the one who incorrectly thinks that an indel outside of an open reading frame will result in a frame shift mutation. That would be you. I am not the one who incorrectly thinks that a 3 base indel occuring in an open reading frame will result in a frame shift mutation. That would be you. I am not the one who incorrectly thinks that frame shift mutations can occur in an RNA gene that is never translated into protein. That would be you. I am not the one who incorrectly thinks that a 10 base indel indicates 10 separate insertion or deletion events. That would be you.

You are the LAST person who should be pointing any fingers when it comes to knowledge of protein translation, RNA transcription, or even DNA replication. You can't even figure out that finding a 2% difference between genes does not refute the argument that there is 98% similarity.

The HERV-K (HML2) is less then 1% of the human genome and yet it is the most studied. When they revive this sequence they actually manage to reconstruct it but with one frameshift. What is interesting about the results is that only two are within genes. The explanation being that they are probably deleterious so their are defenses that prevent this.

No. The explanation is that insertions which occur within genes are almost always deleterious, SO THEY ARE SELECTED AGAINST THROUGH NATURAL SELECTION. ERV insertions that happen outside of the 2-3% of the genome made up of coding regions can be completely neutral, so they are not selected against or for. There are also indications that some ERVs are actually beneficial, and they are selected for.

Doesn't it make sense that the germline cells would be protected as well?

You are imagining things that don't exist.

The amino acids need an open reading frame. When they got it working they they wanted to see how it would interact with living cells and it was introduced to live T cells. Guess what, it really can get into the DNA but I'm still waiting for the part where it's demonstrated that massive germline invasions are possible.

Why aren't they possible?

Let's take a look at a little Darwinian mythology and try to picture what they believe happened here. Our supposed ancestors from about 25 million years ago would have been inundated with a massive dose of these pathological ERV viruses.

Reference?

Or do you not realize that they are spread out through time and did not occur all at once?

As a result the ERVs would replicate at random in the genomes until random mutations disrupted the reading frame, leaving fragments like the HERV K. Getting this far into the ancestry of apes in Darwinian evolution leaves you following a lot of long 'ghost lineages' but geographically always go back to the East African Rift valley. (Nature, 30 May 2013)

It seems that you are making a lot of stuff up.

This is an area that has made a number of paleontologists famous, especially the Leaky family who found so many of the Homo habilis and Homo erectus fossils in and around this area. So in case you were wondering when this supposed ERV onslaught of germline invasions would have happened it would have been right around there. What the Darwinian desperately wants to prove is a correlation between the molecular evidence and the fossil record. What they are doing is taking this highly technical ERV research, molecular clock age estimates and reconcile it with the fossil record. My positive argument here will simply be this, no matter how many ways it's reconstructed ERVs are just another homology argument.

They are a phylogenetic argument.

"Endogenous retrovirus loci provide no less than three sources of phylogenetic signal, which can be used in complementary fashion to obtain much more information than simple distance estimates of homologous sequences."
http://www.pnas.org/content/96/18/10254.full

Phylogenetic signal, Mark. PHYLOGENETIC SIGNAL. That is what evidences evolution. Not homology. How many time do we need to go over this?

That's about it, Talk Origins wants you to accept the assumption that ERVs are the result of germline invasions then drop a probability argument in your lap. The essence of the argument is the strongest argument against germline invasions in the first place. They are rare and they are pretty much random. Once they hook you with the assumption that they must be the result of a germline invasion they use the probability argument for common ancestry.

WE CAN DIRECTLY OBSERVE THAT RETROVIRAL INSERTION IS RANDOM!!!

How many times do we need to go over this? I have shown you this fact over and over and over, and yet here you are pretending to be ignorant once again.

It's just another homology argument buried in highly technical viral research but it really comes down to a false assumption and some anecdotal comparisons.

IT IS A PHYLOGENETIC ARGUMENT!!!!

