Curious about Neo-Darwinian theory

[hopefulcynic]

From the paper you linked to:

It is possible that our assays were not able to detect dramatic phenotypes that under a different setting, for instance, outside the controlled laboratory setting, would become evident. Moreover, possible phenotypes might become evident only on a longer timescale, such as longer generation time.

In science, you need to be careful of jumping to conclusions too quickly. If a gene's function is undefined, that does not mean that the gene is useless.

[godslanguage]

From the paper you linked to:

It is possible that our assays were not able to detect dramatic phenotypes that under a different setting, for instance, outside the controlled laboratory setting, would become evident. Moreover, possible phenotypes might become evident only on a longer timescale, such as longer generation time.

In science, you need to be careful of jumping to conclusions too quickly. If a gene's function is undefined, that does not mean that the gene is useless.

You have not really engaged any of the merits presented. Hand waving is not how science works! What I presented is very good evidence for front-loading. Front-loading, as opposed to the Darwinian fairytale would better explain such events as the Cambrian explosion. Its not my fault you and Bgood are unable (or possibly unwilling? ) to grasp this simple logic.

Abrupt appearance does not equal evidence or support for Darwinian Evolution.
Genes with no adaptive significance with high concentration of coding potential inherent in ancient organisms does not equal evidence or support for Darwinian Evolution.
All this is entirely testable, I have shown merely one example.

What I am also implying is that this is not negative evidence but positive since it better explains the evidence not merely pointing out the inadequacies of evolution. Nowhere did I mention evolution did not occur.

[hopefulcynic]

You have not really engaged any of the merits presented.

On the contrary. Please see my post regarding Trichoplax, your earlier supposed example of useless genes. I presented a reasonable hypothesis that is supported by some evidence from the literature.

Hand waving is not how science works! What I presented is very good evidence for front-loading. Front-loading, as opposed to the Darwinian fairytale would better explain such events as the Cambrian explosion. Its not my fault you and Bgood are unable (or possibly unwilling? ) to grasp this simple logic.

Before we go any further, I want to make sure I understand your frontloading idea. Are you saying that God (or an intelligent designer) created genes that are presently useless to the host organism, but will one day be useful?

If this is indeed your argument, then there is an easy way to test this hypothesis, without resorting to the difficulties inherent in gene knockout experiments.

Suppose a gene is observed to have no adaptive significance in a given organism under a given set of conditions. There are two possibilities:
1.We don't know the gene's function yet.
2.The gene has no function.

If the gene has no function, then mutations within the gene will have no effect on the organism's fitness. Thus, mutations will tend to accumulate over time.

However, if the gene does have a function, then it will have an effect on host fitness. If this is the case, mutations within the gene will likely be detrimental to the organism's fitness. Thus, most mutations will be selected against.

By looking at a gene's sequence over time, we can look at the relative mutation rate, and then determine whether a gene has adaptive value.

[godslanguage]

Before we go any further, I want to make sure I understand your front loading idea. Are you saying that God (or an intelligent designer) created genes that are presently useless to the host organism, but will one day be useful?

First off I am not proposing a mechanism, that would be best handled by the PEH/SMH. Front-loading simply would suggest that a fully fledged template of genes was embedded into some of the first ancient systems. These would serve as the actual building blocks of all subsequent life (hence, I'm not discussing the mechanism). Evolution of body plans (complex function) has basically terminated with the result of homo sapien (the final "terminal" product) rendering subsequent evolution no more.

This is sound logic when we discuss extinction rates since the only thing left after a terminal product of a long gone evolution would be the accumulation of random mutations which inevitably lead to extinction. This is also sound logic when we discuss the fact that no complex function has been observed to evolve in the laboratory, we see evidence pointing to detrimental effects of mutations leading to a degradation of the genome. These are the effects Darwin saw at the Galapagos, these are the effects we see today (micro evolution), we also see extinction rates skyrocket due to our influencing technology on the planet and its species. Modern medicine is unable to catch up with these harmful mutations either, we are devolving.

As for your experiments, they seem reasonable but they are not by any means the fastest.

[Muttaru]

Something interesting I have found, quantum evolution.
Look like it has potential to be very interesting.

[hopefulcynic]

As for your experiments, they seem reasonable but they are not by any means the fastest.

Well, that depends on how you conduct the experiment. The most straightforward way of doing it would be simply to observe the mutation rate over time. For fast growing bacteria this is certainly feasible, but for higher organisms it is simply out of the question. The generation time is simply too long.

