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Human and chimp DNA: They really are about 98% similar

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A few days ago, scientist and young-earth creationist Dr. Jay Wile wrote a post on his Proslogion blog, in which he reported that Dr. Jeff Tomkins had abandoned his claim that human and chimpanzee DNA are only about 70% similar, in favor of a revised figure of 88%. But even that figure is too low, according to the man who spotted the original flaw in Dr. Tomkins’s work.

Dr. Wile reports:

More than two years ago, Dr. Jeffrey P. Tomkins, a former director of the Clemson University Genomics Institute, performed a detailed, chromosome-by-chromosome comparison of human and chimpanzee DNA using a widely-recognized computer program known as BLAST. His analysis indicated that, on average, human and chimpanzee DNA are only about 70% similar. This is far, far, below the 95-99% numbers that are commonly cited by evolutionists, so once I read the study, I wrote a summary of it. Well, Dr. Tomkins has done a new study, and it invalidates the one he did two years ago.

The new study was done because last year, a computer programmer of financial trading algorithms (Glenn Williamson) discovered a bug in the BLAST algorithm that Tomkins used. This bug caused the program to ignore certain matches that should have been identified, which led to an artificially low similarity between the two genomes.

Here is what Glenn Williamson has to say about himself:

Yeah – 36 year old, stay-at-home father of four – including triplets, ha! 🙂

I don’t have any formal qualifications in genetics, or anything biological for that matter. I have a bachelors degree in computing science (i.e. programming) from the University of Technology in Sydney. Started my career as a programmer, but transitioned into derivatives trading, which is a lot more fun…

And for what it’s worth, I believe that my paper is more of a computing science paper than a genetics paper. It’s more my area of expertise than Jeff Tomkins’ area.

Glenn Williamson’s detailed takedown of Dr. Tomkins’s 70% similarity figure can be accessed here. Dr. Tomkins claims he submitted his paper to the creationist publication, Answers Research Journal, but it was never published. Here’s an excerpt from the paper (emphasis mine – VJT):

In this paper I carefully reproduce a subset of Dr Tomkins’ results, and show clearly and unambiguously that Dr Tomkins has fallen victim to a serious bug in the software used to obtain his results. It is this bug that causes Dr Tomkins to report the erroneous figure of 70% similarity. After correcting for both the effects of this bug and some non-trivial errors in Dr Tomkins’ methodology, I report an overall similarity of 96.90% with a standard error of ±0.21%. This figure includes indels, and the result is largely in line with the secular scientific consensus.

What happened next? Dr. Wile takes up the story:

As a result, Dr. Tomkins redid his study, using the one version of BLAST that did not contain the bug. His results are shown above… The overall similarity between the human and chimpanzee genomes was 88%.

In an update at the top of his post, Dr. Wile now admits to having cold feet, even about the revised 88% figure:

Based on comments below by Glenn (who is mentioned in the article) and Aceofspades25, there are questions regarding the analysis used in Dr. Tomkins’s study, upon which this article is based. Until Dr. Tomkins addresses these questions, it is best to be skeptical of his 88% similarity figure.

So what was wrong with Dr. Tomkins’s new study? I’ll let Glenn Williamson explain (emphasis mine – VJT):

October 16, 2015 4:22 pm

As I’ve said many times, if there is a single base pair indel in the middle of a 300bp sequence, Tomkins will say this is a 50% match.

Tomkins is most certainly aware of this, yet he chose to publish it. I think that says pretty much everything.

Another commenter named Aceofspades25 has this to add (emphases mine – VJT):

October 16, 2015 2:13 pm

The other obvious thing that Thompkins hasn’t dealt with in his BLASTN analysis, I talk about here.

There are a few cases where no match will be found because this entire sequence appears de-novo in Chimpanzees as the result of a single mutation (e.g. a novel transposable element – see here) or because humans have had a large deletion which other primates don’t. Deletions like this also likely occurred in a single mutation – see here

Thompkins (sic) would count both of these as being a 0% match (or 600 effective mutations if the sequences he was searching for were 300bp each). In reality, these probably represent just 2 mutations.

I’ll let Glenn Williamson have the final word (emphases mine – VJT):

Thanks Ace, for letting me know about this post. I reiterate here a few things about my (unpublished!) paper, and about Tomkins’ new paper.