You can't look at the actual fossils and comparative genomics in adaptive evolution so you pick the most convoluted argument available.

I have avoided none of the fossils. My argument is simple. The difference between chimps and humans is due to the mutations that separate us.

Nonsense, the a priori assumption of universal common descent

It is a conclusion, not an assumption. Until you face this fact, we can't move any farther.

 

[VirOptimus]

When you get done with your peer reviewed article let me know. What I never quite understand is how a person can think themselves the voice of science without even so much as reading the literature, let alone thinking about the details. If you know and understand so much about science then why have you managed to say nothing substantive, let alone scientific. The approach you are using is about all evolutionists have, it's called an ad hominem fallacy, it's an argument that never happened.

You understand science perfectly? I don't think you know what the word means

Have a nice day
Mark

Heh, no that is not how this works. You make the claim that the science is wrong, you back it up. As you obviously cant its just empty preaching.

 

[mark kennedy]

/

They seemed to have reconciled it just fine: "suggests that synergistic epistasis among harmful mutations may be common". What they are saying is that individuals with two or more mutations are strongly selected against which increases the rate at which deleterious mutations are removed from the population.

Its rather sad to see that deleterious effects are inevitable is absent from the language.

Why is that a problem?

Two reasons, selective constraints and deleterious effects.

No, that isn't true at all. The mutations would have occurred continuously over the last 5 million years, not all at once.

You haven't shown that it is too great. You have simply asserted it. Why would we need to consider your claims when you have no evidence to back them?

Why is that a problem?

Because for obvious reasons mutations, especially on this scale, always result in devastating disease and disorder.

Sometimes it is rather sad that you lack a sense of irony.

What is truly sad is the lack of scientific acumen on the part of those who pretend to be it's defenders.

Have a nice day

 

[mark kennedy]

Heh, no that is not how this works. You make the claim that the science is wrong, you back it up. As you obviously cant its just empty preaching.

Define science and then when you are done you can define evolution. Then we can talk like adults who take the subject matter seriously instead of fielding these pedantic, fallacious one liners.

Have a nice day
Mark

 

[mark kennedy]

I already addressed it. The differences between the human and chimp brain is due to the mutations that separate the two species.

Will you address my response or not?

You categorically assumed they were the result of mutations, you demonstrated nothing.

Then don't question common ancestry between humans and chimps unless you are willing to address the evidence that supports it. Also, if you have to deny the direct observation of retroviruses producing ERVs, what does that say about your argument?

The direct observation of an ERV producing a germline mutation in the human genome when? Bear in mind I mean modern times not some assumed germline invasion from a mythical natural history.

So where have you been shown that the human brain could not have been produced by numerous, successive, and slight modifications?

The effects of mutations on human brain relate genes, they are always deleterious.

That is simply untrue. Phylogenies are objective.

They are semantics.

You can't simply ignore the evidence.

I am the only one in this thread actually appealing to actual evidence, something you manage to ignore. Every single time.

We are using a phylogenetic argument. Please stop misrepresenting our argument.

No you are using semantics to avoid actual evidence.

How many times do we need to go over this?

Till you get dizzy enough from arguing in circles that you argument finally collapses which is usually not that long.

Do you have to assume a suspect is guilty in order to get a DNA match from a blood sample at a crime scene? Do we have to witness a suspect leaving his DNA at a crime scene in order to use it in court?

You need two good samples and a direct comparison.

The evidence that germline invasions occurred are heritable ERVs. ERVs are the evidence that germline invasions leave, just as the DNA at a crime scene is what a criminal leaves.

Unless the invasion is simply impossible due to deleterious effects. Which is the case.

I have forgotten more about protein translation than you have ever known. I am not the one who incorrectly thinks that an indel outside of an open reading frame will result in a frame shift mutation. That would be you. I am not the one who incorrectly thinks that a 3 base indel occuring in an open reading frame will result in a frame shift mutation. That would be you. I am not the one who incorrectly thinks that frame shift mutations can occur in an RNA gene that is never translated into protein. That would be you. I am not the one who incorrectly thinks that a 10 base indel indicates 10 separate insertion or deletion events. That would be you.

