Rumraket wrote:

Shrunk wrote:

MarioNovak wrote:If science shows that evolutionary processes can not create a single gene and someone claims evolutionary processes created all genes we observe in living organisms, then this is pseudoscience.

Still waiting for your example of a "new gene" of the sort you are describing ever arising, anywhere.

We don't just need an example, we need well defined metrics for determining what does and does not qualify as "new".

How much must one gene differ from another to be considered "new"?

Is it not the case that we can distinguish between different genes? If so, then there must already be some sort of biological definition in place sufficient to know when a 'new gene' arises?

jamest wrote:

Shrunk wrote:

jamest wrote:Makes you wonder why Lenski didn't extend his experiment accordingly.

Umm, 'cause then it'd be a different experiment. Not this one.

If you were going to observe bacteria for several decades, it seems like common sense to do so within various environmental contexts. Scientists are more than capable of conducting one experiment at a time.

Well, technically they did test the bacteria in several different environments. They just did not evolve in them.

They are continuously grown in the same environment(with oxygen), but samples are taken and spread on agar plates, which are then incubated under different conditions. For example there is one with oxygen and one without. I don't remember if these are the only conditions tested for this particular experiment, I do remember however that Lenski also did experiments with bacterial adaptation to different incubation temperatures.

On some of the agar plates, the growth medium contains only citrate, no glucose. For the first 31.000 generations of the experiment, there was no growth on these plates. The bacteria could not utilize the citrate because oxygen was present. After 31.000 generations, one lineage had acquired the ability to utilize citrate under oxygenated conditions, so suddenly they saw growth on these plates.

Creationists deal with this result, as you see, by creative reinterpretation. Somehow this result is made to be less impressive than it is. Yeah, so they can now utilize citrate under aerobic conditions, so what? It's not new-newey-new-in-this-particular-sense-of-new-we-never-define. Therefore evolution didn't happen, is powerless to create new genes, is pseudoscience etc. etc.

jamest wrote:

Rumraket wrote:

Shrunk wrote:

MarioNovak wrote:If science shows that evolutionary processes can not create a single gene and someone claims evolutionary processes created all genes we observe in living organisms, then this is pseudoscience.

Still waiting for your example of a "new gene" of the sort you are describing ever arising, anywhere.

We don't just need an example, we need well defined metrics for determining what does and does not qualify as "new".

How much must one gene differ from another to be considered "new"?

Is it not the case that we can distinguish between different genes? If so, then there must already be some sort of biological definition in place sufficient to know when a 'new gene' arises?

Yes, but that definition is rejected by creationists (it's called a new allele, new alleles arise simply through mutation. A single mutation in a single gene would make it a new allele under population genetics). That's why we want THEM to define what would qualify as new, so we can then show them an example that qualifies under their own supplied definition.

They refuse to do that, because they know this. So they rely on this vague term in order to be able to use any of a handful of definitions so they can always avoid conceding something "new" arose.

There has never EVER by ANY ID proponent or creationist been a rigorous definition supplied, for that very reason. Never. I challenge every one who disagrees to prove me wrong.

jamest wrote:

Rumraket wrote:

Shrunk wrote:

MarioNovak wrote:If science shows that evolutionary processes can not create a single gene and someone claims evolutionary processes created all genes we observe in living organisms, then this is pseudoscience.

Still waiting for your example of a "new gene" of the sort you are describing ever arising, anywhere.

We don't just need an example, we need well defined metrics for determining what does and does not qualify as "new".

How much must one gene differ from another to be considered "new"?

Is it not the case that we can distinguish between different genes? If so, then there must already be some sort of biological definition in place sufficient to know when a 'new gene' arises?

It depends. If there is a definition of "new" which, when applied, demonstrates that "new" genes can arise thru evolutionary processes that do not require the intervention of any gods, then it seems that is not the correct definition of "new." It would appear that there is some other type of "new" gene that is regularly observed, but which only pops into existence when some god causes it to happen. We are still awaiting MarioNovak's demonstration of the existence of such "new" genes which, as Rumraket reminds me, also requires that MarioNovak clarify his particular definition of "new".

