Annoying creationists

[hammegk]

Competition for resources by self replicating RNA molecules.

There seems to be a bit of discussion about where we find one of those, today. Better yet, how did we get the first one?

 

[Taffer]

There seems to be a bit of discussion about where we find one of those, today. Better yet, how did we get the first one?

I don't know, hamme, I do not deal with abiogenesis.

ETA: How does this relate to the original point, anyway? You asked for the selective pressures which would lead to the formation of the first novel genes. I proved an example of one. Why, then, did you switch to abiogenesis?

 

[kleinman]

Annoying Creationists

This is your third post, and I'm still waiting for you to compute all the probabilities.

Didn’t you take care of all the probability problems with string theory?

My apologies, I thought my question was clear. Do you have any compelling evidence which would falsify these hypotheses?

Certainly I do. You can start with the results from ev computer model, a peer reviewed and published model of random point mutations and natural selection which shows this mechanism of evolution is so profoundly slow when using realistic genome lengths and mutation rates that nothing can evolve by this mechanism. Then you can again consider the concept of natural selection which can only operate if there is a benefit or detriment to the creature. I have shown that natural selection can not evolve a gene from the beginning. I will repeat it again since so many evolutionarians are in denial about this issue.

A gene is to evolve. The first base in the sequence for the gene is laid down on the genome. One base codes for nothing so there is nothing for natural selection to act upon. A second base added by random chance is laid down in the sequence. Still nothing to code for, natural selection can not act on this sequence. A third base in the sequence is laid down. You now have enough bases to form a codon for a single amino acid. A single amino acid has no functional use so there is still nothing for natural selection to act upon. So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.

Do you evolutionarians see the goal posts or are you so far out of the ball park you need the Hubble telescope just to see the ball park?

Without a selection process, neither abiogenesis nor the theory of evolution are mathematically possible.

You are correct that, without selection pressure, the theory of evolution is not mathematically possible. However, there is and was selective pressure, so that is not a problem. As for abiogenesis, since it does not deal with evolution of anything, it might or might not require selective pressure. You would have to choose one hypothesis for us to discuss, as I am not versed in abiogenesis. I deal only with evolution.

This thread is about mathematically modeling evolution by mutation and selection. If you believe there is and was selective pressure to do this, present a description for this so that you can evolve a gene from the beginning. Feel free not to discuss this topic if you believe that all genes formed during abiogenesis. However, you have acknowledged the first step in disproving the theory of evolution. The next step is understanding that there is no selective pressure that can evolve a gene from the beginning. The only thing that natural selection can do is select for a creature with a beneficial property and select against a creature with a detrimental property. The addition of bases to a sequence which is neither beneficial nor detrimental will not alter the frequency of occurrence of that sequence in the population. Without selection pressure, the theory of evolution is not mathematically possible as you so correctly have said.

Yeah, that is a question being discussed. What did you say those pressures are?

Competition for resources by self replicating RNA molecules.

Taffer, that’s a lovely semantic dance you are doing here.

There seems to be a bit of discussion about where we find one of those, today. Better yet, how did we get the first one?

I don't know, hamme, I do not deal with abiogenesis.

I’m not talking about abiogenesis, I am talking about the evolution of a new gene from the beginning. Here are some examples to consider. The gene that codes for insulin, the gene that codes for globulin, the genes that code for the enzymes for the Krebs cycle, the genes that code for the proteins in the DNA replicase system and so on. Do you believe that all these genes arose during abiogenesis? Unless you can describe a sieve that would give rise to these genes from the beginning, you theory of evolution is mathematically impossible as you so correctly noted earlier.

 

[kjkent1]

Didn’t you take care of all the probability problems with string theory?

Unless you defend your current position, I'll take your statement here as an admission by you that I have, in fact, refuted substantially all of your claims of mathematical impossibility, concerning both evolution and abiogenesis.

