Where did the laws of nature come from?

[Loudmouth]

Then rather then just say it show how it isn't what I claim.

For example, your oft cited paper on protein folds is completely debunked here:

http://www.pandasthumb.org/archives/2007/01/92-second-st-fa.html

You try to claim that it is nearly impossible for any functional protein fold to evolve, yet the paper you cite only looked at one single enzyme function which is beta-lactamase activity. It never looked at all possible functions. It also never looked at completely different protein structures. The paper only looked at one single protein with one specific protein structure, and then only made a few mutations.

You ignore all of these facts, and pronounce that proteins can't evolve. It simply isn't true, and any cursory glance at the evidence demonstrates this.

 

[stevevw]

Because the things you post. You cherrypick and misrepresent whith a clear agenda. Its not the science you mistrust, its the fact that it clashes with your religious beliefs.

Why cant you admit that? Why lie about it? Doesnt your religion consider lying a sin?

Religion has nothing to do with it. The claims are about a quantitative and qualitative argument about evolution and not whether evolution is true or not. I support evolution so how is it a clash with my religious beliefs. You are just trying to come up with something , anything to divert the attention away from what I have posted. Its called an ad hominem where you try to undermine the person rather then deal with the evidence and present a supported case based on the argument.

 

[VirOptimus]

Religion has nothing to do with it. The claims are about a quantitative and qualitative argument about evolution and not whether evolution is true or not. I support evolution so how is it a clash with my religious beliefs. You are just trying to come up with something , anything to divert the attention away from what I have posted.

You support evolution? In what way do you "support evolution"?

Is the ToE correct?

Do chimps and humans share a common ancestor?

 

[stevevw]

Evolution already produces order from chaos, including biological information.

Nucleic Acids Res. 2000 Jul 15; 28(14): 2794–2799.

Evolution of biological information
Thomas D. Schneider

How do genetic systems gain information by evolutionary processes? Answering this question precisely requires a robust, quantitative measure of information. Fortunately, 50 years ago Claude Shannon defined information as a decrease in the uncertainty of a receiver. For molecular systems, uncertainty is closely related to entropy and hence has clear connections to the Second Law of Thermodynamics. These aspects of information theory have allowed the development of a straightforward and practical method of measuring information in genetic control systems. Here this method is used to observe information gain in the binding sites for an artificial ‘protein’ in a computer simulation of evolution. The simulation begins with zero information and, as in naturally occurring genetic systems, the information measured in the fully evolved binding sites is close to that needed to locate the sites in the genome. The transition is rapid, demonstrating that information gain can occur by punctuated equilibrium.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC102656/​

A computer simulation isn't the ideal scientific support. Actual tests done on bacteria for example bacteria that has been able to become antibiotic resistant has been found to be the result of a loss of info or the recombination of existing genetic material. Mutations actually rework existing genetic info and usually to the detriment of the creatures fitness rather then create more complex and fitter creatures. The point is there has to be that info and instruction there in the first place for it to happen. Where did that come from. How did living things get the genetic codes in the first place from what was either non life or simple life.

 

[stevevw]

You support evolution? In what way do you "support evolution"?

Is the ToE correct?

Do chimps and humans share a common ancestor?

I support what has been verified scientifically through tests and this is what people call micro evolution. Limited evolution within a species but not beyond the species level. The evidence for evolution beyond the species level has not been scientifically verified. It is based on assumption of what micro evolution can d and the interpretation of observation of living things with their physical similarities. But molecular evidence doesn't support a tree of life as Darwin had made that shows all life has a common ancestor.

 

[stevevw]

For example, your oft cited paper on protein folds is completely debunked here:

http://www.pandasthumb.org/archives/2007/01/92-second-st-fa.html

You try to claim that it is nearly impossible for any functional protein fold to evolve, yet the paper you cite only looked at one single enzyme function which is beta-lactamase activity. It never looked at all possible functions. It also never looked at completely different protein structures. The paper only looked at one single protein with one specific protein structure, and then only made a few mutations.

