Waiting for Two Mutations
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In 2008 a paper was published that allegedly refuted some of Dr. Behe's claims made in "Edge of Evolution". The title of the paper is "Waiting for two mutations: with applications to regulatory sequence evolution and the limits of Darwinian evolution". You can read it HERE.
The paper has severe consequences for unguided evolution as it says that if specific mutations are required it may be out of the reach of unguided processes. Three such mutations would take millions, if not billions, of years to produce. So once sexual reproduction hit the scene most evolution would be out of reach via mutations.
So forget about gene duplication as a mechanism. For that you need the duplicated gene, a new binding site and then numerous specific mutations to get a new function from the old sequence. So all that is left is to rely solely on sheer dumb luck or miracles. And that means you don't have any science to support your claims.
Now I have an evoTARD claiming that the paper has been disputed and disregarded. That is actually true. It has been disputed and disregarded by IDists who know it does NOT refute anything ID claims. Meaning it did not do what the authors claimed. I don't know of any evolutionary biologists who have challenged it in peer-review and I am sure that Jerad doesn't either.
There hasn't been any work that refutes this paper's claims. There hasn't been any work that refines it such that it makes unguided evolution more plausible.
It is too funny when evolutionists, trying to refute ID, actually refute their own position.
In 2008 a paper was published that allegedly refuted some of Dr. Behe's claims made in "Edge of Evolution". The title of the paper is "Waiting for two mutations: with applications to regulatory sequence evolution and the limits of Darwinian evolution". You can read it HERE.
The paper has severe consequences for unguided evolution as it says that if specific mutations are required it may be out of the reach of unguided processes. Three such mutations would take millions, if not billions, of years to produce. So once sexual reproduction hit the scene most evolution would be out of reach via mutations.
So forget about gene duplication as a mechanism. For that you need the duplicated gene, a new binding site and then numerous specific mutations to get a new function from the old sequence. So all that is left is to rely solely on sheer dumb luck or miracles. And that means you don't have any science to support your claims.
Now I have an evoTARD claiming that the paper has been disputed and disregarded. That is actually true. It has been disputed and disregarded by IDists who know it does NOT refute anything ID claims. Meaning it did not do what the authors claimed. I don't know of any evolutionary biologists who have challenged it in peer-review and I am sure that Jerad doesn't either.
There hasn't been any work that refutes this paper's claims. There hasn't been any work that refines it such that it makes unguided evolution more plausible.
It is too funny when evolutionists, trying to refute ID, actually refute their own position.
posted by Joe G @ 10:20 AM
26 Comments:
At 2:15 AM,
Unknown said…
Too funny. You continue to misunderstand the science.
Read this.
http://sandwalk.blogspot.com/2015/12/waiting-for-multiple-mutations-michael.html
The Barrett and Schmidt paper doesn't say what you think it says. I'll extract a quote just to make sure it's clear:
He's referring to a paper by Durrett and Schmidt (2008). Those authors examined the situation where one transcription factor binding site was disrupted by mutation and another one nearby is created by mutation. The event requires two prespecified coordinated mutations.
Durrett and Schmidt show that in Drosophila such event can occur on a timescale of about 4,300 years. In humans with an effective population size of 10,000 the event would take about 160 million years. The authors point out that such and event—two prespecified mutations—is very unlikely. They also point out that their estimates are 5 million times more likely that those given by Michael Behe in The Edge of Evolution.
This study is not very relevant to the evolution of new functions as described in Behe and Snoke (2004).
PRESPECIFIED mutations are, of course, very unlikely. But evolution doesn't have targets. And this is not relevant to the evolution of new functions.
Once again, the science does not support your claims.
At 10:04 AM,
Joe G said…
Too funny, you continue to be an ignorant ass.
PRESPECIFIED mutations are, of course, very unlikely.
Umm, gene duplications followed by function altering mutations meet that prespecified criteria, moron.
You must be one of the most ignorant people ever.
At 4:40 PM,
Unknown said…
Too funny, you continue to be an ignorant ass.