Edit: you know, there's a lot of genuine brain power in this thread. If you were a litttle more interested in actually searching for answers, rather than ridiculing your opponents because they don't accept your version of universal creation, all of us might just discover something new -- or at least worthy of further investigation.

 

[kleinman]

Annoying Creationists

Didn’t you take care of all the probability problems with string theory?

Unless you defend your current position, I'll take your statement here as an admission by you that I have, in fact, refuted substantially all of your claims of mathematical impossibility, concerning both evolution and abiogenesis.

Little gator, I think your refutation of my claims using string theory should be embraced by evolutionarians far and wide. It has been the only response to my claim that natural selection can not evolve a gene from the beginning.

 

[kjkent1]

Little gator, I think your refutation of my claims using string theory should be embraced by evolutionarians far and wide. It has been the only response to my claim that natural selection can not evolve a gene from the beginning.

I don't know what you mean by "little gator," but if it's a reference to chronological age, I'm probably older than you are.

 

[kleinman]

Annoying Creationists

Little gator, I think your refutation of my claims using string theory should be embraced by evolutionarians far and wide. It has been the only response to my claim that natural selection can not evolve a gene from the beginning.

I don't know what you mean by "little gator," but if it's a reference to chronological age, I'm probably older than you are.

Did you compute that probability?

 

[kjkent1]

Did you compute that probability?

No, but the publicly available empirical evidence suggests to me that you're between 50 and 60 years old.

 

[Dr Richard]

...I’m not talking about abiogenesis, I am talking about the evolution of a new gene from the beginning. The gene that codes for insulin...

Annual review of Genetics: structure and evolution of the insulin gene

Apologies for the block quotations, and long post, but I am not sure that many viewers will have access to Annual Reviews going back to 1985...

Kleinman has evidently forgotten that the insulin gene does not exist in isolation:

The two-chain hormone is derived biosynthetically from the immediate precursor, proinsulin which consists of the B and A chains linked to a connecting peptide (C-peptide) by adjacent pairs basic residues in the following order: NH2-B chain.Arg.Arg.C-peptide. Lys.Arg.A chain-COOH(2 3, 93, 136). However,the initial translation product of the insulin mRNiAs preproinsulin, which contains an N-terminal signal peptide, or prepeptide, of 24 amino acids linked to proinsulin (21).

So, insulin comes from proinsulin...

Although insulin at one time was thought to be a structurally unique hormone, the pioneering studies of Froesch and Humbeal nd their coworkers( 40,110, 111, 159) have shown that other insulin-like activities not suppressed by the addition of anti-insulin antibody are present in the sera of mammals. The successful isolation and amino acid sequence determination of these substances, which have been named IGF-I and II in man (110, 111), clearly demonstrated their structural relationship to proinsulin, particularly in the conservation of the disulfide bridges and the presence of a short connecting peptide segment that is usually not removed. In addition to the insulin-like growth factors, the ovarian peptide hormone, relaxin, has been placed in the insulin superfamily on the basis of its primary and secondary structural homology to insulin (61). The submaxillary nerve growth factor (NGF) may also be a homologue of insulin (38), but in this case the evidence is less compelling (147a).

Insulin is therefore part of a signalling superfamily. This is is of course the case with most signalling/receptor pathways, which exhibit multiple crossovers and redundancies. As might be expected from evolution with natural selection, or perhaps from a sloppy/incompetent designer. This is further evidenced by the fact there is not just one insulin gene, in rodents at least...

In most species the insulin gene exists in a single copy, except rats (79) and mice (18) where 2 nonallelic insulins are produced by closely related genes that are over 90% homologous in nucleotide sequence in the rat (79) (estimated divergence time 25-35 million years). Evidence suggests that the genes for rat and mouse insulin I, which in addition to the absence of IVS-2 (Figure 1) exhibit other hallmarks of retroposition, probably have arisen by RNA-mediaded rna transposition,as a functional gene, of a cDNA copy of an incompletely processed upstream transcript of insulin gene II into the ancestral murine germ line (122).