The first thing is that he uses the “ungapped” parameter in his BLAST comparisons. As I’ve written in a few other places now, using this parameter, and calculating results in the way that Tomkins does is entirely disingenuous. If you are comparing two 300bp sequences, and one of those sequences has a single indel smack bang in the middle, Tomkins counts this as the sequences being only 50% identical.

I’ve told him at least twice that he cannot use ungapped and then calculate the result in this way. He can do one of two things:

1. Use ungapped, which ignores indels and therefore he can only report the substitution rate. (emphasis mine – VJT)If he did this, he would get a result of around 98.8%.

2. Allow gaps, and – this is what he fails to mention in his paper – get a result of around 96.9%. And this is using a very conservative method of calculation as well, since it counts a 50bp indel as having the same weight as 50 individual mutations. If you counted a 50bp indel as a single event (which it probably was), then the overall result would be pushed up towards 98%, which is the figure usually thrown around anyway.

In a comment dated 14 August 2015 (at 03:44) on an article titled, Chimp and Human DNA vs “Sophisticated Nonsense”! on a blog called Marmotism, Glenn Williamson adds:

I’ve actually written a paper on Tomkins’ 70% result, and have _ATTEMPTED_ to get it published in Answers Research Journal. Obviously they are not having a bar of it – Tomkins is the sole peer-reviewer, and he is currently refusing to provide any critique of my work – he has been silent for 8 months, while the ball is in his court ..

See the paper here:

https://www.dropbox.com/sh/dm2lgg0l93sjayv/AAATnWSJdER53EYEYZvcgiwma?dl=0

It’s the two PDFs ..

Dr. Tomkins’s latest article in Answers Research Journal (October 7, 2015) acknowledges Williamson’s work in a single sentence:

As of 2013, the issue of overall genome similarity between chimpanzee and humans seemed to be about 70% based on five different reports, three of which were based on actual data analyses. However, in 2014 , a computer programmer of financial trading algorithms discovered an apparent bug in the BLASTN algorithm and notified this author of the situation (Glenn Williamson, Tibra Capital, personal communication).

So, a submitted article only counts as a “personal communication”? Perhaps Dr. Tomkins needs to be a little more up-front about giving credit where credit is due, and acknowledging his mistakes. At any rate, the ball is definitely in his court, and his latest 88% similarity figure warrants skepticism. I have to say that Dr. Tomkins’s methodology sounds rather suspicious to me.

What do readers think?