Because I referenced a respected, published academic about such matters?
Umm, gene duplications followed by function altering mutations meet that prespecified criteria, moron.
Oh wow. You really don't understand the issue.
You must be one of the most ignorant people ever.
It's possible, which is why I look to others for insight and knowledge and experience.
At 9:46 AM,
Joe G said…
?Because I referenced a respected, published academic about such matters?
The reference that didn't help you at all?
Oh wow. You really don't understand the issue.
Nice projection, asshole. Clearly you are just an ignorant ass, Jerad.
Umm, gene duplications followed by function altering mutations meet that prespecified criteria, moron.
And nothing Jerad says will ever change that fact.
Try making a coherent argument supported by evidence, Jerad
At 10:23 AM,
Joe G said…
Again, for a duplicated gene you also need a binding site. And most likely you will need more than one mutation to make that so.
All unguided evolution has to do that is sheer dumb luck.
At 4:34 PM,
Unknown said…
The reference that didn't help you at all?
You can't show a mechanism that guides mutations. It doesn't exists.
Nice projection, asshole. Clearly you are just an ignorant ass, Jerad.
Seriously, you really don't understand the science.
Umm, gene duplications followed by function altering mutations meet that prespecified criteria, moron.
Proof again that you really don't understand the science.
Again, for a duplicated gene you also need a binding site. And most likely you will need more than one mutation to make that so.
And you wonder why no one is taking you seriously?
All unguided evolution has to do that is sheer dumb luck.
Incredible. Deny, deny, deny and misunderstand. Thank goodness it doesn't matter how badly you mangle the science since you don't teach.
At 5:34 PM,
Joe G said…
You can't show a mechanism that guides mutations.
You can't show anything, hypocrite
Seriously, you really don't understand the science.
Seriously, you are an ignorant coward. Try forming a coherent argument, Jerad.
Proof again that you really don't understand the science.
Actually it is proof that you don't.
And you wonder why no one is taking you seriously?
The fact that you are a coward who cannot form a coherent argument that refutes anything I have said proves that you cannot be taken seriously.
. Deny, deny, deny and misunderstand.
So you say. Unfortunately for you Ernst Mayr supports what I posted:
"The first step in selection, the production of genetic variation, is almost exclusively a chance phenomenon except that the nature of the changes at a given locus is strongly constrained. Chance plays an important role even at the second step, the process of elimination of the less fit individuals. Chance may be particularly important in the haphazard survival during periods of mass extinction." Ernst Mayr, "What Evolution Is"
jerad, you are ignorant of science, ignorant of biology and ignorant of evolution
At 5:59 PM,
Joe G said…
for a duplicated gene you also need a binding site.
If a gene doesn't have an accompanying binding site it cannot be expressed. It is very telling that Jerad doesn't understand that simple fact. And seeing that Jerad agrees with there not being a target then it is clear that all that is left is sheer dumb luck- all chance, just as Mayr said.
At 2:55 AM,
Unknown said…
The fact that you are a coward who cannot form a coherent argument that refutes anything I have said proves that you cannot be taken seriously.
I've tried many, many times and you just deny results and data that contradict your beliefs.
Dr Ernst Mayr's quote does not disagree with mutations being random with respect to fitness. I have no idea why you keep repeating it. His main point is that evolution has no goal or target and that genetic variation is pure chance. AND, sometimes, who survives has nothing to do with fitness.
If a gene doesn't have an accompanying binding site it cannot be expressed. It is very telling that Jerad doesn't understand that simple fact. And seeing that Jerad agrees with there not being a target then it is clear that all that is left is sheer dumb luck- all chance, just as Mayr said.
