Original Research--join In

[Split Rock]

I was just thinking about mentioning that. They say you can take all the
phones, computers, tablets, etc. in the world today, put them all together
and it would all equal the power of one human brain.

Apparently nature just came about developing something like that
by mere time and chance. And that is just your brain.

Why do you continue to ignore SELECTION???? There is a mechanism called Natural Selection... look it up!

 

[WisdomSpy]

The import of my research continues to be misunderstood and mischaracterized, often using straw-man arguments and continued assumptions of what natural selection (NS) is capable of doing. Gould did not deny that NS occurs and neither do I—he pointed out that it must occur at the organismal level. Individual areas of DNA or RNA simply “do not have [access] to NS”, was his point [or really, that NS does not have access to them within individual cells]:

““‘…no matter how much power [Richard] Dawkins wishes to assign to genes, there is one thing that he cannot give them – direct visibility to natural selection’. Rather, the unit of selection is the phenotype, not the genotype, because it is phenotypes which interact with the environment at the natural-selection interface.”

 

[WisdomSpy]

Now, returning to the most salient point regarding expected genomes and proteomes, if naturalistic processes were in fact responsible for their origins:

“The genetic code allows making some theoretical predictions about average protein size and frequency distribution [1,2,3]. Since stop codons can appear stochastically after any start codon, then larger proteins should always be less frequent than smaller proteins. The most frequent protein sizes should be 1 aa in length [4].”[5]

But this is not at all consistent with empirical data. Furthermore, calculations can be made of the expected amount of junk DNA within cells, IF naturalistic processes were the only ones involved in their genesis.

Where is the mechanism within cells, to clean up the 99.9999% of junk that would naturally accompany the random search for necessarily lengthy genes? Do the math on ONE gene of 2500 codons in length. How much junk would occur under random naturalistic chemical processes? What amount of molecular resources do you think were really present in the hypothetical primordial ooz? It is irresponsible to assume unlimited resources.

1. Zhang JZ: Protein-length distributions for the three domains of life. Trends Genet 2000, 16(3):107-109.
2. Brocchieri L, Karlin S: Protein length in eukaryotic and prokaryotic proteomes. Nucleic Acids Res 2005, 33(10):3390-3400.
3. Jukes TH, Holmquist R, Moise H: Average proteins and genetic code. Science 1976, 194(4265):642-643.
4. Oliver JL, Marin A: A relationship between GC content and coding sequence
length. J Mol Evol 1996, 43(3):216-223.
5. Tiessen et al.: Mathematical modeling and comparison of protein size distribution in different plant, animal, fungal and microbial species reveals a negative correlation between protein size and protein number, thus providing insight into the evolution of proteomes. BMC Research Notes 2012 5:85.

 

[Split Rock]

The import of my research continues to be misunderstood and mischaracterized, often using straw-man arguments and continued assumptions of what natural selection (NS) is capable of doing. Gould did not deny that NS occurs and neither do I—he pointed out that it must occur at the organismal level. Individual areas of DNA or RNA simply “do not have [access] to NS”, was his point [or really, that NS does not have access to them within individual cells]:

““‘…no matter how much power [Richard] Dawkins wishes to assign to genes, there is one thing that he cannot give them – direct visibility to natural selection’. Rather, the unit of selection is the phenotype, not the genotype, because it is phenotypes which interact with the environment at the natural-selection interface.”

What happens to the frequency of an allele in a population that confers a detrimental phenotype (reduced fitness) upon an individual?

 

[Split Rock]

Now, returning to the most salient point regarding expected genomes and proteomes, if naturalistic processes were in fact responsible for their origins:

“The genetic code allows making some theoretical predictions about average protein size and frequency distribution [1,2,3]. Since stop codons can appear stochastically after any start codon, then larger proteins should always be less frequent than smaller proteins. The most frequent protein sizes should be 1 aa in length [4].”[5]

But this is not at all consistent with empirical data. Furthermore, calculations can be made of the expected amount of junk DNA within cells, IF naturalistic processes were the only ones involved in their genesis.

Where is the mechanism within cells, to clean up the 99.9999% of junk that would naturally accompany the random search for necessarily lengthy genes? Do the math on ONE gene of 2500 codons in length. How much junk would occur under random naturalistic chemical processes? What amount of molecular resources do you think were really present in the hypothetical primordial ooz? It is irresponsible to assume unlimited resources.

1. Zhang JZ: Protein-length distributions for the three domains of life. Trends Genet 2000, 16(3):107-109.
2. Brocchieri L, Karlin S: Protein length in eukaryotic and prokaryotic proteomes. Nucleic Acids Res 2005, 33(10):3390-3400.
3. Jukes TH, Holmquist R, Moise H: Average proteins and genetic code. Science 1976, 194(4265):642-643.
4. Oliver JL, Marin A: A relationship between GC content and coding sequence
length. J Mol Evol 1996, 43(3):216-223.
5. Tiessen et al.: Mathematical modeling and comparison of protein size distribution in different plant, animal, fungal and microbial species reveals a negative correlation between protein size and protein number, thus providing insight into the evolution of proteomes. BMC Research Notes 2012 5:85.

