Harsh Truth: If Intelligent Design is Untestable . . .

[JM2C]

Before you can learn something new, you have to stop buying into outdated, inaccurate, ignorant information...

You wouldn't step into a Calculus classroom and try to argue that Calculus is a flawed science because of what you learned in Elementary school, would you?

So, likewise, you shouldn't make bold statements or claims about biology when you very obviously don't know what you're talking about.


CB102: Mutations adding information


Adding New Genetic Information


Evolution myths: Mutations can only destroy information - New Scientist


Question 1: How Does Evolution Add Information? - How Evolution Works


Gene duplication - Wikipedia, the free encyclopedia


Molecular evolution - Wikipedia, the free encyclopedia

Enough with the rhetoric please. Summarize those links on how you understand them then I would be interested in reading your post.

 

[Monk Of Reason]

Enough with the rhetoric please. Summarize those links on how you understand them then I would be interested in reading your post.

Essentially in the most laymen of terms we can put it;

Mutations are changes in the DNA coding. This is done when a "mistake" during the replication process occurs. It has the ability to add or subtract total amount of genetic information with each mutation. However there is always a change of "new" information even if total information is less. But there still stands that some mutations add to the total genetic information.

What are you confused about?

 

[jonathan180iq]

Enough with the rhetoric please. Summarize those links on how you understand them then I would be interested in reading your post.

• Gene duplication happens.
  It causes an increase in genetic information from one generation to another. It can happen anywhere from individual alleles in complex organisms all the way up to a simpler organism's entire genome.

• Mutations happen.
  They can lead to distinct observed changes (called changes in phenotype) or they can lead to nonphysical changes, which occur directly at the genetic level but do not produce observed external changes (called changes in genotype). Genotypical changes, while not manifesting themselves physically, are still passed on from one generation to another.
  
  
• Mutations do more than simple "destroy information"
  This one is self explanatory.

It's quite humorous that you ask me to "stop with the rhetoric" on a post that has detailed supporting documents attached which explain these things to you.

You made the claim that genetic information cannot increase.
You were shown to be wrong.

You made the claim that Macroevolution has no observable substantiation.
You were shown to be wrong.

You made a claim about your understanding of transitional forms.
You were shown to be mistaken.

You made the claim that Microevolution was factual, but that it somehow breaks down at the Macroevolutionary level.
I have shown you that your claim is inaccurate. Unless you have some data which suggests that there is a genetic barrier which limits microevolutionary changes, then your argument is null.

You have expressed all of these claims with the underlying belief that evolution is a hoax or a fraud or some other nonsense, and you've supported that belief with terribly outdated information, straight up inaccuracies, and simple ignorance. You've provided very little to express even the most basic understanding of biology, and yet you're attempting to disprove the foundation of modern biology... In what other real life scenario would that be a wise thing to do? Like I said, you're attempting to disprove calculus with what little you know about addition. It's foolish.

You can quote all of the Creationists that you like, but it won't change what actual observable science predicts, demonstrates, or supports.

 

[Shad]

Your ignorance is leading you to believe that modern ToE has nothing to do with Darwin’s ToE and using this modern ToE as your STRAWMAN so you can get away from the main argument, i.e., man came from a dead molecule.

No I am just pointing out you are attacking the theory as it was not what it is now. Thus you are attacking a strawman based on ToE over a century ago.

Really? What is the point of our arguments here then?

The point was that a theory that specifically addresses concepts and objects which already exists do not need to account for the origins Evolution deals with life which already exists just as orbit models deal with planets which already exist.

 

[Shad]

I don’t think you understand what a genetic basis for the change means. What I meant is, from eating glucose to eating citrate is not a genetic change as in gain new genetic information or gain new mechanism, i.e., by means of mutation, to digest citrate. In the case of E.coli the genetic change [NO NEW G.I. AND NO N.M.] is just the rearranging of the genetic sequence caused by mutation that is beneficial for survival. Remember in the experiment, Lenski placed the E.coli in a beaker with 10 to 1 ratio of citrate to glucose, in an aerobic environment, and after they consumed the glucose, they started to eat the citrate. What causes them to eat citrate? Starvation!

Actually the genetic basis was a change in a mechanic which did not function in the environment of the experiment. It was a mutation of this mechanic into a function it did not have before. This change did not occur in every sample nor at once. A mechanic that is alter becomes a new mechanic as it is no longer the same as the one before. Thus is new information thus a gain of function not a loss of.

Starvation is frequently a state that bacteria have to endure. In order to survive, they need to have special adaptive capabilities. Both adaptive mutation and antagonistic pleiotropy come into play.

Still a gain of function phenotype

Anderson and Purdom sum up the conclusions rather concisely:

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. (Anderson and Purdom 78)

A citation from creationist wiki, yawn. Refuted above and by the very experiment you cited. A random citation is useless especially from Purdom who is a YEC.