Dr Mayr did not say it's all down to luck. A duplicated gene has the same binding site as the original. After the duplication then variation can change things.
https://www.ncbi.nlm.nih.gov/pubmed/25644246
"Gene duplication provides large numbers of new genes that can lead to the evolution of new functions. Duplicated genes can diverge by changes in sequences, expression patterns, and functions. MicroRNAs play an important role in the regulation of gene expression in many eukaryotes. After duplication, two paralogs may diverge in their microRNA binding sites, which might impact their expression and function. Little is known about conservation and divergence of microRNA binding sites in duplicated genes in plants. We analyzed microRNA binding sites in duplicated genes in Arabidopsis thaliana and Brassica rapa. We found that duplicates are more often targeted by microRNAs than singletons. T"
At 3:03 AM,
Unknown said…
From the same abstract:
"Close to half of the cases of binding site divergence are caused by microRNAs that are specific to the Arabidopsis genus, indicating evolutionarily recent gain of binding sites after target gene duplication. We also show rapid evolution of microRNA binding sites in a jacalin gene family. Our analyses reveal a dynamic process of changes in microRNA binding sites after gene duplication in Arabidopsis and highlight the role of microRNA regulation in the divergence and contrasting evolutionary fates of duplicated genes."
At 9:34 AM,
Joe G said…
I've tried many, many times and you just deny results and data that contradict your beliefs.
You have failed, every time, to produce anything that supports unguided evolution.
Dr Ernst Mayr's quote does not disagree with mutations being random with respect to fitness.
Yes, it does. It says they are just chance events. Period.
Dr Mayr did not say it's all down to luck.
What is chance besides luck?
A duplicated gene has the same binding site as the original
No, it does not. Lenski's experiment demonstrated that it does not as his duplicated gene did NOT also duplicate its binding site.
And again to change a duplicated gene requires specific mutations. Unguided evolution just doesn't have enough time in the universe to do such a thing.
At 5:05 PM,
Unknown said…
You have failed, every time, to produce anything that supports unguided evolution.
Provide a mechanism that guides mutations.
Yes, it does. It says they are just chance events. Period.
Oh, right. I didn't understand that you didn't understand what random means.
What is chance besides luck?
Again, I didn't understand that you didn't understand what random means.
No, it does not. Lenski's experiment demonstrated that it does not as his duplicated gene did NOT also duplicate its binding site.
If something is duplicated, i.e. copied, then it will have the same characteristics.
And again to change a duplicated gene requires specific mutations. Unguided evolution just doesn't have enough time in the universe to do such a thing.
To change a duplicated gene does not require guidance. If you have a particular target or goal in mind then you might come to a different conclusion.
Anyway, you're repeating the same old creationists' tropes.
At 3:26 AM,
Unknown said…
Yes, it does. It says they are just chance events. Period.
What do you think random means? If I role a die, a random event, and I get a 3 was that not just a chance event?
What is chance besides luck?
Dr Mayr does not disagree with mutations being random with respect to fitness. You are quote mining and misinterpreting what he wrote.
No, it does not. Lenski's experiment demonstrated that it does not as his duplicated gene did NOT also duplicate its binding site.
Reference please.
And again to change a duplicated gene requires specific mutations. Unguided evolution just doesn't have enough time in the universe to do such a thing.
To change a gene to hit a prespecified target would be highly improbably. For some mutations to occur is very likely. Most of the mutations will be deleterious, some will be neutral and some will convey some kind of advantage.
I even linked to a paper that discusses such processes.
At 10:59 AM,
Joe G said…
Provide a mechanism that guides mutations.
Already have
Oh, right. I didn't understand that you didn't understand what random means.
Fuck you, loser
Again, I didn't understand that you didn't understand what random means.
Again, you are a liar and a coward
If something is duplicated, i.e. copied, then it will have the same characteristics.
The GENE is duplicated. The BINDING site is NOT part of the gene, moron
To change a duplicated gene does not require guidance.
It requires lucky just-so mutations that also just happen to get past proof-reading and error correction- sheer dumb luck
Anyway, you're repeating the same old creationists' tropes.
Fuck you. All you are doing is lying and bluffing. You can't even form an argument
At 11:02 AM,
Joe G said…
What do you think random means?