Comments
Zachriel:
The Lederberg experiment shows that mutations are random with respect to fitness.
In what way did that experiment show that mutations are random with respect to fitness? Be specific or go home.Virgil Cain
October 26, 2015
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Zachriel:
Actually, we are here to discuss ID and evolutionary biology, and try to support our position with relevant facts and argument.
And yet you refuse to learn what ID is and you equivocate when you talk about evolutionary biology. That means to don't know the relevant facts and you don't have an argument.Virgil Cain
October 26, 2015
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And you can ignore the same reference as many times as you want
Is this coming from the same guy that ignored:
In the case of many adaptations, we can show they are random with respect to fitness.
Virgil: So something that aids fitness is random with respect to it? Really?
???
The Lederberg experiment shows that mutations are random with respect to fitness.
My, my, my. A few umpteen comments ago, it was the Lenski experiments that showed it and now it's this one. Uh uh, you may like to move around in circles but not me.Vy
October 26, 2015
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Vy: You can refer to that same reference as many times as you want. And you can ignore the same reference as many times as you want, but it doesn't go away. The Lederberg experiment shows that mutations are random with respect to fitness.Zachriel
October 26, 2015
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No. We can observe that mutations are random with respect to fitness. We can observe how selection causes heritable changes in populations. One experiments showing mutation is random with respect to fitness is Lederberg & Lederberg, Replica Plating and Indirect Selection of Bacterial Mutants, Journal of Bacteriology 1952.
Still the same rapping as last time and it is still false. Moving along, nothing new to see . . .
No
So they're not evodelusionists like yourself? Are you even reading your comments???
but it does support the claim that “per the researchers, they evolved to adapt to the laboratory conditions”.
Do you have reading comprehension issues? The level of inanity in your comments is at a critical level, damn! You saw this:
Maybe the title of the project is a clue to the researchers’ thinking
Oh yes, I’m fully aware of the fact that they happen to be evodelusionists like you but that doesn’t affect reality. Just because I see a madman on TV because of a sloppily positioned video camera saying “madmen matchsticks ignite when you strike them” doesn’t mean I should believe the nonsense. No way, I take the “non-“, “madmen” in this case, and keep the” sense”, which is the rest of the statement. It’s easy.
and you still had the audacity to post the comment? Come on! What do the claims of seemingly madmen, as per the analogy, have to do with a logical interpretation of said claims?
Evolution largely works by incremental change of existing structures.
I lost interest in any of your other redefinitions of what evolution is and isn't two redefinitions ago so that your statement is as logical as "blahita maggiooop dd kd smiggles we worldiia tak overrrrr" and as useful as a stain on the wall. ___ It was all nice and good in the beginning but having to repeat myself over and over has made this discussion become quite tiresome. You have shown, to me as well as others and even across threads, that the only thing you're capable of doing is being consistently inconsistent (and I'm not even joking), selectively blind, ignore questions and/or give non-answers to simple yes/no questions, repeat the same refuted things over and over, bait-and-switch, and make comments that contradict your very own words and the inner workings of your pet theories. I guess I should have listened to Mapou and Virgil earlier on, whew!Vy
October 26, 2015
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computerist: If you’re saying ANYTHING can be modified, then the underlying protocols would be subsequently affected sooner rather than later, rendering the network non-functional. No, but largely robust to changes, contrary to your statement above. Nearly every single sexually reproducing organism is a unique combination of traits, and nearly all carry a number of mutations, yet the vast majority are viable.Zachriel
October 26, 2015
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Changes in a complex network can occur at most places within such networks without disrupting the entire network.
Networks operate within restrictions in the form of protocols. If you're saying biology is like a network, it's governed by strict protocols. I do not modify the transport control protocol when I send a message or make a request. The arbitrary message is "encapsulated" within the OSI layers (in the case of computer networks). If you're saying ANYTHING can be modified, then the underlying protocols would be subsequently affected sooner rather than later, rendering the network non-functional.computerist
October 26, 2015
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computerist: The way I see it, biology is composed of multiple interdependent systems. Organisms are organized at many levels throughout. They can be modeled as networks which have been built through preferential attachment. computerist: If the mutation can occur in any arbitrary position affecting any of those systems, you cannot constructively or positively “evolve” anything. Changes in a complex network can occur at most places within such networks without disrupting the entire network.Zachriel
October 26, 2015
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There is definitely a strong degree of delusion with respect to evolution, so in that case I would say it would be in a way synonymous with evoillusion and/or pseudo-evolution. Whichever one sounds better I guess :)computerist
October 26, 2015
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Computerist, how about evodelusion?Vy
October 26, 2015
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This is why it's more in-line with Evoillusion than Evolution. or maybe "pseudo-Evolution"? sounds good to me.computerist