If you continue reading the Tiessen paper, they offer explanations for why proteins are longer:

"One can interpret this as evidence of a selective pressure for the avoidance of proteins smaller than 100 aa and the selective advantage of functional proteins of > 250 aa. The characteristic increase of proteins in the range 50-200 aa can be explained with the abovementioned selection force, whereas the monotonic decrease of frequency in the range 500-1,000 aa can be explained by the probable occurrence of stop codons in the coding determining sequence (CDS).

If one considers simple models, the average protein size should be ~21 aa [7]. If one considers more sophisticated models explaining the length of random open reading frames (ORFs) in the intergenic regions of yeast [8], random ORFs of ~33 aa can be explained by the mummy and baby ORF theory alone [8,39]. However, the average eukaryotic protein is much larger than 100 aa (Table 1). We assume that the frequent occurrence proteins of size 150-250 aa is due to protein folding stability (for example TIM barrels) that generates a selective pressures avoiding stop codons within exons or genes. We postulate that this force is so strong in eukaryotic species, that it overcomes the influence of the GC content of DNA on average ORF length as indeed found in prokaryotic genomes. "

 

[EternalDragon]

Why do you continue to ignore SELECTION???? There is a mechanism called Natural Selection... look it up!

Are you saying natural selection built something that humans
can't even begin to do? From the bottom up?

 

[Paul of Eugene OR]

Are you saying natural selection built something that humans
can't even begin to do? From the bottom up?

Well, you also have to include the random mutations and the ongoing reproduction and competition, but, including all that, yes.

You see, advantages accumulate. One comes along, gets established, and then another gets added to it that enhances it or complements it . . . that gets established, another comes along gets added, enhances or complements it. . . .etc etc.

Clearly, such a process would take a looooong time but, given long enough time, there is no limit to the number of enhancements that can be added.

And the end results would be . . . wonderful!

 

[WisdomSpy]

Split Rock posted: "...We assume that the frequent occurrence proteins of size 150-250 aa is due to protein folding stability..."

Yes, I read the entire article. What I also did was to separate in my mind empirical science from pure speculation. Anyone can tell stories about wishful events. The key is to test the actual feasibility of those things, using the evidence you have.

Isn't it interesting that this article offers glib reasoning as to why very long proteins are "usually not seen" (referencing the effects of stop codons) and yet it utterly fails to apply that math to known genes in virtually every type of cell which are very long. Instead of doing the math, as I have done in my research, they simply add more mythology to the equation.

They simply assume that function dictates selection--without providing any step-by-step example of how that would occur--how would it clean up the incredible volumes of mess that you would see if you only followed through with the challenge I posted numerous times--sit down and calculate the total molecules which would be used up, on overage, for EACH trial at producing a single ORF of 500 codons (a very "average" size BTW).

And notice that in the article, none of their models was even 50% accurate in explaining the empirical data. What kind of a grade would you give it?

 

[Paul of Eugene OR]

Split Rock posted: "...We assume that the frequent occurrence proteins of size 150-250 aa is due to protein folding stability..."

Yes, I read the entire article. What I also did was to separate in my mind empirical science from pure speculation. Anyone can tell stories about wishful events. The key is to test the actual feasibility of those things, using the evidence you have.

Isn't it interesting that this article offers glib reasoning as to why very long proteins are "usually not seen" (referencing the effects of stop codons) and yet it utterly fails to apply that math to known genes in virtually every type of cell which are very long. Instead of doing the math, as I have done in my research, they simply add more mythology to the equation.

They simply assume that function dictates selection--without providing any step-by-step example of how that would occur--how would it clean up the incredible volumes of mess that you would see if you only followed through with the challenge I posted numerous times--sit down and calculate the total molecules which would be used up, on overage, for EACH trial at producing a single ORF of 500 codons (a very "average" size BTW).

And notice that in the article, none of their models was even 50% accurate in explaining the empirical data. What kind of a grade would you give it?

Sounds like you are explaining why so much DNA is junk DNA.

 

[WisdomSpy]

Evolutionists stack the deck in their favor by several common tactics:
1. Assume unlimited powers of mutations
2. Assume unlimited powers of natural selection
3. Assume unlimited supplies of resources were available in the past
4. Assume virtually unlimited amounts of time
5. When evidence surfaces that refutes your theory or hypothesis, come up with ad hoc retrospective alterations to it and pretend that none of the criticisms matter.

"We assume that the frequent occurrence proteins of size 150-250 aa is due to protein folding stability (for example TIM barrels) that generates a selective pressures avoiding stop codons within exons or genes."