You ignore all of these facts, and pronounce that proteins can't evolve. It simply isn't true, and any cursory glance at the evidence demonstrates this.

There are many other papers that show that mutations will cause fitness lose rather then a gain in fitness which is what evolution proposes. I think the particular paper I linked from memory or one of them was showing results for a number of different species of bacteria and it was showing a more general support that bacteria dont produce pathways to new functions so easy. But here is more support.

Stability effects of mutations and protein evolvability.
Abstract
The past several years have seen novel insights at the interface of protein biophysics and evolution. The accepted paradigm that proteins can tolerate nearly any amino acid substitution has been replaced by the view that the deleterious effects of mutations, and especially their tendency to undermine the thermodynamic and kinetic stability of protein, is a major constraint on protein evolvability--the ability of proteins to acquire changes in sequence and function. We summarize recent findings regarding how mutations affect protein stability, and how stability affects protein evolution. We describe ways of predicting and analyzing stability effects of mutations, and mechanisms that buffer or compensate for these destabilizing effects and thereby promote protein evolvabilty, in nature and in the laboratory.
http://www.ncbi.nlm.nih.gov/pubmed/19765975

Negative Epistasis Between Beneficial Mutations in an Evolving Bacterial Population
We analyzed the effects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returns with genotype fitness,

http://www.sciencemag.org/content/332/6034/1193.abstract

Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations?
It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favorable mutations (and their effects) is still a matter for debate.
http://www.ncbi.nlm.nih.gov/pubmed/10849074

Distribution of fitness effects caused by random insertion mutations in Escherichia coli.
In this study, we took a direct approach to measuring the effects of mutations on fitness. We used transposon-mutagenesis to create 226 mutant clones of Escherichia coli. Each mutant clone carried a single random insertion of a derivative of Tn10. All 226 mutants were independently derived from the same progenitor clone, which was obtained from a population that had evolved in a constant laboratory environment for 10,000 generations. We then performed competition experiments to measure the effect of each mutation on fitness relative to a common competitor. At least 80% of the mutations had a significant negative effect on fitness, whereas none of the mutations had a significant positive effect.
http://www.ncbi.nlm.nih.gov/pubmed/9720287

Why Proteins Aren't Easily Recombined

There seems to be an idea floating about among some biologists that it is easy to recombine protein domains or swap bits of protein structure to generate new function. I suppose it comes from looking at simplified drawings of protein structure, and forgetting about the detailed atomic interactions required.

For non-biologists, let me explain why proteins aren’t easily recombined. A protein fold is typically composed of smaller structural elements called alpha helices or beta sheets, with unstructured loops of protein connecting them. These elements adopt a stereotyped pattern of folding because of hydrogen bonding patterns between amino acids. The illustration below from Axe (2010) shows these hydrogen bonding patterns as red dashed lines between the linked amino acids. For clarity, the side chains of each amino acid are faded out, while the backbone trace is in full color.

Below each helix (a) or sheet (b) is a simplified geometric shape that illustrates how the element assembles and what edges are available for extension (magenta faces). We see each kind of structure from the side (on the left) and face on (on the right).

It is important to know that different amino acid combinations can form each of these elements—many different sequence combinations can form alpha helices or beta sheets. As a result, each particular helix or sheet has a distinct set of side chains sticking out from it, requiring a distinct set of chemical interactions with any nearby protein sequence. Thus, helices and sheets are sequence-dependent structural elements within protein folds. You can’t swap them around like lego bricks.

This necessarily means that when you bring new secondary structure elements into contact by some sort of rearrangement, they will be unlikely to form a stable three dimensional fold without significant modification.

But you don’t have to take my word for it—it is possible to test these things. Our next post will introduce one such experiment.
http://www.biologicinstitute.org/post/22595615671/why-proteins-arent-easily-recombined

 

[KCfromNC]

If you would have read the papers that were linked in the reply and all the other papers which I have posted in our debates you would have all the info and supporting evidence you need.