MarioNovak wrote:

Shrunk wrote:

The evolutionary origin of orphan genes

Nature Reviews Genetics 12, 692-702 (October 2011) | doi:10.1038/nrg3053

Diethard Tautz & Tomislav Domazet-Lošo

Abstract

Gene evolution has long been thought to be primarily driven by duplication and rearrangement mechanisms. However, every evolutionary lineage harbours orphan genes that lack homologues in other lineages and whose evolutionary origin is only poorly understood. Orphan genes might arise from duplication and rearrangement processes followed by fast divergence; however, de novo evolution out of non-coding genomic regions is emerging as an important additional mechanism. This process appears to provide raw material continuously for the evolution of new gene functions, which can become relevant for lineage-specific adaptations.

http://www.nature.com/nrg/journal/v12/n ... g3053.html

Just reading this now. So far, no mention of orphan genes being magically created by Jesus as a viable hypothesis, and from the title and the abstract I don't expect that to be included. But I'll let everyone know if it comes up...

As I said above, people must learn to

As I said above, you can stuff your patronising lecturing where the sun doesn't shine. You're in no position to deride others for lack of knowledge when you present such a profound lack of requisite knowledge yourself.

MarioNovak wrote: differentiate between scientific knowledge - cognizance of a fact or phenomenon acquired through experiments and observations - and mental constructs of a human mind - ideas, explanations, theories, hipoteses, ad hoc hypothesis, conjectures, etc. I have no doubt that proponents of evolution will find an "explanation" of how orphan genes come into existance. But this is not science, but storytelling.

History of evolutionary thought in biology explaining emergence of observable biological organization is full of mental constructs and magic words like: "might arise". Evolutionary explanations of orphan genes emergence is not different.
"Might appeared", "emerged", "gave rise to", "burst onto the scene", "evolved itself," "derived", "was on the way to becoming", "radiated into", "modified itself", "manufactured itself", "evolution's way of dealing with", "derived emergent properties", "was lucky"...

Stevebee, is that you?

MarioNovak wrote:

Fenrir wrote:

MarioNovak wrote:...snipped some whimpering...
"Evolutionary book" will not change the results of experimental science which shows total impossibility of random mutation and natural selection to create a new genes.

That's all well and fine, now all you need to do is actually link some genuine experimental science which shows, or even suggests, any such thing.

I suspect I have quite a wait ahead of me.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3461117/

Don't expect people to do your work for you.
Stop blindly copy-pasting links and cite the actual passages that support your position.
Given your disengenuous representation of the article in the OP, I won't take your word for it that this article supports it either.

MarioNovak wrote:Have you ever heard of the terms like logic or rational?

Have you heard of the terms patronising or presumptive?

MarioNovak wrote:The evolutionary community get all excited when Lenski discovered changes that involved moving one pre-existing gene from one location to another. They refer this as a "key innovation", and a "fascinating case of evolution in action".

Stop lying Mario, it will only contribute to the erosion of your credibility.

MarioNovak wrote:If moving one pre-existing gene from one location to another is "key innovation", in the longest evolution experiment, what can you rationally and logically conclude: did experiment produced new gene or not?

Except that's not what the experiment or it's scientists claim is it Mario?

Rumraket wrote:

jamest wrote:

Rumraket wrote:

Shrunk wrote:

Still waiting for your example of a "new gene" of the sort you are describing ever arising, anywhere.

We don't just need an example, we need well defined metrics for determining what does and does not qualify as "new".

How much must one gene differ from another to be considered "new"?

Is it not the case that we can distinguish between different genes? If so, then there must already be some sort of biological definition in place sufficient to know when a 'new gene' arises?

Yes, but that definition is rejected by creationists (it's called a new allele, new alleles arise simply through mutation. A single mutation in a single gene would make it a new allele under population genetics). That's why we want THEM to define what would qualify as new, so we can then show them an example that qualifies under their own supplied definition.

Then MN really needs to respond to this post of yours, for his whole argument hinges upon it. Actually, it doesn't, since I don't think that the experiment suffices to make the sort of claims that have been made here. And as you know, I'm a theist.

Yep, thank you jamest.

Wonders whether acquiring the ability to digest a substrate which itself is novel would count as newness but suspect not. There's always a out when you make it up as you go along. Maybe god made nylon to test us?

Wriggle wriggle wriggle.

Rumraket wrote:Yep, thank you jamest.

It is I who should thank you, for providing us with information sufficient to arrive at that conclusion.

Happy New Year everyone.

Thomas Eshuis wrote:Stevebee, is that you?

Maybe he misses the butt-kicking he received with each and every reply when he was last here.

Rumraket wrote:
Some hypotheses cannot be directly empirically tested because the timescales involved are practically not achievable. That's when we use phylogenetics or computer simulations instead. These testify that evolution did in point of fact happen, get over it.