However, there is another way of doing the experiment, which is easier, but not as straightforward. Bear with me and I'll do my best to explain the logic.

Genes are composed of codons. Three base pairs comprise one codon, and each codon specifies one amino acid. However, multiple codons can encode the exact same amino acid. Thus, it is possible to have mutations within a gene that do not affect the amino acid sequence of the protein the gene encodes. These are known as synonymous mutations, in contrast to non-synonymous mutations which do alter the amino acid sequence. So for example, the amino acid histidine has two codons: CAT and CAC. A T-->C in the third position would be an example of a synonymous mutation. If a mutation has no effect on the amino acid sequence, it is unlikely that the mutation will have much effect on fitness. Thus synonymous mutations are generally neutral with respect to fitness.

If a gene has no function, then you can compare the gene in two different lineages and look at the relative frequency of synonymous versus non-synonymous mutations. Suppose your gene of interest is found in both rats and mice. You argue that the gene is an example of frontloading and is therefore useless to either organism. Thus, there is no selection pressure to prevent the accumulation of mutations. Thus, non-synonymous mutations will be predominant.

However, if the gene does have function, then non-synonymous mutations will be selected against, and the primary differences between the two genes will be in the form of synonymous mutations. If this is the case, then we can argue that the gene has a function, without ever knowing what it is.

[Proinsias]

Evolution of body plans (complex function) has basically terminated with the result of homo sapien (the final "terminal" product) rendering subsequent evolution no more.

This seems presumptuous. How can you know that we are the end result of evolution and not just another branch that came to an end. Or that we are in a lull as opposed to an end.

[godslanguage]

Evolution of body plans (complex function) has basically terminated with the result of homo sapien (the final "terminal" product) rendering subsequent evolution no more.

This seems presumptuous. How can you know that we are the end result of evolution and not just another branch that came to an end. Or that we are in a lull as opposed to an end.

Do we assume one tree consisting of many branches ( and we are an extension of a branch on that tree ), or many trees (several blueprints)? No evidence of complex function has arisen, should we assume "evolution in action"? Perhaps I'm being presumptious, but there absolutely no reason to insist that evolution is actually occuring right now in real-time. As far as anyone can tell, deleterious and neutral mutations have no significance on evolution of complex functions leading up to new body plans. Natural selection can only select from what already exists. Couple just these two facts, what is the correct model we should be looking at, is it the Darwinian model? Or is it something else. If the evidence in the laboratory and nature itself isn't in sync with this model its time for a replacement. As far as a correct model, I believe John A. Davison presents something substantial, an actual mechanism that the evidence is in sync with. The simplest real-life analagous system I can think of that illustrates this type of evolution logically, I believe, is an odometer. I haven't had the time to cover the details but when I do and I make a new thread it will definetely be about this.

[godslanguage]

Genes are composed of codons. Three base pairs comprise one codon, and each codon specifies one amino acid. However, multiple codons can encode the exact same amino acid. Thus, it is possible to have mutations within a gene that do not affect the amino acid sequence of the protein the gene encodes. These are known as synonymous mutations, in contrast to non-synonymous mutations which do alter the amino acid sequence. So for example, the amino acid histidine has two codons: CAT and CAC. A T-->C in the third position would be an example of a synonymous mutation. If a mutation has no effect on the amino acid sequence, it is unlikely that the mutation will have much effect on fitness. Thus synonymous mutations are generally neutral with respect to fitness.

If a gene has no function, then you can compare the gene in two different lineages and look at the relative frequency of synonymous versus non-synonymous mutations. Suppose your gene of interest is found in both rats and mice. You argue that the gene is an example of frontloading and is therefore useless to either organism. Thus, there is no selection pressure to prevent the accumulation of mutations. Thus, non-synonymous mutations will be predominant.

However, if the gene does have function, then non-synonymous mutations will be selected against, and the primary differences between the two genes will be in the form of synonymous mutations. If this is the case, then we can argue that the gene has a function, without ever knowing what it is.

Very good explanation. Another way front-loading could be tested is if two distinct lineages have been seperated for millions of years between continents, from a front-loading perspective one would expect that there would be striking similarity in form and function in the relative same time frame. Surprisingly, that is exactly what we find in the fossil record, how Darwinian Evolution persists nobody knows.

[hopefulcynic]

Very good explanation.