Again, this seems entirely consistent with an evolutionary explanation of a mutation within the rodent precursor after separation from the mammalian superfamily. Personally, I find in incomprehensible why an intelluigent designer would duplicate the insulin gene in these two species alone, and as we know argument from personal incredulity constitutes proof...

But this will not be good enough for Kleinman, we need to know how these insulin link genes could have evolved in the first place...

As noted earlier, it is now clear that several insulin-like growth factors (also known as multiplication stimulating activity (MSA) or somatomedin) circulate in mammals (e.g. rat MSA and human IGFs I and II).

The gene for IGF I is located on human chromosome 12, which may be evolutionarily related to chromosome (14, 143). The recent demonstration
of a larger variant form of IGFI I in humans suggests the existence of an
additional gene for IGF II in man (162). Although the exact time of divergence
of these molecules from insulin cannot be predicted with accuracy, they differ
more in amino acid sequence (-45% homology) than do the vertebrate insulins
(e.g. hagfish vs human -60% homology) suggesting an earlier separation time (>0.5 billion years). The recent finding of IGF-like peptides in Bombyxm orii
(90) tentatively supports this conclusion, although it is unclear as yet whether insulin, as such, also exists in such invertebrates. Thus far the evidence on putative invertebrate or prokaryotic insulins is fragmentary (35, 36, 78a, 105,140).

But where did these earlier genes come from?

The above findings, coupled with evidence that IGF-I production is under control of pituitary growth hormone and may, in fact, be largely responsible for mediating postnatal somatic growth in the organism (1, 17, 40), strongly suggest the evolution of a complex and well-integrated system for the regulation of growth and metabolism in which insulin-like peptides (insulin and somatomedins) play a central role and are regulated by both nutritional and neural influences

...It is tempting to speculate that protoinsulin in simpler organisms was a metabolic hormone whose actions led to increased uptake and utilization of foodstuffs and, perhaps as a direct consequence, stimulated growth. However, as organisms became more complex and food supplies more limited, these two activities - nutrition and growth - had to be uncoupled. To accomplish this the primitive "insulin" system becamed diversified in evolution into superfamilies of related proteins and receptors, with differing relative potencies for regulating fuel metabolism on the one hand, or growth on the other. This hypothesis is supported by studies of the relative growth-promoting vs metabolic activities of insulin and the IGF peptides (40, 47, 70, 71, 160).

And these genes form part of an even older family of proteins - remember the ovarian hormone relaxin mentioned above?

Relaxin has no insulin-like activity and little is known of its cell surface receptors, at present. However, as discussed in more detail below, recent studies of its mode of biosynthesis via preprorelaxin (74, 153) and of its gene structure support its probable evolutionary divergence from an ancestral antecedent of insulin.

So, insulin is part of a superfamily of proteins whose comparatve structures in various species support the hypothesis that they evolved from primitive organisms where they regulated growth and metabolism.

Remember that Kleinman specifically did not ask for abiogenesis here, so haveing covered >500million years of evolution of the insulin gene, I will leave things there.

I realise that most JREF forum readers will realise that similar cases can be made for the other genes/proteins he mentions, but it is worth pointing out that such evolutionary genetics is not simply a sterile theoretical field. Genuine scientific and medical breakthroughs have been made by comparative genomic studies that are based on the assumption that both coding and non-coding sections of the genome are subject to evolutionary change over millions of years.

My favorite recent paper is on the importance of the non-coding (so-called junk) DNA in the pathogenesis of Hirschsprung's disease; note the application within the paper of evolutionary theory to achieve a clinically relevant result.

So, question to Kleinman in return. What did God evolve from? Or did he just suddenly appear? What is the mathematical probability of that happening?

 

[Schneibster]

How does this relate to the original point, anyway? You asked for the selective pressures which would lead to the formation of the first novel genes. I proved an example of one. Why, then, did you switch to abiogenesis?

Because it doesn't know the difference.