In biology it means the mutations are happenstance- they just occur- they are accidents, errors and mistakes
You are quote mining and misinterpreting what he wrote.
Fuck you. Try forming an argument, pussy
Lenski's experiment demonstrated that it does not as his duplicated gene did NOT also duplicate its binding site.Reference please.
So you are ignorant. Figures.
To change a gene to hit a prespecified target would be highly improbably.
A change that changes the protein is prespecified, moron
I even linked to a paper that discusses such processes.
It doesn't sat anything about unguided processes.
At 11:12 AM,
Joe G said…
gene duplications followed by function altering mutations meet that prespecified criteria, moron.
At 11:14 AM,
Joe G said…
https://en.wikipedia.org/wiki/E._coli_long-term_evolution_experiment#Genomic_analysis_of_the_Cit+_trait_and_implications_for_evolutionary_innovation
The researchers also found that all Cit+ clones had mutations in which 2933 base pair segment of DNA was duplicated or amplified. The duplicated segment contained the gene for the citrate transporter protein used in anaerobic growth on citrate, citT. The duplication is tandem, and resulted in copies that were head-to-tail with respect to each other. This new configuration placed a copy of the previously silent, unexpressed citT under the control of the adjacent rnk gene's promoter, which directs expression when oxygen is present. This new rnk-citT module produced a novel regulatory pattern for citT, activating expression of the citrate transporter when oxygen was present, and thereby enabled aerobic growth on citrate.
At 4:44 PM,
Unknown said…
Already have
Nope. Even one of the reviewers of Dr Shapiro's book noted that no new mechanism was put forth.
Fuck you, loser
Well, you do get random, chance and luck all muddled up.
It requires lucky just-so mutations that also just happen to get past proof-reading and error correction- sheer dumb luck
Only if you consider a particular target. Mutations happen all the time which are deleterious.
In biology it means the mutations are happenstance- they just occur- they are accidents, errors and mistakes
Good enough. And that's what Dr Mayr was talking about. You muddle everything up.
A change that changes the protein is prespecified, moron
No, it's just random. Lots of changes/mutations are deleterious.
For you, the development of life on earth has a purpose, a target. So you think you can qualify mutations as being 'good' or 'directed' when they point to that target. But it doesn't work that way. The development of life on earth is full of waste and suffering because of bad variations and evolutionary branches that died out.
gene duplications followed by function altering mutations meet that prespecified criteria, moron.
And how many mutations occurred before that one that was 'beneficial' came about?
Your Wikipedia quotes does not support your guided hypothesis. Sometimes good mutations or changes do occur. Mostly they don't. And besides . . .
Dr Lenski's experiment started with a single strain which was then split into multiple strains. That implies that the strains all started with the same cellular material, your extra programming included. And yet, one (and only one) strain went through the beneficial change observed. From your perspective why is that? Why didn't all the strains go through the same change at the same time? If the mutations were guided then surely that's what should have happened. If not then how do you explain the difference?
The mechanism you hypothesise has to be able to match the experimental data. So tell us what the mechanism is and how it matches the data.
At 5:03 PM,
Joe G said…
Jerad- Built-in responses to environmental cues is such a mechanism, asshole.
Well, you do get random, chance and luck all muddled up.
Liar
Only if you consider a particular target.
Nope
And that's what Dr Mayr was talking about. You muddle everything up.
No, you muddle up everything because you are ignorant
A change that changes the protein is prespecified, moron
No, it's just random.
It meets the prespecified criteria, asshole
gene duplications followed by function altering mutations meet that prespecified criteria, moron.
And how many mutations occurred before that one that was 'beneficial' came about?
What does that have to do with anything?
Your Wikipedia quotes does not support your guided hypothesis.
It wasn't supposed to. It shows that gene duplication does NOT include the binding site.
At 2:33 AM,
Unknown said…
Jerad- Built-in responses to environmental cues is such a mechanism, asshole.
Where are these built-in responses? How are they stored? How are they triggered? How do they affect mutations?