October 26, 2015
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Zachriel, The way I see it, biology is composed of multiple interdependent systems. If the mutation can occur in any arbitrary position affecting any of those systems, you cannot constructively or positively "evolve" anything. Now, the only way this can be circumvented, is if there are specific restrictions and controls in the cell similar to object oriented software design, where you have limited access to certain methods/properties, ie: public/protected/private. The evidence shows (for example dog breeds) that there are key mutational hot spots that are common and are responsible for determining a wide range of characteristics including size, color etc...aka: variation. These hot spots would be analogous to public properties/methods. They can be accessed and modified but also have modifier restrictions in place. This however still preserves the underlying functionality, and evolution can move forward, but in a limited way, that's good.computerist
October 26, 2015
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EugeneS: What I mean by a working gene duplication machinery is specific protein-protein interactions achieving controlled gene duplication such that one copy is there for integrity, the other is for alleged unguided exploration of the search space. Mistakes in duplication are intrinsic to the replication process, so inhere to the origin of replication. Vy: We observe adaptation and evodelusionary twisting of adaptation, like all your comments on the issue. No. We can observe that mutations are random with respect to fitness. We can observe how selection causes heritable changes in populations. One experiments showing mutation is random with respect to fitness is Lederberg & Lederberg, Replica Plating and Indirect Selection of Bacterial Mutants, Journal of Bacteriology 1952. Vy: I’m fully aware of the fact that they happen to be evodelusionists like you but that doesn’t affect reality. No, but it does support the claim that "per the researchers, they evolved to adapt to the laboratory conditions". Vy: However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial. Evolution largely works by incremental change of existing structures.Zachriel
October 26, 2015
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OFF TOPIC Mapou: we should be working on expanding ID in order to come up with serious scientific predictions. Thought this site was for general discussion. Perhaps that should be clarified in the comment policy, right next to the policies about germaneness, politeness, and tolerance. https://uncommondescent.com/comment-policy/ Mapou: People like Zachriel are not here to discuss or argue anything. Actually, we are here to discuss ID and evolutionary biology, and try to support our position with relevant facts and argument. However, you seem to be more concerned with other issues. Good luck with that.Zachriel
October 26, 2015
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Dr JDD, you said:
Finally such behaviour quite frankly puts off people in general – why would they want to participate in a place where if you disagree someone goes on a hunt for your personal info and plasters it over a public board for all to see?
The way I see it this is the Internet, and it's now more social than ever. If you expose any sort of details and you're a person of interest, there is a chance someone will do some detective work, trace it to the source and expose it to the public. Ironically, this is also similar to how ID investigation works! :) This is exactly what happened to Zachriel, he probably said more than he should have in some online exchanges somewhere sometime ago (at ATBC or wherever), and/or gave too many clues pertaining to his identity. In that case, maybe he just doesn't care about anonymity? I pasted a link pertaining to existing information posted a while back on a sub-blog (darwins-god.blogspot.com) to UD. Who knows if it's even accurate, but the question of singular vs. plural Zachriel/s came up, and since I read much of Zachriels material for many years now as an ID supporter, I will admit I was a bit curious to know who/what Zachriel even is, whether it's really some paid group of Darwin lobby trolls etc...and confirm here. I'm completely for taking down the link and understand privacy controls and concerns, but it's still really weird that people are annoyed when this information is freely available online with a simple google search. That's all I really have to say on this matter.computerist
October 25, 2015
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We can directly observe evolutionary adaptation.
In your daydreams? Absolutely. In reality? We observe adaptation and evodelusionary twisting of adaptation, like all your comments on the issue.
Maybe the title of the project is a clue to the researchers’ thinking
Oh yes, I'm fully aware of the fact that they happen to be evodelusionists like you but that doesn't affect reality. Just because I see a madman on TV because of a sloppily positioned video camera saying "madmen matchsticks ignite when you strike them" doesn't mean I should believe the nonsense. No way, I take the "non-", "madmen" in this case, and keep the" sense", which is the rest of the statement. It's easy.
Instead, it was cooption of an existing transporter. That the new trait evolved by modification of an existing system
Again:
More from Anderson and Purdom:
Each of these mutant strains has an antagonistic pleiotropy characteristic. An existing system is traded for an altered phenotype that is better suited to survive the specific stressful environment. Regulation is reduced to enable overexpression. DNA repair and DNA polymerase fidelity are reduced to enable increased mutation rates (increasing the probability of a “beneficial” mutation). A gene is inactivated by a process that concurrently activates a silent gene. Such trade-offs provide a temporary benefit to the bacterium, increasing its chances of surviving specific starvation conditions. However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial.
Sheesh!
is exactly how evolution is posited to work.