 

[RecoveringYuppy]

Kleinman has evidently forgotten that the insulin gene does not exist in isolation:

Probably never knew it. And based on his repetition of a similar error regarding hemoglobin probably isn't capable of learning it.

 

[Schneibster]

I realise that most JREF forum readers will realise that similar cases can be made for the other genes/proteins he mentions, but it is worth pointing out that such evolutionary genetics is not simply a sterile theoretical field. Genuine scientific and medical breakthroughs have been made by comparative genomic studies that are based on the assumption that both coding and non-coding sections of the genome are subject to evolutionary change over millions of years.

See, this is why Kleinman bothers me. Let me ask him this: suppose that a patient of his had a condition that could only be treated by acknowledging some of this research. Would he use that treatment? Would he even know it exists, since he denies this stuff is real?

We can't have doctors who ignore science. It comes perilously close to ignoring their Hippocratic Oath.

 

[kleinman]

Annoying Creationists

...I’m not talking about abiogenesis, I am talking about the evolution of a new gene from the beginning. The gene that codes for insulin...

Annual review of Genetics: structure and evolution of the insulin gene

Apologies for the block quotations, and long post, but I am not sure that many viewers will have access to Annual Reviews going back to 1985...

Kleinman has evidently forgotten that the insulin gene does not exist in isolation:

Dr Richard, welcome to this discussion. I particularly appreciate that you quote the portion of your link that feel address my argument.

The two-chain hormone is derived biosynthetically from the immediate precursor, proinsulin which consists of the B and A chains linked to a connecting peptide (C-peptide) by adjacent pairs basic residues in the following order: NH2-B chain.Arg.Arg.C-peptide. Lys.Arg.A chain-COOH(2 3, 93, 136). However,the initial translation product of the insulin mRNiAs preproinsulin, which contains an N-terminal signal peptide, or prepeptide, of 24 amino acids linked to proinsulin (21).

And

Although insulin at one time was thought to be a structurally unique hormone, the pioneering studies of Froesch and Humbeal nd their coworkers( 40,110, 111, 159) have shown that other insulin-like activities not suppressed by the addition of anti-insulin antibody are present in the sera of mammals. The successful isolation and amino acid sequence determination of these substances, which have been named IGF-I and II in man (110, 111), clearly demonstrated their structural relationship to proinsulin, particularly in the conservation of the disulfide bridges and the presence of a short connecting peptide segment that is usually not removed. In addition to the insulin-like growth factors, the ovarian peptide hormone, relaxin, has been placed in the insulin superfamily on the basis of its primary and secondary structural homology to insulin (61). The submaxillary nerve growth factor (NGF) may also be a homologue of insulin (38), but in this case the evidence is less compelling (147a).

Insulin is therefore part of a signalling superfamily. This is is of course the case with most signalling/receptor pathways, which exhibit multiple crossovers and redundancies. As might be expected from evolution with natural selection, or perhaps from a sloppy/incompetent designer. This is further evidenced by the fact there is not just one insulin gene, in rodents at least...

In most species the insulin gene exists in a single copy, except rats (79) and mice (18) where 2 nonallelic insulins are produced by closely related genes that are over 90% homologous in nucleotide sequence in the rat (79) (estimated divergence time 25-35 million years). Evidence suggests that the genes for rat and mouse insulin I, which in addition to the absence of IVS-2 (Figure 1) exhibit other hallmarks of retroposition, probably have arisen by RNA-mediaded rna transposition,as a functional gene, of a cDNA copy of an incompletely processed upstream transcript of insulin gene II into the ancestral murine germ line (122).

And so on…
But this is the crucial quote from this link.

Relaxin has no insulin-like activity and little is known of its cell surface receptors, at present. However, as discussed in more detail below, recent studies of its mode of biosynthesis via preprorelaxin (74, 153) and of its gene structure support its probable evolutionary divergence from an ancestral antecedent of insulin.