There's a peer-reviewed paper which specifically gives a quantitative measure of the level of design for the 4 random objects I asked about? What an interesting world you live in. Please, tell us more.

It is unreal to ask for specific scientific support or papers on lawn mower or border collie design.

So wait, the answer really isn't in the papers you just said it was? I think I mentioned before that it is best to make up just one excuse when you're avoiding a question you can't answer.

These papers go into detail to explain and show the difference between the high levels of info and order needed for intelligent design

Exactly how many bits of information are needed before you know a design is intelligent? How exactly do you measure the number of bits of information in a design? How many bits make up your design versus that of your phone? Please be specific and show your work - you wouldn't want people to think you're just making up this nonsense as you go along.

 

[KCfromNC]

A computer simulation isn't the ideal scientific support.

And yet just a few pages back you were offering up the fact that someone proposed a model as evidence for your claims about reality. There seem to be a lot of inconsistencies popping up the deeper we dig into your writings.

 

[KCfromNC]

There are many other papers that show that mutations will cause fitness lose rather then a gain in fitness which is what evolution proposes.

Some mutations are detrimental, yes. That doesn't mean all of them are. What's your point?

 

[Loudmouth]

A computer simulation isn't the ideal scientific support.

We see the same increases in information in biological organisms.

Actual tests done on bacteria for example bacteria that has been able to become antibiotic resistant has been found to be the result of a loss of info or the recombination of existing genetic material.

Show us how you measure information and how all cases of antibiotic resistance result from a loss in information. I bet you can't do it. Why? Because you reject evolution because of your religious beliefs, not the evidence.

Also, recombination is mutation.

Mutations actually rework existing genetic info and usually to the detriment of the creatures fitness rather then create more complex and fitter creatures.

Yet another claim that you can not back up with evidence. Why? Because you reject evolution because of your religious beliefs, not the evidence.

The point is there has to be that info and instruction there in the first place for it to happen.

Yet another claim I know you can't back up, and I also know that it is false. I can cite experiments from 60 years ago which illustrate that antibiotic resistance only arises after mutation, and that the information for resistance did not exist before those mutations.

Here is that 60+ year old paper:
http://jb.asm.org/content/63/3/399.full.pdf

Where did that come from. How did living things get the genetic codes in the first place from what was either non life or simple life.

Abiogenesis is not evolution. How many times have we gone over that?

 

[Loudmouth]

There are many other papers that show that mutations will cause fitness lose rather then a gain in fitness which is what evolution proposes.

There are instances where we can show that airplanes kill people. Does that mean that most airplane trips end in death?

You are claiming that MOST mutations are detrimental. Where is your support for this ludicrous claim? You know why you can't produce evidence for this claim? Because you don't reject evolution because of the evidence. You reject evolution because of your religious beliefs.

 

[Loudmouth]

Stability effects of mutations and protein evolvability.
Abstract
The past several years have seen novel insights at the interface of protein biophysics and evolution. The accepted paradigm that proteins can tolerate nearly any amino acid substitution has been replaced by the view that the deleterious effects of mutations, and especially their tendency to undermine the thermodynamic and kinetic stability of protein, is a major constraint on protein evolvability--the ability of proteins to acquire changes in sequence and function. We summarize recent findings regarding how mutations affect protein stability, and how stability affects protein evolution. We describe ways of predicting and analyzing stability effects of mutations, and mechanisms that buffer or compensate for these destabilizing effects and thereby promote protein evolvabilty, in nature and in the laboratory.
http://www.ncbi.nlm.nih.gov/pubmed/19765975

Negative Epistasis Between Beneficial Mutations in an Evolving Bacterial Population
We analyzed the effects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returns with genotype fitness,

http://www.sciencemag.org/content/332/6034/1193.abstract

Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations?
It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favorable mutations (and their effects) is still a matter for debate.
http://www.ncbi.nlm.nih.gov/pubmed/10849074