As an analogy, nobody has seen an entire star form from a coalescing disc of interstellar dust and gas. We can only see snapshots of the process by taking pictures of distant stars, but the timescales are still way beyond practical human timescales. It's the same with evolution and geological time. We cannot practically reconstruct this process in the laboratory, stars are bigger than our planet, the masses, distances and timescales involved are beyond all human capacity to control. Some things really just are too big, or take too long a time, for us to be able to directly observe and control them in nice experimental fashion. This is where we build models instead, out of practical necessity. And then we test the predictions of the models against observations in the real world, whether those be pictures of distant stars and galaxies, or sequences of proteins in living organisms.

These models in turn then serve as justification for the claim that evolution (or gravity) produced the diversity of life (stars).

Bad rationalization(making excuses). Apeal to a large time scale is really funny if we consider the recent development of evolutionary thought. Have you heard of the new phrase that originated(evolved) in evolutionary Think Tank : "rapid evolution"? In a study of Caenorhabditis briggsae and related species, researchers compared over 2000 genes. They proposed that these genes must be evolving too quickly to be detected and are consequently sites of very rapid evolution. So, at first evolution is not observable and empirically testable because it is too slow, but now evolution is not observable and empirically testable because it is too quick.

Rumraket wrote:You cannot compare the rate of origin of de novo genes in an experimental bacterial population to the evolution of large multicellular eukaryotes WHEN THE FORMER HAVE NO JUNK-DNA.

So, the new ad hoc hypotheses(excuse for science ignorance) in evolutionary thought is as follows: organisms that have junk in their genomes can evolve new genes. But when junk is missing, evolution of new genes is not possible or is to slow to be detectable and empirically testable. Gotcha.

But... your ad hoc excuse have been debunked by science, again.

http://genome.cshlp.org/content/14/6/1036.full

However, most bacteria contain large numbers of ORFans, that is, annotated genes that are restricted to a particular genome and that possess no known homologs.
...
The high frequencies of ORFans detected in bacterial genomes were originally attributed to the limited set of sequenced genomes then available for comparison, and it was predicted that this category of genes would dwindle as databases expanded. Nevertheless, the number of ORFans in databases has grown despite an increase in the number and diversity of complete genome sequences. A recent survey estimated their frequency to be 14% of the total genes from 60 completely sequenced genomes.

Rumraket wrote:Wait, new alleles did not arise and take control? What qualifies as a "new" allele? What does that even mean "and take control"? Where has this prediction been made?
Where's the problem? The experiment shows that even strong natural selection does not successfully weed out large genetic variation.

In a population genetics new allele is a new gene variation. Mutation is the primary source of those variations(new alleles). "To take control" - to increase allele frequency in population(gene pool).

The researchers were looking for the fixation of positive mutations within the genome and within the whole population. This is referred to using the term "selection sweep". When it occurs, the new mutation at a base pair (a novel single nucleotide polymorphism or SNP) not only experiences replication to be transmitted to the descendants of the organism, but the gene pool of variation is effectively swept clean as the new mutation becomes dominant in the whole population. However, such sweeping was conspicuous by its absence.

"Recent research on evolutionary genetics has focused on classic selective sweeps, which are evolutionary processes involving the fixation of newly arising beneficialmutations. In a recombining region, a selected sweep is expected to reduce heterozygosity at SNPs flanking the selected site. . . . Notably, we observe no location in the genome where heterozygosity is reduced to anywhere near zero, and this lack of evidence for a classic sweep is a feature of the data regardless of window size."
http://www.nature.com/nature/journal/v4 ... bal=remove

This empirical work is worth noting because we are considering a mechanism that is central to Darwinian evolution. Positive natural selection of hereditable variation is the key to understanding how descent with modification occurs. However, the empirical data relating to a sexually reproducing species does not confirm that modification works this way. This is why the primary investigator, ecology and evolutionary biology professor, Anthony Longsaid said: "This research really upends the dominant paradigm about how species evolve".

http://news.uci.edu/press-releases/uci- ... uit-flies/

Rumraket wrote:As just shown, they do nothing of the sort. By the way, you have never detailed a rigorous metric for "newness". And regardless, we already know evolution has created basically the entire biosphere, we know this from phylogenetic evidence.

You haven't shown anything scientifically important, you just offered(produced) a mental construct of a human mind(excuse) - a rationalization for ignorance of scientific discoveries. When an orderly long term procedure is carried out(long term evolution experiment) and empirical connection with the two causes - random variation and natural selection is established, a new gene, as na effect is not produced. So, the scientific fact is that evolutionary processes can not create new genes. Your rationalizations will not make this fact ceases to exist.