Correction: That's how adaptation works. The evolution part is more twisting.Vy
October 25, 2015
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We can directly observe evolutionary adaptation.
In your daydreams? Absolutely. In reality? We observe adaptation and evodelusionary twisting of adaptation, like all your comments on the issue.
Maybe the title of the project is a clue to the researchers’ thinking
Oh yes, I'm fully aware of the fact that they happen to be evodelusionists like you but that doesn't affect reality. Just because I see a madman on TV because of a sloppily positioned video camera saying "madmen matchsticks ignite when you strike them" doesn't mean I should believe the nonsense. No way, I take the "non-", "madmen" in this case, and keep the sense, which is the rest of the statement. It's easy.
Instead, it was cooption of an existing transporter. That the new trait evolved by modification of an existing system
Again:
More from Anderson and Purdom:
Each of these mutant strains has an antagonistic pleiotropy characteristic. An existing system is traded for an altered phenotype that is better suited to survive the specific stressful environment. Regulation is reduced to enable overexpression. DNA repair and DNA polymerase fidelity are reduced to enable increased mutation rates (increasing the probability of a “beneficial” mutation). A gene is inactivated by a process that concurrently activates a silent gene. Such trade-offs provide a temporary benefit to the bacterium, increasing its chances of surviving specific starvation conditions. However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial.
Sheesh!
is exactly how evolution is posited to work.
Correction: That's how adaptation works. The evolution part is more twisting.Vy
October 25, 2015
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In the case of many adaptations, we can show they are random with respect to fitness.
So something that aids fitness is random with respect to it? Really?Virgil Cain
October 25, 2015
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EugeneS: We can directly observe effects of adaptation. Whether it is evolutionary (e.g. Darwinian) or pre-programmed is open for discussion. Evolution refers to hereditary changes. In the case of many adaptations, we can show they are random with respect to fitness.Zachriel
October 25, 2015
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Zachriel, "We can directly observe evolutionary adaptation." We can directly observe effects of adaptation. Whether it is evolutionary (e.g. Darwinian) or pre-programmed is open for discussion. No evolution is capable of producing a program together with a processor taking the program as input.EugeneS
October 25, 2015
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Zachriel, "If there is replication, there is duplication." What I mean by a working gene duplication machinery is specific protein-protein interactions achieving controlled gene duplication such that one copy is there for integrity, the other is for alleged unguided exploration of the search space. How did a protein machinery that achieves no less than that function ever appear? Show in detail how you think such a system arose.EugeneS
October 25, 2015
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Vy: The fact that you’ve successfully deceived yourself into believing that simply because evodelusionists have taken up adaptation as an evolutionary mechanism, it makes it one doesn’t affect reality. We can directly observe evolutionary adaptation. Zachriel: Yes, per the researchers, they evolved to adapt to the laboratory conditions Vy: False, they adapted Maybe the title of the project is a clue to the researchers' thinking: E. coli long-term evolution experiment. See Blount et al., Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli, PNAS 2008: "All twelve populations underwent rapid improvement in fitness that decelerated over time. All evolved higher maximum growth rates on glucose, shorter lag phases upon transfer into fresh medium, reduced peak population densities, and larger average cell sizes relative to their ancestor." It's clear that, per the researchers, they evolved to adapt to the laboratory conditions. Vy: Neither of those involve the creation of anything Your claim was that Cit+ was due to the "breaking of a molecular feature — a repressor switch". Instead, it was cooption of an existing transporter. That the new trait evolved by modification of an existing system is exactly how evolution is posited to work.Zachriel
October 25, 2015
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Does anybody know who Upright BiPed is? LOL.Mapou
October 25, 2015
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Your inability to understand doesn’t make the statement nonsensical.
Your illusory view that the statement is not nonsensical doesn't make it so*.
More simply, while evolutionary adaptation is a subset of evolution, not all evolution is adaptation.
* - this being a case-in-point. The fact that you've successfully deceived yourself into believing that simply because evodelusionists have taken up adaptation as an evolutionary mechanism, it makes it one doesn't affect reality.
.. .they adapted to the glucose environment, but lacking in other sugars (except citrate, which was added as an chelating agent). They adapted to the glucose-deficient environment they were kept to get the most out or the little glucose they had till the next "lunch-break".
Only in anaerobic conditions, yes
Redundant. A simple yes would've sufficed.
The broth had glucose, as well as citrate added as a chelating agent.
Not what I asked. Read before you respond.
Yes, per the researchers, they evolved to adapt to the laboratory conditions
False, they adapted, nothing evolves to do anything despite your assumptions in the other thread that evolution is purposeful and has goals.
Yes, it’s typical to allow the bacteria to fill the flask before cloning it.
What? That is not what I asked. Are you talking to an imaginary image in front of you?
That’s what Behe and other ID proponents had supposed before the genomic analysis had been completed.
Whoops, sorry. You've used so many numbers I taught you understood math. Is 2015 later or earlier than 2012?