Distribution of fitness effects caused by random insertion mutations in Escherichia coli.
In this study, we took a direct approach to measuring the effects of mutations on fitness. We used transposon-mutagenesis to create 226 mutant clones of Escherichia coli. Each mutant clone carried a single random insertion of a derivative of Tn10. All 226 mutants were independently derived from the same progenitor clone, which was obtained from a population that had evolved in a constant laboratory environment for 10,000 generations. We then performed competition experiments to measure the effect of each mutation on fitness relative to a common competitor. At least 80% of the mutations had a significant negative effect on fitness, whereas none of the mutations had a significant positive effect.
http://www.ncbi.nlm.nih.gov/pubmed/9720287

Why Proteins Aren't Easily Recombined

There seems to be an idea floating about among some biologists that it is easy to recombine protein domains or swap bits of protein structure to generate new function. I suppose it comes from looking at simplified drawings of protein structure, and forgetting about the detailed atomic interactions required.

For non-biologists, let me explain why proteins aren’t easily recombined. A protein fold is typically composed of smaller structural elements called alpha helices or beta sheets, with unstructured loops of protein connecting them. These elements adopt a stereotyped pattern of folding because of hydrogen bonding patterns between amino acids. The illustration below from Axe (2010) shows these hydrogen bonding patterns as red dashed lines between the linked amino acids. For clarity, the side chains of each amino acid are faded out, while the backbone trace is in full color.

Below each helix (a) or sheet (b) is a simplified geometric shape that illustrates how the element assembles and what edges are available for extension (magenta faces). We see each kind of structure from the side (on the left) and face on (on the right).

It is important to know that different amino acid combinations can form each of these elements—many different sequence combinations can form alpha helices or beta sheets. As a result, each particular helix or sheet has a distinct set of side chains sticking out from it, requiring a distinct set of chemical interactions with any nearby protein sequence. Thus, helices and sheets are sequence-dependent structural elements within protein folds. You can’t swap them around like lego bricks.

This necessarily means that when you bring new secondary structure elements into contact by some sort of rearrangement, they will be unlikely to form a stable three dimensional fold without significant modification.

But you don’t have to take my word for it—it is possible to test these things. Our next post will introduce one such experiment.
http://www.biologicinstitute.org/post/22595615671/why-proteins-arent-easily-recombined

Notice that you didn't address a single thing that I wrote.

This is what I am talking about.

 

[VirOptimus]

I support what has been verified scientifically through tests and this is what people call micro evolution. Limited evolution within a species but not beyond the species level. The evidence for evolution beyond the species level has not been scientifically verified. It is based on assumption of what micro evolution can d and the interpretation of observation of living things with their physical similarities. But molecular evidence doesn't support a tree of life as Darwin had made that shows all life has a common ancestor.

So, no to the ToE being correct and no to common descent. You dont support evolution in any meaningful way. And yes, its only because of your religious beliefs.

Why all the tapdancing? Dont you have the honesty to state your convictions?

 

[Gracchus]

There are many other papers that show that mutations will cause fitness lose rather then a gain in fitness which is what evolution proposes.

What evolution "proposes" is that those mutations that cause a loss in fitness will be culled, selected out, leaving only those mutations that do not effect fitness, and those that are beneficial. That's what a thinking person would expect.

 

[stevevw]

There's a peer-reviewed paper which specifically gives a quantitative measure of the level of design for the 4 random objects I asked about? What an interesting world you live in. Please, tell us more.

If you read what I said , I stated that it is unfair for you to demand specific papers on the items like a lawn mower and border collie dog as it would be hard to find. So I said that a more general paper covering the concept of what these items are would suffice IE a paper on biological design for animals (border collie and a paper on engineering design for machines ( lawn mower) would be relevant.

So wait, the answer really isn't in the papers you just said it was? I think I mentioned before that it is best to make up just one excuse when you're avoiding a question you can't answer.