A change that changes the protein is prespecified, moron
How do you know that? What if it changes the protein in a deleterious way?
gene duplications followed by function altering mutations meet that prespecified criteria, moron.
Even if it's a 'bad' change?
What does that have to do with anything?
Many mutations have negative effects. So, if there were more negative mutations before the 'good' one occurred then how was you built-in responses triggered?
At 8:22 PM,
Joe G said…
Where are these built-in responses?
In cells.
What is your mechanism?
How do you know that?
It fits the criteria.
What if it changes the protein in a deleterious way?
How does that help you?
Many mutations have negative effects.
How does that help you?
At 3:02 AM,
Unknown said…
In cells.
Where in cells? How is it encoded? How is triggered? How does it affect mutations? How does it avoid degradation? How come only one of Dr Lenski's lines developed a beneficial change when all the lines started out with the same in-built programming?
Is anyone actually trying to answer any of these questions?
What is your mechanism?
Differential survival depending on inheritable variation along with other factors like sexual selection. It's all very easy to find.
It fits the criteria.
Spell out the criteria please. Unless it's just: beneficial changers are 'programmed', non-beneficial ones are not because that doesn't work.
How does that help you?
I'm talking about how your view cannot tell which mutations are programmed and which are random. Since most mutations are NOT beneficial (most being negative or neutral) then your in-built programming seems to only work sporadically which is why I keep asking how it's triggered!
I don't think you've really thought your position through very well. You can't find the in-built programming. You can't say how it's stored or encoded. You don't know how it's triggered or how it affects mutations. You can't say how it avoids degradation. It's all just a bit of handwaving.
So, if you can't show that any kind of guiding, in-built programming exists then it must all be down to unguided processes. You are making a claim and you can't support it. Lashing out with vague accusations doesn't cut it. You have to support your claim.
.
At 10:17 AM,
Joe G said…
Differential survival depending on inheritable variation along with other factors like sexual selection. It's all very easy to find.
What a dunce. That says nothing of being unguided.
Spell out the criteria please.
It's in the paper. Read it.
I don't think you've really thought your position through very well.
Nice projection. You cannot support anything you post.
At 1:10 PM,
Unknown said…
What a dunce. That says nothing of being unguided.
You haven't found any physical evidence of in-built programming that could influence mutations. You can't say where precisely it is, how it's encoded, how it's triggered, how it influences mutations or how it avoids degradation. So I'll stick with unguided for now.
t's in the paper. Read it.
Uh huh. Point me to the particular passage since I'm so dense.
Nice projection. You cannot support anything you post.
You haven't found any in-built programming in cells. You can't say how it's encoded, how it's triggered, how it affects mutations or how it avoids degradation. Seems to me like you should get to work.
At 1:21 PM,
Joe G said…
You haven't found any physical evidence of in-built programming that could influence mutations.
You haven't found anything. We have observed mutations happening to outside stimuli.
Point me to the particular passage since I'm so dense.
The paper is about specific mutations, dumbass. The same type that would change the functionality of the protein.
You haven't found anything. You don't have a mechanism capable of producing living organisms. And even given starting populations of prokaryotes you don't have a mechanism capable of producing eukaryotes.
Your entire position lacks work.
At 2:44 PM,
Unknown said…
You haven't found anything. We have observed mutations happening to outside stimuli.
Uh huh. How are mutations affected by outside stimuli? What is the physical mechanism? Where is it stored? How is it encoded? How does it affect mutations? How is it triggered? How does it avoid degradation?
The paper is about specific mutations, dumbass. The same type that would change the functionality of the protein.
How do you know it was a random mutation? Because you think it was beneficial? If there were thousands of previous deleterious mutations first would you still feel the same way?
What is the mechanism that affects mutations? How is it stored? How is it triggered? You have a lot to address.
You haven't found anything. You don't have a mechanism capable of producing living organisms. And even given starting populations of prokaryotes you don't have a mechanism capable of producing eukaryotes.
Can you find a mechanism for guiding mutations or not? I'm guessing no.
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