The most likely result of an indel in an open reading frame would be a frameshift, the likely hood of a triplet codon replacement would be astronomical. I refuse your assumption as mythical, not methodological.

You are the LAST person who should be pointing any fingers when it comes to knowledge of protein translation, RNA transcription, or even DNA replication. You can't even figure out that finding a 2% difference between genes does not refute the argument that there is 98% similarity.

96% at best and you have seen the actual research enough times to know that. Now if you just mean the actual protein coding genes it's, on average, on substitution per genome per gene on average. Given the deleterious effects of mutations it's a statistical impossibility by even the most conservative estimations. It's only believed because it's assumed.

No. The explanation is that insertions which occur within genes are almost always deleterious, SO THEY ARE SELECTED AGAINST THROUGH NATURAL SELECTION. ERV insertions that happen outside of the 2-3% of the genome made up of coding regions can be completely neutral, so they are not selected against or for. There are also indications that some ERVs are actually beneficial, and they are selected for.

Which assumes they are the result of germline invasions rather then actual reading frames simply broken by mutations. The odds of mutations breaking the reading frames fall into expected averages, the odds of them happening as the result of viral infections are laughable.

You are imagining things that don't exist.

The stone age ape man myth is laughable.

Why aren't they possible?

Reference?

Or do you not realize that they are spread out through time and did not occur all at once?

More circular questions, points refuted a thousand times.

It seems that you are making a lot of stuff up.

I at least have source material, something you cannot be bothered with.

At this point I'm going to wait for you to argue the same thing in circles at a later time. You always do...

Have a nice day
Mark

 

[Loudmouth]

Its rather sad to see that deleterious effects are inevitable is absent from the language.

Why would they write something that isn't true?

There is absolutely no evidence that every single mutation is deleterious. In fact, there is tons of evidence that demonstrates most mutations are neutral, and a few are beneficial.

Two reasons, selective constraints and deleterious effects.

Please show that all mutations are deleterious and that none are beneficial.

Because for obvious reasons mutations, especially on this scale, always result in devastating disease and disorder.

Yet another bare assertion with no science to back it up.

What is truly sad is the lack of scientific acumen on the part of those who pretend to be it's defenders.

My irony meter just broke.

You are the one claiming that chimp and human genes can not be 98% identical because they differ by 2%. This is your actual argument. Who lacks acumen?

 

[Loudmouth]

You categorically assumed they were the result of mutations, you demonstrated nothing.

I made no such assumption. The evidence is conserved sequence within functional parts of the genome, and a phylogeny of DNA differences and similarities. That is the evidence which allows us to CONCLUDE that those differences are due to mutations. Again, we have the evidence. We aren't assuming.

The direct observation of an ERV producing a germline mutation in the human genome when?

The direct observation of a retrovirus producing an ERV in a human cell. We have directly observed it. Why do you have to run away from this observation?

Bear in mind I mean modern times not some assumed germline invasion from a mythical natural history.

Then why ask for any modern observations if you are just going to ignore them?

The effects of mutations on human brain relate genes, they are always deleterious.

Still waiting for evidence to back this up.

They are semantics.

No, they aren't. We are using a phylogenetic argument, not a homology argument. Please stop lying about the argument we are using.

I am the only one in this thread actually appealing to actual evidence, something you manage to ignore. Every single time.

Where is the evidence that every single mutation is deleterious?

Why are you ignoring the direct observation of retroviruses creating ERVs as shown in this scientific paper?

http://www.ncbi.nlm.nih.gov/pubmed/15314653

Why are you ignoring the PHYLOGENETIC ERV evidence supplied in this paper?

http://www.pnas.org/content/96/18/10254.full

No you are using semantics to avoid actual evidence.