Rumraket wrote:I notice you have completely ignored the rather large first post I made in this thread where I present some of this evidence. Why is it that ID proponents are invariably always totally silent on phylogenetics? It's almost as if the field does not exist in your minds.

Because the phylogenetics is just the construct of a human mind, which can conceptually be applied to any set of objects with similar characteristics, such as vehicles. So, by your reasoning, if vehicles are recognized, differentiated and grouped into categories that proves that random processes create vehicles.

Rumraket wrote:Yes, because we have actual concrete empirical evidence that it did from phylogenetics.

We have actual concrete empirical evidence that vw golf 6 and vw golf 7 are related. How this proves eventual assumption that the blueprint for golf 7 resulted from random change in the blueprint that shows how golf 6 will be made?

MarioNovak wrote:

Rumraket wrote:
Some hypotheses cannot be directly empirically tested because the timescales involved are practically not achievable. That's when we use phylogenetics or computer simulations instead. These testify that evolution did in point of fact happen, get over it.

As an analogy, nobody has seen an entire star form from a coalescing disc of interstellar dust and gas. We can only see snapshots of the process by taking pictures of distant stars, but the timescales are still way beyond practical human timescales. It's the same with evolution and geological time. We cannot practically reconstruct this process in the laboratory, stars are bigger than our planet, the masses, distances and timescales involved are beyond all human capacity to control. Some things really just are too big, or take too long a time, for us to be able to directly observe and control them in nice experimental fashion. This is where we build models instead, out of practical necessity. And then we test the predictions of the models against observations in the real world, whether those be pictures of distant stars and galaxies, or sequences of proteins in living organisms.

These models in turn then serve as justification for the claim that evolution (or gravity) produced the diversity of life (stars).

Bad rationalization(making excuses).

These are concrete empirical facts, things really just do take the time they do. You don't grow a 300 foot redwood tree in a week either. Stop being ridiculous please.

MarioNovak wrote:Appeal to a large time scale is really funny if we consider the recent development of evolutionary thought. Have you heard of the new phrase that originated(evolved) in evolutionary Think Tank : "rapid evolution"? In a study of Caenorhabditis briggsae and related species, researchers compared over 2000 genes. They proposed that these genes must be evolving too quickly to be detected and are consequently sites of very rapid evolution. So, at first evolution is not observable and empirically testable because it is too slow, but now evolution is not observable and empirically testable because it is too quick.

Wait, it is testable, just not directly. We cannot reconstruct ancient historical progressions before our very eyes. Tough shit, that's just an inherent limitation of being human.
Once again you get it wrong. What we can do, If we postulate some event happened in the past, and took a very long time, we can test this through building a model of the event and making predictions about what we should be able to find if the event really took place. One of the ways we do this is through phylogenetics. If these predictions are confirmed, we can start having confidence that the event/process postulated really did take place.

MarioNovak wrote:

Rumraket wrote:You cannot compare the rate of origin of de novo genes in an experimental bacterial population to the evolution of large multicellular eukaryotes WHEN THE FORMER HAVE NO JUNK-DNA.

So, the new ad hoc hypotheses(excuse for science ignorance) in evolutionary thought is as follows: organisms that have junk in their genomes can evolve new genes. But when junk is missing, evolution of new genes is not possible or is to slow to be detectable and empirically testable. Gotcha.

Wrong again. What is being said is that you cannot test the hypothesis for the rate of origin of ORFan genes in multicellular eukaryotes with an experimental bacterial population. That's it.

MarioNovak wrote:But... your ad hoc excuse have been debunked by science, again.

http://genome.cshlp.org/content/14/6/1036.full

However, most bacteria contain large numbers of ORFans, that is, annotated genes that are restricted to a particular genome and that possess no known homologs.
...
The high frequencies of ORFans detected in bacterial genomes were originally attributed to the limited set of sequenced genomes then available for comparison, and it was predicted that this category of genes would dwindle as databases expanded. Nevertheless, the number of ORFans in databases has grown despite an increase in the number and diversity of complete genome sequences. A recent survey estimated their frequency to be 14% of the total genes from 60 completely sequenced genomes.

Nobody is saying, nor did any one even insinuate that bacteria do not contain ORFan genes.

Why do you also link a paper that explains the origin of these ORFans by testing a hypothesis?:

If ORFans originate in phages, it is anticipated that their sequences will harbor additional characteristics of bacteriophage genes. Because dinucleotide frequencies can provide signatures that discriminate among sequences from different organisms and have been used to identify alien genes within genomes (Karlin 1998), we compared the dinucleotide frequencies from native genes, ORFans, and bacteriophages known to infect E. coli (see Supplemental material). Recent ORFans and phages are similarly biased for CpG, TpC, ApG, CpC, and ApA, whereas the older ORFans progressively approach the dinucleotide compositions of native genes. These results provide further support of an ancestral relationship between the ORFans present in the E. coli genomes and bacteriophages.