There are two issues you have to account for in your story in order to make it mathematically and scientifically consistent. The first is how did the ancestral antecedent of insulin arise from the beginning and the second is how did this ancestral antecedent of insulin morph into the other related hormones. You have no selection process that will evolve any gene from the beginning including your so called ancestral antecedent of insulin. And any process of morphing this so called ancestral antecedent of insulin into other hormones must have selective benefit to those creatures as it is morphing step by step from one hormone to the next. Do you care to describe this selective process that morphs these hormones from one to another so that it can be included in Dr Schneider’s mathematical model and the process demonstrated. Otherwise, mutation and selection is nothing more than a slogan with no mathematical or scientific basis.

It is not enough to observe similarities between genetic structures. You must demonstrate how these structures could have arisen initially and how they can transform from one to another. You have done neither.

I realise that most JREF forum readers will realise that similar cases can be made for the other genes/proteins he mentions, but it is worth pointing out that such evolutionary genetics is not simply a sterile theoretical field. Genuine scientific and medical breakthroughs have been made by comparative genomic studies that are based on the assumption that both coding and non-coding sections of the genome are subject to evolutionary change over millions of years.

See, this is why Kleinman bothers me. Let me ask him this: suppose that a patient of his had a condition that could only be treated by acknowledging some of this research. Would he use that treatment? Would he even know it exists, since he denies this stuff is real?

We can't have doctors who ignore science. It comes perilously close to ignoring their Hippocratic Oath.

You can make similar cases for any genes you want and I will ask you how the ancestral gene formed from the beginning and how these genes transformed from one to another. I don’t consider a slogan as a scientific answer.

Dr Richard, perhaps you could tell us what the ancestral genes were for the DNA replicase system? I would be interested in hearing that case.

 

[hammegk]

Genuine ... medical breakthroughs have been made by comparative genomic studies that are based on the assumption that both coding and non-coding sections of the genome are subject to evolutionary change over millions of years.

What medical breakthroughs depend on millions of years? Is it not really years or decades of evolutionary change for any such breakthroughs you might cite?

 

[RecoveringYuppy]

We've found parts of our genome that we didn't know were active by comparing the rate of accumulation of change in the various regions of DNA. Look back through Scientific American over the past two years for an article about the subject.

 

[Schneibster]

Well, I guess that was about what I expected. No answer. OK, fine, back on ignore.

 

[Dr Richard]

Dr Richard, welcome to this discussion. I particularly appreciate that you quote the portion of your link that feel address my argument.

I am however somewhat diappointed that you did not actually bother to read the article before firing off your response. I was, after all, merely quoting excerpts from the article; it would be somewhat foolish to base your arguments solely on what I have quoted.

Firstly, I need to clarify a point:

You asked for a demonstration of the evolution of insulin.

I provided evidence back to the precursor from which proto insulin and proto relaxin diverged; this would seem not to be sufficient.

Definition and acceptable base sequence please.

You did not answer my other questions, hence I feel we must stall on this point for now.

 

[Kotatsu]

You can start with the results from ev computer model, a peer reviewed and published model of random point mutations and natural selection which shows this mechanism of evolution is so profoundly slow when using realistic genome lengths and mutation rates that nothing can evolve by this mechanism.

Notwithstanding, again, that the results of Ev regarding random point mutations does not in any way whatsoever preclude the possibility of evolution either entirely through other means, or through a combination of random point mutations and other means, your latest formulation of your hypothesis (1) can easily be countered by the example of what I believe is called the FMRFamide-like neuropeptide family (2), many members of which have appeared exactly due to random point mutations, but which are still useable by the organisms, with a varied degree of success.

---
(1) i.e. "nothing can evolve by th[is] mechanism [random point mutation and natural selection]" (Emphasis mine).
(2) I don't have the papers in front of me, as I am at home, and I have only become superficially acquianted with them, as my study on a certain oligochaete (3) have involved working with a guy in Florida who studies this family from an evolutionary perspective (among other things).
(3) Submitted today after over a year of hard work! Hoorah!