Did you catch the word "assume" beginning the sentence? Natural selection cannot prevent stop codons from occurring when mutations or random generation of sequences makes the sequences with then in the reading frames. The only think NS can do is bury the entire organism or cell, IF a "fitter" organism or cell is there to compete for sustenance or reproduction. That's a really big if, and it doesn't address the junk DNA question.

Also, did you catch this quote from the article? -- "The evolutionary forces that have shaped protein number and size distributions in modern organisms are unknown."

As I reflected back on this article, it seemed to me that the authors, if they were completely candid and honest, were essentially saying; "we have no earthly idea why the observed distributions of gene and protein lengths do not conform to any modeling of evolutionary origins". I would suggest that by going a bit further and doing the appropriate math, you should be looking at a model of origins that begins with design/creation and then adds mutation and natural selection over time.

 

[WisdomSpy]

Paul said: "Sounds like you are explaining why so much DNA is junk DNA."

Look at the results of the ENCODE project. There is far less junk than previously thought and we are just beginning to understand a small portion of the epigenetic regions.

If you will do the simple desktop "experiments" I have suggested and follow them through, you will notice that even the amount of junk touted by some evolutionists for certain cells is multiple orders of magnitude less than what would occur under random or naturalistic generation processes. I challenge you to do the math.

 

[WisdomSpy]

Regarding the discussion about the earth standing still or not...

Quick lesson on theology: if one refuses to realize that the Bible contains poetry, metaphors and symbols galore, and instead tries to make it literal, you are walking on very dangerous grounds. Also, if you fail to recognize the difficulty in accurately translating ancient languages, ditto. I would suggest looking up Psalms 7:11 in every modern translation and then tell me what you think it is saying.

Several versions say that God is angry with the wicked every day.
At least one version says that God is NOT angry with the wicked every day.
Another version frames it as a question; "is God angry with the wicked every day?"

The amazing thing is that the discrepancy in these translations of the original poetic thoughts do not bother me. There is an underlying consistency when one views it in context. All three interpretations are saying that God is not ambivalent, uncaring, unmoved or unconcerned with how the wicked mistreat others.

 

[sfs]

The import of my research continues to be misunderstood and mischaracterized, often using straw-man arguments and continued assumptions of what natural selection (NS) is capable of doing. Gould did not deny that NS occurs and neither do I—he pointed out that it must occur at the organismal level. Individual areas of DNA or RNA simply “do not have [access] to NS”, was his point [or really, that NS does not have access to them within individual cells]:

““‘…no matter how much power [Richard] Dawkins wishes to assign to genes, there is one thing that he cannot give them – direct visibility to natural selection’. Rather, the unit of selection is the phenotype, not the genotype, because it is phenotypes which interact with the environment at the natural-selection interface.”

Um, so? Both Gould and Dawkins were in complete agreement that deleterious mutations are eliminated by natural selection. Their disagreement has nothing to do with your denial of the effectiveness of natural selection at removing new, harmful mutations.

 

[sfs]

Split Rock posted: "...We assume that the frequent occurrence proteins of size 150-250 aa is due to protein folding stability..."

Yes, I read the entire article. What I also did was to separate in my mind empirical science from pure speculation. Anyone can tell stories about wishful events. The key is to test the actual feasibility of those things, using the evidence you have.

Isn't it interesting that this article offers glib reasoning as to why very long proteins are "usually not seen" (referencing the effects of stop codons) and yet it utterly fails to apply that math to known genes in virtually every type of cell which are very long. Instead of doing the math, as I have done in my research, they simply add more mythology to the equation.

You didn't do the math. You calculated part of the easy bit -- how quickly will mutations break down ORFs (although you don't seem to know how often such mutations actually occur) -- but have done no calculations about the creation of ORFs, by any mechanism.

They simply assume that function dictates selection--without providing any step-by-step example of how that would occur--how would it clean up the incredible volumes of mess that you would see if you only followed through with the challenge I posted numerous times--sit down and calculate the total molecules which would be used up, on overage, for EACH trial at producing a single ORF of 500 codons (a very "average" size BTW).

Produced how? You can't calculate anything until you specify the model, and you've insisted that only one model -- creation from random sequence -- be considered. Why?

And notice that in the article, none of their models was even 50% accurate in explaining the empirical data. What kind of a grade would you give it?

Compared to the 0% of the empirical data that any creationist model explains? I'd give it quite a good grade. When has a creationist offered a calculation of the expected distribution of gene lengths in their model?

 

[justlookinla]

Why do you continue to ignore SELECTION???? There is a mechanism called Natural Selection... look it up!

SELECTION creates nothing.

 

[sfs]

Evolutionists stack the deck in their favor by several common tactics:
1. Assume unlimited powers of mutations

We never assume that -- biologists have done extensive research on the limitations of mutation.