My other irony meter just exploded.

You are ignoring the phylogenetic argument by calling it semantics.

Till you get dizzy enough from arguing in circles that you argument finally collapses which is usually not that long.

And you are still ignoring the phylogenetic argument.

You need two good samples and a direct comparison.

Don't you have to "assume" that the suspect is guilty in order to get a DNA match?

Unless the invasion is simply impossible due to deleterious effects. Which is the case.

Which is still just a bare assertion backed by zero science.

The most likely result of an indel in an open reading frame would be a frameshift, the likely hood of a triplet codon replacement would be astronomical.

Then lets see your probability calculations and the science that backs it. Why is a 3 base indel nearly impossible while a 1, 2, 4, or 5 base indel completely possible?

96% at best and you have seen the actual research enough times to know that.

And yet you would point to a 4% difference as a refutation of the 96% similarity. Do you see the problem with your argument or not?

Now if you just mean the actual protein coding genes it's, on average, on substitution per genome per gene on average. Given the deleterious effects of mutations it's a statistical impossibility by even the most conservative estimations. It's only believed because it's assumed.

We only assume that human and chimp genes are 98% identical? We haven't held them up side by side and compared them?

Which assumes they are the result of germline invasions rather then actual reading frames simply broken by mutations.

We assume no such thing. We have the evidence of germline invasions. We have the ERVs. It is no different than finding a criminal's DNA at a crime scene.

The odds of mutations breaking the reading frames fall into expected averages, the odds of them happening as the result of viral infections are laughable.

And yet you haven't shown us those odds, or that they even need to be broken in order to insert into a germline cell and become heritable.

The stone age ape man myth is laughable.

And you avoid the evidence once again.

More circular questions, points refuted a thousand times.

And you avoid the evidence once again.

I at least have source material, something you cannot be bothered with.

You haven't produced a single source demonstrating that every single mutation is deleterious.

Just produce a single peer reviewed paper which states that every single mutation is deleterious. Just one.

 

[mark kennedy]

I made no such assumption. The evidence is conserved sequence within functional parts of the genome, and a phylogeny of DNA differences and similarities. That is the evidence which allows us to CONCLUDE that those differences are due to mutations. Again, we have the evidence. We aren't assuming.

That's not how Molecular Phylogentics works, you are either oblivious or otherwise unaware that these kind of
phylogenetic trees go back to Linnaeus and Darwin. It was a foregone conclusion long before Mendelian genetics had been developed and phylogentic markers were finally utilized.

Molecular phylogenetics predates DNA sequencing by several decades. It is derived from the traditional method for classifying organisms according to their similarities and differences, as first practiced in a comprehensive fashion by Linnaeus in the 18th century. Linnaeus was a systematicist not an evolutionist, his objective being to place all known organisms into a logical classification which he believed would reveal the great plan used by the Creator - the Systema Naturae. (Chapter 16 Molecular Phylogenetics. Genomes. 2nd edition NCBI Books)
​

I have enjoyed reading about phylogentics for years, these taxonomic schemes while fascinating do not prove anything. They are a semantic systematic organization.

The direct observation of a retrovirus producing an ERV in a human cell. We have directly observed it. Why do you have to run away from this observation?

There is no we, it's just you using a worn out Talk Origins argument that proves nothing either way.

Then why ask for any modern observations if you are just going to ignore them?

Waiting for you to start an exposition of relevant source material.

Still waiting for evidence to back this up.

Likewise.

No, they aren't. We are using a phylogenetic argument, not a homology argument. Please stop lying about the argument we are using.

It's not we it's you and it's a homology argument, phylogentic arguments are a homology argument if you assume common ancestry based on similar traits or alleles.

Where is the evidence that every single mutation is deleterious?

At every turn, a beneficial effect is on of the rarest of mutations.