Notice how they start out by making a prediction from their postulated model(as I explained above is how we can test hypotheses about ancient and slow events), then test it against observations in extant life.

They invariably always take on this general form:
If X happened, we would expect to find Z in entity Y because of process A. That's how you test hypotheses about things you can't directly observe. It works in science and in criminal forensics. We throw people to jail on this general principle.

MarioNovak wrote:

Rumraket wrote:Yes, because we have actual concrete empirical evidence that it did from phylogenetics.

We have actual concrete empirical evidence that vw golf 6 and vw golf 7 are related.

We do? I didn't know cars gave birth to other cars. I thought they were built in factories.

But here's another opportunity for empirical verification of your "hypothesis". Try construct a phylogenetic tree of all extant models of cars, based on the various components from which they are constructed, compared to the models from the past. If you're able to produce a branching pattern with a nested hierarchical arrangement, then you've shown that phylogenetics cannot be used to demonstrate common ancestry (or that cars actually do give birth to other cars.)

Rumraket wrote:These are concrete empirical facts, things really just do take the time they do. You don't grow a 300 foot redwood tree in a week either. Stop being ridiculous please.

Wait, it is testable, just not directly. We cannot reconstruct ancient historical progressions before our very eyes. Tough shit, that's just an inherent limitation of being human.
Once again you get it wrong. What we can do, If we postulate some event happened in the past, and took a very long time, we can test this through building a model of the event and making predictions about what we should be able to find if the event really took place. One of the ways we do this is through phylogenetics. If these predictions are confirmed, we can start having confidence that the event/process postulated really did take place.

Ok, models. Check this out: this "model" show that the appearance of only two coordinated mutations in humans would have an expected time of appearance of 216 million years.
Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution, http://www.genetics.org/content/180/3/1501.full

If these calculations are put alongside the research which identified a total of 60 protein-coding genes that originated de novo on the human lineage since divergence from chimpanzee, failure of evolutionary ideas is even more obvious. If absurd assumption is made, that only two coordinated mutation are nedded to create one protein coding gene from junk DNA, the appearance of this gene in humans would have an expected time of appearance of 216 million years. Since, ancestors of humans and chimps diverged 5-7 million years ago, it is obvious that evolutionary hypothesis are in complete contradiction with science.

Rumraket wrote:Nobody is saying, nor did any one even insinuate that bacteria do not contain ORFan genes.

Why do you also link a paper that explains the origin of these ORFans by testing a hypothesis?:

If ORFans originate in phages, it is anticipated that their sequences will harbor additional characteristics of bacteriophage genes. Because dinucleotide frequencies can provide signatures that discriminate among sequences from different organisms and have been used to identify alien genes within genomes (Karlin 1998), we compared the dinucleotide frequencies from native genes, ORFans, and bacteriophages known to infect E. coli (see Supplemental material). Recent ORFans and phages are similarly biased for CpG, TpC, ApG, CpC, and ApA, whereas the older ORFans progressively approach the dinucleotide compositions of native genes. These results provide further support of an ancestral relationship between the ORFans present in the E. coli genomes and bacteriophages.

Notice how they start out by making a prediction from their postulated model(as I explained above is how we can test hypotheses about ancient and slow events), then test it against observations in extant life.

They invariably always take on this general form:
If X happened, we would expect to find Z in entity Y because of process A. That's how you test hypotheses about things you can't directly observe. It works in science and in criminal forensics. We throw people to jail on this general principle.

How pre-existing genes derived from phage genomes by horizontal gene transfer proves that process of evolution can create new genes?

In my first post I wrote :

Why are new genes important? Because the hypothetical first self-replicator did not contain genes for three-dimensional cellular structures and arrangements like lungs, heart, blood vessels, stomach, liver, kidneys, muscles, brain, nerves, skin, hair, ovaries, uterus, testes, prostate, penis, bones, ligaments, ... etc. All these arrangements are significantly different in their three-dimensional shape, and function, so the information written in genes that represent them also have to be significantly diferent. Ear is different than eye, heart is different than kidneys, DNA polymerase is different ATP synthase, mechanical gears in jumping insects are diferent then bacterial flagellum, knee is different than jaw, liver is differnt then stomach...