Rather, a new “switch” was created.
Truth from constantly repeated lies, carry on. In reality-ville, Blount says:
One possibility is that the Cit+ lineage activated a ‘cryptic’ [preexisting but dormant] transporter, that is, some once-functional gene that has been silenced by mutation accumulation ... 2. A more likely possibility, in our view, is that an existing transporter has been coopted for citrate transport under oxic conditions. This transporter may previously have transported citrate under anoxic conditions or, alternatively, it may have transported another substrate in the presence of oxygen. ...
Neither of those involve the creation of anything, in fact, it's quite the opposite as already explained in the ENV article. More from Anderson and Purdom:
Each of these mutant strains has an antagonistic pleiotropy characteristic. An existing system is traded for an altered phenotype that is better suited to survive the specific stressful environment. Regulation is reduced to enable overexpression. DNA repair and DNA polymerase fidelity are reduced to enable increased mutation rates (increasing the probability of a “beneficial” mutation). A gene is inactivated by a process that concurrently activates a silent gene. Such trade-offs provide a temporary benefit to the bacterium, increasing its chances of surviving specific starvation conditions. However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial.
So far, you have been unable to understand simple English and answer simple questions directly. Do you need me to dumb it down with crayons and shiny graphics so that your selective blindness, mental gymnastics and delusions will be reduced to a fairer minimum?
Vy
October 25, 2015
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Moderators, comments #110 and #111 need to be removed from this thread.Upright BiPed
October 25, 2015
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Mapou: Free will is a beautiful thing and we are all entitled to our opinion and we have each stated ours, so that is that. I'm not one to argue simply for the sake of it. I just sincerely hope certain behaviours (trolls or not) do not put off the type of crowd that UD wishes to draw. Best Wishes.Dr JDD
October 25, 2015
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JDD:
So yes, I stand by the word “stoop” as this “outing” to me does nothing to add to the argument and is a bit immature in the grand scheme of things quite frankly. Sadly, if this is what UD thinks is acceptable it’s not a place I would want to associate with personally for much longer.
I don't care. You got your opinion and I got mine. People like Zachriel are not here to discuss or argue anything. The jackass is a dishonest troll. He's here to bog us down in interminable and worthless debates when we should be working on expanding ID in order to come up with serious scientific predictions. If this site belonged to me, I would have kicked his arse off this forum a long time ago, along with his buddies. Heck I would not even allow people like Larry Moran to comment here. Know thine enemy.Mapou
October 25, 2015
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Vy: Still as nonsensical a statement as it was the first time but enjoy the gymnastics. Your inability to understand doesn't make the statement nonsensical. More simply, while evolutionary adaptation is a subset of evolution, not all evolution is adaptation. Vy: that reality contradicts your “adaptation to a glucose-rich environment” assertion. "while they grow faster on a meager diet of glucose, they’ve gotten worse at feeding on some other kinds of sugars." In other words, they adapted to the glucose environment, but lacking in other sugars (except citrate, which was added as an chelating agent). Vy: – Did they or did they not have a perfectly working mechanism to use citrate albeit under anaerobic conditions? Only in anaerobic conditions, yes. Vy: – Were they or were they not put in a medium that had little glucose and more citrate? The broth had glucose, as well as citrate added as a chelating agent. Vy: – Did they or did they not initially become very efficient in using glucose as an energy thus temporarily increasing their survival rate? Yes, per the researchers, they evolved to adapt to the laboratory conditions. Vy: – Did they or did they not finish up the glucose before the next day leaving them starving in the presence of something they could very well use if not for one variable for several hours before the next “lunch break”? Yes, it's typical to allow the bacteria to fill the flask before cloning it. Vy: A switch that normally represses expression of CitT under oxic conditions was broken, so the citrate-uptake pathway got turned on. This isn’t the evolution of a new molecular feature. It’s the breaking of a molecular feature — a repressor switch. That's not what happened. That's what Behe and other ID proponents had supposed before the genomic analysis had been completed. Rather, a new "switch" was created. This required potentiating mutations and a duplication, then this was followed by optimizing mutations. Vy: The only “novel pathway” is the one in your imagination. Blount, Genomic analysis of a key innovation in an experimental Escherichia coli population, Nature 2012: "Our findings highlight the less-appreciated capacity of duplications to produce new functions by promoter capture events that change gene regulatory networks." Vy: please, you gotta let reality in once in a while. Antibiotics, and therefore antibiotic resistance, occur in nature, and probably have for billions of years. Indeed, the first antibiotic was discovered in mold.Zachriel
October 25, 2015
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As for your allusions to the fact that because antibiotic resistant bacteria exist, it somehow puts your absurd assumptions on solid ground, please, you gotta let reality in once in a while. @Virgil: A massive seemingly D.I.Ded troll!Vy
October 25, 2015
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It is so awesome having other people see Zachriel for what it is- an insipid troll.Virgil Cain
October 25, 2015
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