Why are you ignoring the direct observation of retroviruses creating ERVs as shown in this scientific paper?
http://www.ncbi.nlm.nih.gov/pubmed/15314653

Ok we can take a look at this:

The completion of the human genome sequence has made possible genome-wide studies of retroviral DNA integration. Here we report an analysis of 3,127 integration site sequences from human cells. We compared retroviral vectors derived from human immunodeficiency virus (HIV), avian sarcoma-leukosis virus (ASLV), and murine leukemia virus (MLV).(Retroviral DNA integration: ASLV, HIV, and MLV show distinct target site preferences.)​

It seems to be these are viral infections with highly deleterious effects. You wanted proof, it's in the abstract of you own source material. HIV is an especially deadly one that integrates itself into T cells with devastating consequences.

Why are you ignoring the PHYLOGENETIC ERV evidence supplied in this paper?

http://www.pnas.org/content/96/18/10254.full

How many times do you want me to read this paper? It's from 1999 and assumes these sequences are the result of germline viral invasions and includes an abstract, methodology then jumps right into a discussion. It's a conclusion based on an assumption wrapped in a genomic comparison. There is nothing here, whether or not the assumption of germ line invasions is valid this tells us nothing about adaptive evolution.

Typically, ancient proviruses have sustained numerous point mutations, deletions, and insertions, rendering them incapable of expressing virus. No biologically active viruses have been associated with the ancient proviruses. (Constructing primate phylogenies from ancient retrovirus sequences, PNAS)​

It's nothing but broken reading frames.

My other irony meter just exploded.

You are ignoring the phylogenetic argument by calling it semantics.

Because that's what taxonomy is, systematic semantics.

Then lets see your probability calculations and the science that backs it. Why is a 3 base indel nearly impossible while a 1, 2, 4, or 5 base indel completely possible?

Because they represent over 90 million base pairs, some millions of base pairs long.

Both the total number of candidate human insertions/chimpanzee deletions (blue) and the number of bases altered (red) are shown. FIGURE 6. Length distribution of large indel events (> 15 kb), as determined using paired-end sequences from chimpanzee mapped against the human genome.

And yet you would point to a 4% difference as a refutation of the 96% similarity. Do you see the problem with your argument or not?

90 million base pairs of divergence, some sequences in the millions of base pairs that include the sequence that includes the HAR1f sequence and Pterv sequence that represent at least a million base pairs. I see a problem with the absence of an argument for this even being conceivable.

We only assume that human and chimp genes are 98% identical? We haven't held them up side by side and compared them?

Yes the have made direct comparisons and found 40,000 differences in the 20,000 genes representing one change per gene, per lineage in each of the genomes respectively.

~29% being identical and the typical orthologue differing by only two amino acids, one per lineage. (Chimpanzee Genome, Nature 2005)​

What is fascinating is how many fundamentally flawed statements you make.

We assume no such thing. We have the evidence of germline invasions. We have the ERVs. It is no different than finding a criminal's DNA at a crime scene.

A criminal's DNA identifies him, the argument you are using is a comparison of genomic sequences. Two fundamentally different things. To say nothing of the fact you keep saying we when you are doing nothing but making a worn out homology argument to an empty theater. They are gone LM, I don't even have a resident troller in these discussions any more.

And yet you haven't shown us those odds, or that they even need to be broken in order to insert into a germline cell and become heritable.

Don't need them, I know what the rate of permanently fixed, highly deleterious germ line invasions risk. It's a formula for extinction, not adaptive evolution and you have utterly abandoned the comparative anatomy and molecular basis for the evolution of the human brain from that of apes. This is a red herring, nothing more.

And you avoid the evidence once again.

Now you are begging the question of proof, another close encounters of the pedantic one liners.

You haven't produced a single source demonstrating that every single mutation is deleterious.

We can talk about the deleterious effects of mutations any time

Just produce a single peer reviewed paper which states that every single mutation is deleterious. Just one.

And he ends it with a strawman argument. Typical...

Have a nice day
Mark