So evolutionary biologists make predictions from their postulated model that genes CpG, TpC, ApG, CpC, and ApA are derived from phage genomes by horizontal gene transfer, then test it and voila, they were right. So, how that proves that process of evolution can create new genes? How that proves that process of evolution can create ORFans without homologues in phage genomes? This prediction games played by evolutionists are scientifically totally irrelevant.

MarioNovak wrote:

Rumraket wrote:Wait, new alleles did not arise and take control? What qualifies as a "new" allele? What does that even mean "and take control"? Where has this prediction been made?
Where's the problem? The experiment shows that even strong natural selection does not successfully weed out large genetic variation.

In a population genetics new allele is a new gene variation. Mutation is the primary source of those variations(new alleles). "To take control" - to increase allele frequency in population(gene pool).

The researchers were looking for the fixation of positive mutations within the genome and within the whole population. This is referred to using the term "selection sweep". When it occurs, the new mutation at a base pair (a novel single nucleotide polymorphism or SNP) not only experiences replication to be transmitted to the descendants of the organism, but the gene pool of variation is effectively swept clean as the new mutation becomes dominant in the whole population. However, such sweeping was conspicuous by its absence.

"Recent research on evolutionary genetics has focused on classic selective sweeps, which are evolutionary processes involving the fixation of newly arising beneficialmutations. In a recombining region, a selected sweep is expected to reduce heterozygosity at SNPs flanking the selected site. . . . Notably, we observe no location in the genome where heterozygosity is reduced to anywhere near zero, and this lack of evidence for a classic sweep is a feature of the data regardless of window size."
http://www.nature.com/nature/journal/v4 ... bal=remove

This empirical work is worth noting because we are considering a mechanism that is central to Darwinian evolution. Positive natural selection of hereditable variation is the key to understanding how descent with modification occurs. However, the empirical data relating to a sexually reproducing species does not confirm that modification works this way. This is why the primary investigator, ecology and evolutionary biology professor, Anthony Longsaid said: "This research really upends the dominant paradigm about how species evolve".

http://news.uci.edu/press-releases/uci- ... uit-flies/

Thank you for answering my questions, so that's what you mean by "arise and take control".

Well this leads me to ask, since they're testing models of selection. What does this have to do with the ability of evolution to create new genes, or your mistaken views of model and hypothesis testing? Or the applicability of bacterial experiments to eukaryotic genome evolution?

Rumraket wrote:As just shown, they do nothing of the sort. By the way, you have never detailed a rigorous metric for "newness". And regardless, we already know evolution has created basically the entire biosphere, we know this from phylogenetic evidence.

You haven't shown anything scientifically important, you just offered(produced) a mental construct of a human mind(excuse) - a rationalization for ignorance of scientific discoveries. When an orderly long term procedure is carried out(long term evolution experiment) and empirical connection with the two causes - random variation and natural selection is established, a new gene, as na effect is not produced. So, the scientific fact is that evolutionary processes can not create new genes. Your rationalizations will not make this fact ceases to exist.

Rumraket wrote:I notice you have completely ignored the rather large first post I made in this thread where I present some of this evidence. Why is it that ID proponents are invariably always totally silent on phylogenetics? It's almost as if the field does not exist in your minds.

Because the phylogenetics is just the construct of a human mind, which can conceptually be applied to any set of objects with similar characteristics, such as vehicles. So, by your reasoning, if vehicles are recognized, differentiated and grouped into categories that proves that random processes create vehicles.

Ohhh, this is excellent news for your career in law. You'll be earning millions getting people off paternity lawsuits and settlements because, as you imply, patterns of genetic similarity do not imply a genealogical relationship, it's "just the construct of a human mind".

Rumraket wrote:Yes, because we have actual concrete empirical evidence that it did from phylogenetics.

We have actual concrete empirical evidence that vw golf 6 and vw golf 7 are related. How this proves eventual assumption that the blueprint for golf 7 resulted from random change in the blueprint that shows how golf 6 will be made?

You know we actually observe the process of descent with modification, right? You are born with mutations and a combination of alleles from your parents. You also have a phenotypical mix of their attributes. I'm sure you've heard the expression "you have your mother's eyes" and things like that?

Cars don't make copies of themselves, or even reproduce sexually. Organisms do. Changes accumulate over time. You are more different from your great-great-great-great grandparents, than their immediate children were. The corroboration between these two empirically extremely well established processes (what we call the twin nested hierachies, twin because it is corroborated both by morphology and genetics) is simply being extended to longer timescales.

The timescales implied through genetics are roughly correlated with the timescales implied by the fossil record. The process makes specific predictions, which is what allowed researchers to predict the approximate age at which a fossil transitional species like Tiktaalik was eventually found.