2. Assume unlimited powers of natural selection

Natural selection has many well-known limitations. You should know these things if you're going to attack the science.

3. Assume unlimited supplies of resources were available in the past

I have no idea where you got this notion. It resembles nothing in evolutionary biology.

4. Assume virtually unlimited amounts of time

The amounts of time are known very well, thanks to geologists and physicists and paleontologists.

5. When evidence surfaces that refutes your theory or hypothesis, come up with ad hoc retrospective alterations to it and pretend that none of the criticisms matter.

Adjusting theories to evidence is a good thing if you want to model reality. Of course, you could choose instead the creationist path: decide in advance what the theory is, ignore all evidence to the contrary, and spend your energies attacking scientists rather than trying to understand the natural world.

"We assume that the frequent occurrence proteins of size 150-250 aa is due to protein folding stability (for example TIM barrels) that generates a selective pressures avoiding stop codons within exons or genes."

Did you catch the word "assume" beginning the sentence? Natural selection cannot prevent stop codons from occurring when mutations or random generation of sequences makes the sequences with then in the reading frames. The only think NS can do is bury the entire organism or cell, IF a "fitter" organism or cell is there to compete for sustenance or reproduction. That's a really big if,

How is it a big if? If a mutation causes one wombat, say, to have a premature stop codon in a gene, it's going to be worse off than all of the other wombats, right?

and it doesn't address the junk DNA question.

What junk DNA question?

Also, did you catch this quote from the article? -- "The evolutionary forces that have shaped protein number and size distributions in modern organisms are unknown."

No, I didn't catch it. Sounds like a reasonable statement. Were you under the impression that scientists knew everything already?

As I reflected back on this article, it seemed to me that the authors, if they were completely candid and honest, were essentially saying; "we have no earthly idea why the observed distributions of gene and protein lengths do not conform to any modeling of evolutionary origins". I would suggest that by going a bit further and doing the appropriate math, you should be looking at a model of origins that begins with design/creation and then adds mutation and natural selection over time.

Okay, let's get started. In a designed organism, what distribution of gene lengths should we find -- before evolution has any effect, say. Should we find any duplicated genes? Will genes come in families? Will there be genes that combine parts of other genes? Will there be functional genes that look exactly like retroposed transcripts of other genes?

 

[EternalDragon]

Well, you also have to include the random mutations and the ongoing reproduction and competition, but, including all that, yes.

You see, advantages accumulate. One comes along, gets established, and then another gets added to it that enhances it or complements it . . . that gets established, another comes along gets added, enhances or complements it. . . .etc etc.

Clearly, such a process would take a looooong time but, given long enough time, there is no limit to the number of enhancements that can be added.

And the end results would be . . . wonderful!

That sounds awesome but how does it work? You have at the start a
small worm or bacteria or something with very little working parts.
How do the complex mechanisms such as the brain, heart, blood clotting
system, immune system, etc. etc. get built?

Natural selection just selects mainly characteristics and ones that are
already there. It does not build complex biological machinery nor write
code. It certainly does not build a human brain. Name the mechanism
that does please.

 

[Split Rock]

Are you saying natural selection built something that humans
can't even begin to do? From the bottom up?

Yes.

 

[Split Rock]

Paul said: "Sounds like you are explaining why so much DNA is junk DNA."

Look at the results of the ENCODE project. There is far less junk than previously thought and we are just beginning to understand a small portion of the epigenetic regions.

If you will do the simple desktop "experiments" I have suggested and follow them through, you will notice that even the amount of junk touted by some evolutionists for certain cells is multiple orders of magnitude less than what would occur under random or naturalistic generation processes. I challenge you to do the math.

ENCODE showed that 80% of the human genome is transcribed... not that it has a function.

 

[Split Rock]

Split Rock posted: "...We assume that the frequent occurrence proteins of size 150-250 aa is due to protein folding stability..."

Yes, I read the entire article. What I also did was to separate in my mind empirical science from pure speculation. Anyone can tell stories about wishful events. The key is to test the actual feasibility of those things, using the evidence you have.

Isn't it interesting that this article offers glib reasoning as to why very long proteins are "usually not seen" (referencing the effects of stop codons) and yet it utterly fails to apply that math to known genes in virtually every type of cell which are very long. Instead of doing the math, as I have done in my research, they simply add more mythology to the equation.

They simply assume that function dictates selection--without providing any step-by-step example of how that would occur--how would it clean up the incredible volumes of mess that you would see if you only followed through with the challenge I posted numerous times--sit down and calculate the total molecules which would be used up, on overage, for EACH trial at producing a single ORF of 500 codons (a very "average" size BTW).

And notice that in the article, none of their models was even 50% accurate in explaining the empirical data. What kind of a grade would you give it?

These hypotheses can now be tested. That is how science works.