Excellent! Now let's put it into practice.

In recent years, the genomes of hundreds of species have been sequenced, and many more species have at least some genes sequenced. What's more, this information is freely available on the internet.

This allows you to present direct evidence for your frontloading idea. So, I will repeat the question that I asked at the beginning of this thread:

What is the ratio of synonymous to non-synonymous mutations in your genes of interest?

[godslanguage]

Very good explanation.

Excellent! Now let's put it into practice.

In recent years, the genomes of hundreds of species have been sequenced, and many more species have at least some genes sequenced. What's more, this information is freely available on the internet.

This allows you to present direct evidence for your frontloading idea. So, I will repeat the question that I asked at the beginning of this thread:

What is the ratio of synonymous to non-synonymous mutations in your genes of interest?

I hope you realize that the idea of frontloading is not new with me. Front loading is actually a key concept in computer programming and software engineering. Many have already proposed frontloading including Mike Gene and John A. Davison directly, but many, many more in the past and present have proposed front loading indirectly. A limited few have actually realized what the data implies.

[hopefulcynic]

Very good explanation.

Excellent! Now let's put it into practice.

In recent years, the genomes of hundreds of species have been sequenced, and many more species have at least some genes sequenced. What's more, this information is freely available on the internet.

This allows you to present direct evidence for your frontloading idea. So, I will repeat the question that I asked at the beginning of this thread:

What is the ratio of synonymous to non-synonymous mutations in your genes of interest?

I hope you realize that the idea of frontloading is not new with me. Front loading is actually a key concept in computer programming and software engineering. Many have already proposed frontlloading including Mike Gene and John A. Davison directly, but many, many more in the past and present have proposed front loading indirectly. A limited few have actually realized what the data implies.

Ok....The fact that other people agree with you doesn't mean you don't have to provide evidence in support of your position.

[godslanguage]

Very good explanation.

Excellent! Now let's put it into practice.

In recent years, the genomes of hundreds of species have been sequenced, and many more species have at least some genes sequenced. What's more, this information is freely available on the internet.

This allows you to present direct evidence for your frontloading idea. So, I will repeat the question that I asked at the beginning of this thread:

What is the ratio of synonymous to non-synonymous mutations in your genes of interest?

I hope you realize that the idea of frontloading is not new with me. Front loading is actually a key concept in computer programming and software engineering. Many have already proposed frontlloading including Mike Gene and John A. Davison directly, but many, many more in the past and present have proposed front loading indirectly. A limited few have actually realized what the data implies.

Ok....The fact that other people agree with you doesn't mean you don't have to provide evidence in support of your position.

What does the word "evidence" mean to you exactly? I have already provided evidence that supports front-loading. These very recent peer-reviewed published papers are incompatible within a Darwinian framework , they indirectly support a front-loading hypothesis. Even if said tests are performed and they again support front-loading will that conclusively change peoples minds? I doubt it.

[hopefulcynic]

What does the word "evidence" mean to you exactly? I have already provided evidence that supports front-loading. These very recent peer-reviewed published papers are incompatible within a Darwinian framework , they indirectly support a front-loading hypothesis. Even if said tests are performed and they again support front-loading will that conclusively change peoples minds? I doubt it.

I have already explained why your examples do not constitute evidence for frontloading. In the case of Trichoplax, you failed to consider the possibility of a cryptic life cycle. In the case of the rats, you failed to consider the possibility that those genes would be essential outside of a controlled laboratory setting.

The evidence you presented is consistent with frontloading, but by no means conclusive. In order to demonstrate that the genes are dispensible, and thus an example of frontloading, you must show that there is no selection pressure preventing the accumulation of non-synonymous mutations. Since gene sequences are freely available online, this should be trivial for you to do, if in fact the genes are an example of frontloading.

[godslanguage]

I did not fail to see anything. Any objections you raise seem to be futile in comparison. It should be trivial for you to demonstrate how they came about via RM & NS, especially the RM part. It should be trivial for you to demonstrate that they are useless genes that are not loaded for future contingency.

You say:

I have already explained why your examples do not constitute evidence for frontloading.

Then you say:

The evidence you presented is consistent with frontloading, but by no means conclusive.

Do you see any conflict?

I realize they are not conclusive, but I also realize they do not fit within the Darwinian framework. Question is, do you realize that? Seems the only real answer you and Bgood could give me is that they are because they are.