No if anyone uses their logic and reasoning you will see the connections. stop playing cat and mouse games.

Exactly how many bits of information are needed before you know a design is intelligent? How exactly do you measure the number of bits of information in a design? How many bits make up your design versus that of your phone? Please be specific and show your work - you wouldn't want people to think you're just making up this nonsense as you go along.

Its not as simple as how many bits of information. In fact the amount of information is not necessarily what makes something designed. It is more to do with highly ordered and structured info. The level of complexity is not a measure of design and high complexity can be something that is randomly created as it has no pattern and order and is hard to work out. Design should show a high order of pattern and structure as well as info, be measurable and have a high probability against happening by a random and chance event. The higher the ordered structures, patterns , algorithms are the more improbable it is to have been created by a random chance event. These qualities are found in things like DNA and physics. In fact if anything is measured in bits it is uncertainty of order and patterns which is related to a non designed structure. The higher the number of bits of uncertainty, the greater the degree of complexity, and the closer we move toward a random string: If you read the papers you will see.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2662469/

 

[stevevw]

What evolution "proposes" is that those mutations that cause a loss in fitness will be culled, selected out, leaving only those mutations that do not effect fitness, and those that are beneficial. That's what a thinking person would expect.

Three things, first that is not what happens from tests done. Even beneficial mutations are affected by other beneficial ones which eventually work towards a fitness cost overall. Proteins are not good at dealing with any mutations no matter what their contribution is that change the structure of them period. Secondly the rarity of any beneficial mutation is not enough to justify the amount of high level of ordered complexity and info needed to create a living thing. Thirdly function proteins let alone functional organs and features require multiple beneficial mutations to all work towards the same objective without each knowing it needs to. For that level of benefit and direction it would be impossible and require a multitude of negative mutations to achieve which need to be dealt with. It would make a hell of a lot of unfit features and creatures. yet we dont see a lot of that.

Its a nice idea and as you said something that can be thought up as logical way of making a living thing. But in reality and in tests it doesn't work that way. Mutations are mostly deleterious and even when beneficial work against each other because they are changing what already was working well. Thats why our DNA has a great ability to rectify errors caused by mutations. When it doesn't it is nearly always a cost to fitness and when those rare times it does benefit it is so small and isolated that it doesn't amount to much.

 

[stevevw]

So, no to the ToE being correct and no to common descent. You dont support evolution in any meaningful way. And yes, its only because of your religious beliefs.

Why all the tapdancing? Dont you have the honesty to state your convictions?

I support what the evidence shows for evolution with scientific verifiable tests. That is that tests have shown that micro change can happen to a limited extent and this gives variation within a species or type of creature. I say type because evolution hasn't really clarified what a species is. A type of animal can be a group such as bats which have hundreds of species but have remained the same shape for millions of years. So common decent can be limited as well within that scenario. But as for animals being able to use the same mechanisms for morphing into completely different shaped ones that steps beyond those limits and requires massive amounts of mutations which are mostly a cost to fitness well that hasn't been scientifically verified. How do you support what you believe and how do you know you are not being exactly what you are accusing me of. How do you know that you are not faithfully believing an idea that hasn't been scientifically verified because some scientist guru told you so.

 

[stevevw]

Notice that you didn't address a single thing that I wrote.

This is what I am talking about.

Notice that you didn't address a single thing that I wrote.

This is what I am talking about.

So you reject peer reviewed papers which do relate to the ability of proteins to evolve functional folds and show examples in a wide variety of examples. IE
The accepted paradigm that proteins can tolerate nearly any amino acid substitution has been replaced by the view that the deleterious effects of mutations, and especially their tendency to undermine the thermodynamic and kinetic stability of protein, is a major constraint on protein evolvability--the ability of proteins to acquire changes in sequence and function.
If proteins cannot tolerate amino acid substitutions which is needed to create new protein folds and it diminishes the fitness of them then how does this not relate to Axes paper which states the same thing.