This same general principle can be used to test phylogenetic methodology. You've skipped a very important question I posed to you in my post on phylogenetics:
Key question to be answered by the people who deny the phylogenetic evidence for the evolution of novel enzymatic functions through novel protein coding genes:
If ancestral sequence reconstruction is based entirely on phylogenetic trees and substitution models(as it is), but the inferred evolutionary transitions did not actually take place, WHY IS IT POSSIBLE TO RECONSTRUCT FUNCTIONALLY PROMISCOUS ANCESTRAL STAGES OF EXTANT PROTEINS?

This should simply not be possible if evolution did not take place. The artificially reconstructed and inserted mutations, derived from algorithms build on assumptions about how molecular evolution takes place (which in turn are derived from empirical data about how real-world and laboratory populations evolve), should simply not be able to produce functional ancestral states.

Yet they do.

Explain why this is possible when, as you say, these inferred phylogenetic relationships are "just the construct of a human mind".

Edit: Edited for spelling and grammar.

MarioNovak wrote:Ok, models. Check this out: this "model" show that the appearance of only two coordinated mutations in humans would have an expected time of appearance of 216 million years.
Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution, http://www.genetics.org/content/180/3/1501.full

Did you even read that paper? Here is what they say near the end:

The edge of evolution?

Our final example of waiting for two mutations concerns the emergence of chloroquine resistance in P. falciparum. Genetic studies have shown, see Wooton et al. (2002), that this is due to changes in a protein PfCRT and that in the mutant strains two amino acid changes are almost always present—one switch at position 76 and another at position 220. This example plays a key role in the chapter titled “The mathematical limits of Darwinism” in Michael Behe's book, The Edge of Evolution (Behe 2007).

Arguing that (i) there are 1 trillion parasitic cells in an infected person, (ii) there are 1 billion infected persons on the planet, and (ii) chloroquine resistance has arisen only 10 times in the past 50 years, he concludes that the odds of one parasite developing resistance to chloroquine, an event he calls a chloroquine complexity cluster (CCC), are ∼1 in 1020. Ignoring the fact that humans and P. falciparum have different mutation rates, he then concludes that “On the average, for humans to achieve a mutation like this by chance, we would have to wait a hundred million times ten million years” (Behe 2007, p. 61), which is 5 million times larger than the calculation we have just given.

Indeed his error is much worse. To further sensationalize his conclusion, he argues that “There are 5000 species of modern mammals. If each species had an average of a million members, and if a new generation appeared each year, and if this went on for two hundred million years, the likelihood of a single CCC appearing in the whole bunch over that entire time would only be about 1 in 100” (Behe 2007, p. 61). Taking 2N = 106 and μ1 = μ2 = 10−9, Theorem 1 predicts a waiting time of 31.6 million generations for one prespecified pair of mutations in one species, with (Formula) having reduced the answer by a factor of 31,600.

We are certainly not the first to have criticized Behe's work. Lynch (2005) has written a rebuttal to Behe and Snoke (2004), which is widely cited by proponents of intelligent design (see the Wikipedia entry on Michael Behe). Behe and Snoke (2004) consider evolutionary steps that require changes in two amino acids and argue that to become fixed in 108 generations would require a population size of 109. One obvious problem with their analysis is that they do their calculations for N = 1 individual, ignoring the population genetic effects that produce the factor of (Formula). Lynch (2005) also raises other objections.

(Some of the mathematical symbols are not reproduced, and replaced by the term Formula.)

This paper says the exact opposite of what you think it says. It shows that the emergence of novel genes thru normal evolutionary mechanisms is common place, and provides the math to prove it. The 216 million year figure you quote is the odds of a specific pair of mutations occurring. Not of any pair of mutations.

Own goal!

MarioNovak wrote:

Rumraket wrote:These are concrete empirical facts, things really just do take the time they do. You don't grow a 300 foot redwood tree in a week either. Stop being ridiculous please.

Wait, it is testable, just not directly. We cannot reconstruct ancient historical progressions before our very eyes. Tough shit, that's just an inherent limitation of being human.
Once again you get it wrong. What we can do, If we postulate some event happened in the past, and took a very long time, we can test this through building a model of the event and making predictions about what we should be able to find if the event really took place. One of the ways we do this is through phylogenetics. If these predictions are confirmed, we can start having confidence that the event/process postulated really did take place.