 

[kleinman]

Annoying Creationists

We've found parts of our genome that we didn't know were active by comparing the rate of accumulation of change in the various regions of DNA. Look back through Scientific American over the past two years for an article about the subject.

At least Dr Richard quotes the portions of his link that he thinks makes a valid argument. Now RecoveringYuppy simply says read Scientific American. Let me bring this discussion back on topic.

This is a discussion on the mathematics of mutation and selection. I have focused on Dr Tom Schneider’s ev computer model of random point mutation and natural selection since it was peer reviewed and published in Nucleic Acids Research. It is clear from this stylized model that random point mutations and natural selection is a profoundly slow process when realistic genome lengths and mutation rates are used in the model, too slow to evolve anything in the time available. Unnamed altered Dr Schneider’s selection process and achieved more rapid convergence which moved the center of discussion to the selection process. Since neither Dr Schneider’s nor Unnamed’s selection process have any relationship to any realistic selection process, I have challenge the evolutionarians reading this thread to describe a selection process that would evolve a gene from the beginning. We can add to this challenge to describe a selection process that would evolve a gene from one form to another such that every step of the evolutionary process gives a selective benefit to those creatures in which this process is occurring.

As an example of this additional challenge, consider a gene which produces a protein that acts as a selective channel for transporting sodium. Describe a selection process that would evolve this gene to a protein that would transport calcium such that every step along the way this gene offers selective benefit to the creatures in which this gene is evolving.

It is not enough to say that there are genetic similarities between different life forms and therefore the theory of evolution is true. You must show how the bookkeeping of your slogan of mutation and natural selection accomplishes these transformations and the origin of the so called ancestral genes initially. Dr Schneider’s model shows that you don’t have your bookkeeping in order. In fact, Dr Schneider’s model shows how important the selection process is for accomplishing any gain in information in a genome. Without a valid selection process that can evolve a gene from the beginning and a selection process that allows the transformation of one gene to another, you have no theory of evolution with a mathematical/scientific basis. However, you do have a slogan that has duped many scientists for more than 150 years.

Firstly, I need to clarify a point:

You asked for a demonstration of the evolution of insulin.

I provided evidence back to the precursor from which proto insulin and proto relaxin diverged; this would seem not to be sufficient.

My contention is that natural selection does not have the capability of evolving a gene from the beginning. I will repeat my argument again here.

A gene is to evolve. The first base in the sequence for the gene is laid down on the genome. One base codes for nothing so there is nothing for natural selection to act upon. A second base added by random chance is laid down in the sequence. Still nothing to code for, natural selection can not act on this sequence. A third base in the sequence is laid down. You now have enough bases to form a codon for a single amino acid. A single amino acid has no functional use so there is still nothing for natural selection to act upon. So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.

Do you suggest there is a proto DNA replicase system?

Definition and acceptable base sequence please.

A sequence that gives benefit to the creature, something which a partially evolved gene can not do.

You did not answer my other questions, hence I feel we must stall on this point for now.

You have not answered my questions either. What is the selection mechanism which would evolve a gene from the beginning? Your entire first post simply describes similarities between insulin and insulin like molecules and that satisfies you as a proof for the theory of evolution. I on the other hand require you show how proto insulin evolved from the beginning and how these insulin like molecules transform from one to another by mutation and selection. Using the slogan “mutation and natural selection” is not a satisfactory scientific explanation. Mutations have been described and measured extensively however natural selection is an amorphous mushy term as shown by Dr Schneider’s ev model of random point mutations and natural selection. It is your theory of evolution which is stalled without a valid selection mechanism that would evolve a gene from the beginning.

 

[Kotatsu]

What medical breakthroughs depend on millions of years?

[/serious mode]
Didn't people use to eat powdered diamonds to counter some syndrom or other? Or is that just a myth, or perhaps something I've just made up?
[serious mode]