We analyzed the effects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returns with genotype fitness,
So the combined mutations which are needed to produce a change in function for a protein all work together to have a fitness cost and not make fitter and more functional proteins. Isn't that exactly what Axe had determined.

It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious
If most if not all mutations are deleterious then how can they create complex varieties of features and life that is functional and fit when it would need a multitude of beneficial mutations.

Methods for inferring genome-wide mutation parameters are presented, and results stemming from these studies are reviewed.
In this study, we took a direct approach to measuring the effects of mutations on fitness. We used transposon-mutagenesis to create 226 mutant clones of Escherichia coli.
Doesn't this cover a wide area in determining the evolvability of proteins from random mutations.

And you would rather use a blog page to refute Axes paper. Here is a link to Douglas Axe's reply to the claims you make that his paper has been completely shown to be wrong and points out where the critics have either got it wrong or completely misinterpreted him. But the reason I also posted the other papers that also support what Axe says is because it gives a wide variety of support for what Axe says which therefore gives more credibility to it.
Correcting Four Misconceptions about my 2004 Article in JMB
http://www.biologicinstitute.org/post/19310918874/correcting-four-misconceptions-about-my-2004

 

[Ophiolite]

How do you know that you are not faithfully believing an idea that hasn't been scientifically verified because some scientist guru told you so.

Simply because, unlike yourself, I have studied several phyla in fossil form. I have noted the slow development of features such as sutures on ammonites, or thecae on graptolites, or a host of characteristics on trilobites and thus witnessed the morphing of one species into another, one genera into another, one family into another.

And then I have studied the research reports of scientists, not restricting myself to their conclusions and blindly following those, but exploring their methodology and detailed results, before accepting or rejecting their findings. You would be right to criticise my position if I had done what you suggested and believed something "some scientist guru" told me. But that is not what I have done.

Now, may I ask you - have you studied many hundreds of fossils, have you collected numerous fossils in the field, have you read scores of research papers on palaeontology, have you discussed the work of palaeontologists, at length, in a critical fashion, with those palaeontologists? If not, it would seem you have arrived at your belief by accepting what "some theologist guru" told you.

You would be quite right to ignore my beliefs if I had acquired them second hand, but I did not do so. If you have not explored the original material upon which your beliefs surrounding evolution are based then I question your right to have that opinion given any attention. In that regard we seem to be in complete agreement - if one hasn't studied a subject in depth then one isn't really entitled to an opinion.

 

[stevevw]

There are instances where we can show that airplanes kill people. Does that mean that most airplane trips end in death?

This is exactly what evolution does. They take what happens in micro evolution which has been scientifically verified in tests and then apply it to macro evolution. If we have proof of evolution in micro examples does that mean evolution can end up evolving anything and everything beyond the micro that doesn't have the evidence by assumption.

The problem with your example is that there are no examples of verified science that show that mutations can evolve fit and functional features and creatures. So its like saying all we have are instances where we see airplanes that kill people and so far we havnt got proof that people survive them.

You are claiming that MOST mutations are detrimental. Where is your support for this ludicrous claim? You know why you can't produce evidence for this claim? Because you don't reject evolution because of the evidence. You reject evolution because of your religious beliefs.[/QUOTE] I have already posted this many times.

Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations?
It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favorable mutations (and their effects) is still a matter for debate.
http://www.ncbi.nlm.nih.gov/pubmed/10849074

Negative Epistasis Between Beneficial Mutations in an Evolving Bacterial Population
We analyzed the effects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returns with genotype fitness,
http://www.sciencemag.org/content/332/6034/1193.abstract

Distribution of fitness effects caused by random insertion mutations in Escherichia coli.
At least 80% of the mutations had a significant negative effect on fitness, whereas none of the mutations had a significant positive effect.
http://www.ncbi.nlm.nih.gov/pubmed/9720287