Ok, models. Check this out: this "model" show that the appearance of only two coordinated mutations in humans would have an expected time of appearance of 216 million years.
Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution, http://www.genetics.org/content/180/3/1501.full

If these calculations are put alongside the research which identified a total of 60 protein-coding genes that originated de novo on the human lineage since divergence from chimpanzee, failure of evolutionary ideas is even more obvious. If absurd assumption is made, that only two coordinated mutation are nedded to create one protein coding gene from junk DNA, the appearance of this gene in humans would have an expected time of appearance of 216 million years. Since, ancestors of humans and chimps diverged 5-7 million years ago, it is obvious that evolutionary hypothesis are in complete contradiction with science.

No, the problem is you are not understanding what this paper actually calculates. This paper is trying to establish the waiting time for two specific mutation to happen out of the total space of possible mutations. Obviously if you wait for two specific mutations, instead of just any two mutations, you're going to have to wait a very long time.

You know that over 150 neutral mutations are fixed in the human population, yes, fixed, every generation. Right? Seemingly through nothing but genetic drift. http://en.wikipedia.org/wiki/Fixation_(population_genetics)#Probability_of_fixation

Any two specific of these mutations you could have picked out beforehand and derived some extremely low probability that they would arise and become fixed, leading you to conclude as the paper you supply does, that it would on average take an extremely long time for such two specific mutations to arise and become fixed in the population.

It is amazing to me how frequently these silly and trivial mistakes are made by ID proponents. I guess if you're desperate to find something wrong with evolutionary biology, you're not actually bothering to check your own reasoning through. Anything that might superficially seem to confirm your presuppostions is instantantly seized upon and upheld as unavoidable falsifying facts.

Might I suggest that in the future, you ask yourself before you post silly mistakes like this, that you take some time to ponder if you've maybe not really understood it?

MarioNovak wrote:

Rumraket wrote:Nobody is saying, nor did any one even insinuate that bacteria do not contain ORFan genes.

Why do you also link a paper that explains the origin of these ORFans by testing a hypothesis?:

If ORFans originate in phages, it is anticipated that their sequences will harbor additional characteristics of bacteriophage genes. Because dinucleotide frequencies can provide signatures that discriminate among sequences from different organisms and have been used to identify alien genes within genomes (Karlin 1998), we compared the dinucleotide frequencies from native genes, ORFans, and bacteriophages known to infect E. coli (see Supplemental material). Recent ORFans and phages are similarly biased for CpG, TpC, ApG, CpC, and ApA, whereas the older ORFans progressively approach the dinucleotide compositions of native genes. These results provide further support of an ancestral relationship between the ORFans present in the E. coli genomes and bacteriophages.

Notice how they start out by making a prediction from their postulated model(as I explained above is how we can test hypotheses about ancient and slow events), then test it against observations in extant life.

They invariably always take on this general form:
If X happened, we would expect to find Z in entity Y because of process A. That's how you test hypotheses about things you can't directly observe. It works in science and in criminal forensics. We throw people to jail on this general principle.

How pre-existing genes derived from phage genomes by horizontal gene transfer proves that process of evolution can create new genes?

In my first post I wrote :

Why are new genes important? Because the hypothetical first self-replicator did not contain genes for three-dimensional cellular structures and arrangements like lungs, heart, blood vessels, stomach, liver, kidneys, muscles, brain, nerves, skin, hair, ovaries, uterus, testes, prostate, penis, bones, ligaments, ... etc. All these arrangements are significantly different in their three-dimensional shape, and function, so the information written in genes that represent them also have to be significantly diferent. Ear is different than eye, heart is different than kidneys, DNA polymerase is different ATP synthase, mechanical gears in jumping insects are diferent then bacterial flagellum, knee is different than jaw, liver is differnt then stomach...

So evolutionary biologists make predictions from their postulated model that genes CpG, TpC, ApG, CpC, and ApA are derived from phage genomes by horizontal gene transfer, then test it and voila, they were right. So, how that proves that process of evolution can create new genes? How that proves that process of evolution can create ORFans without homologues in phage genomes? This prediction games played by evolutionists are scientifically totally irrelevant.

You're the one who posted this paper as an example of a study that shows bacteria contain ORFan genes, supposedly to refute my claim that you cannot test hypotheses for the origin of ORFan genes in multicellular eukaryotes with experimental bacterial populations.

While I have already explained why you can't actually do that, you now turn around and complain that the paper you linked yourself, for a different purpose, does not answer the question you set out to pose with this thread? I'm not the one you should be complaining to then.

You really need to spend some time to think about this some more I'm afraid.

Comedy gold!

Notice how we didn't get a rigorous definition of "new" either.