The Italian wall lizards were insectivorous before transferring them into the island of Pod Mrcaru. They can’t find their food so they ate what was there, and that is, the plant. On the human side not having the right food and nutrient can cause mutation. Environment can change the appearance of the creature and human, but not the code. Go search for that.

The Wall Lizard already ate plants. The cecal valves value changes were not from the origin organisms, control group.

http://www.sciencedaily.com/releases/2008/04/080417112433.htm

You need to understand what MUTATION means. The E.coli were digesting glucose in an aerobic environment and they have the ability to digest citrate in an anaerobic environment, and as demonstrated in the experiment, with citrate as the only food, they have adapted into that environment, the aerobic environment, because of starvation.

Which is mutation which changes a mechanic into a new mechanic.

 

[JM2C]

So not only did you completely ignore my post explaining how the genetic basis for the change in the E.coli was found (genes were found to be present in the Cit+ strains that were absent in the Cit- strains), but now you are claiming that starvation can cause mutation?

How? How can starvation possibly cause genetic mutations? Do you even know what genetic mutation is? I really want an explanation for that one.

About information again, one of the most fundamental measures of information is computational: bits. There is no simpler way to express information content. So let's say that you have a computer drive that is just barely large enough to store the genomic sequence of a Cit- bacterium. Now you have computationally quantified the amount of information in the Cit- genome in terms of bits. The question then becomes, can the genomic sequence of a Cit+ bacterium be stored on this same drive? If it can, then that means Cit+ has the same amount of information or less than Cit-. However, since it was found that Cit+ has extra genes in it, that means that it would require extra bits to encode it computationally. Since the drive in question was stated to be just barely large enough to hold the Cit- code, it will not fit. You cannot put 6 gallons in a 5 gallon bucket. The Cit+ bacterium therefore has to have more information than the Cit- bacteria.


I also want to point out that information is not the same as functionality. A system can contain new information without gaining new functionality. Imagine you have two computer codes, each 10,000 bits long. One is a random string of 1s and 0s whereas the other one has 1s and 0s arranged in a way that allows it to successfully excute programs. Both codes contain the same amount of computational information since they are both 10,000 bits long, but only one has functionality. So please keep in mind that when you are arguing about new information and new functionality, you are talking about two different things.

The Cit- phenotype, the old species of E.coli, was replaced by the Cit+ phenotype, the new species of E.coli, right?

To digest citrate it needs a transporter protein, right?

How did the bacteria “know” when to switch on the genes for making the proteins that could pull citrate into the cell and matabolize it in the absence of glucose?

There is a defective mutant bacterium that makes citrate using proteins all the time even in the absence of citrate. It lacks a control mechanism to shut off these citrate-using proteins. This mutant bacterium contained hidden protein called a “repressor” is broken.

“The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions.” -Lenski

IOW, all it needed is a way to get the citrate into the cells, right?

Lenski proposed two mechanisms:

1. 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. The evolved changes might involve gene regulation, protein structure, or both. (Blount, Borland and Lenski)

Did it say NEW MECHANISM AND NEW INFORMATION here? Neither one is evidence for a new system.

 

[JM2C]

Actually the genetic basis was a change in a mechanic which did not function in the environment of the experiment. It was a mutation of this mechanic into a function it did not have before.

You are just guessing. Please read the report.

This change did not occur in every sample nor at once.

What change are you talking about or at what generation?

A mechanic that is alter becomes a new mechanic as it is no longer the same as the one before. Thus is new information thus a gain of function not a loss of.

[/quote]And if you return them into the glucose environment, will they change back into the old mechanism or is the mechanism was there all the time? Have you ever thought of that?

Still a gain of function phenotype

Cit- phenotype changed into Cit+ phenotype, but did the genotype change also?

 

[JM2C]

Wrong. There was no starvation.

10 to 1 ratio of citrate to glucose can cause starvation.

Wrong. They identified the exact mutations that led to the ability to metabolise citrate.

And what is it again?

Wrong, new information and a completely new mechanism.

Your opinion only generates ignorance. You don’t have any proof of your claim, and this is only coming from your own ignorance, because if you do, like your math skills, you would have posted it already.

 

[JM2C]

Wrong, there was no starvation.

Yes, starvation was the cause.

Wrong, the mutation has not been identified yet because no one has sequenced the lizards' genome.

So, where is the new information came from again?

The lizards have evolved, and rapidly..

There is no question they have evolved. The question is did they gain new information and new mechanism. According to you ignorance

no one has sequenced the lizards' genome

Meaning you can’t tell the difference between the before and after they were taken to the island, right?

Wrong, ignorant or deliberately misrepresenting the facts. Take your pick.

Neither one! So, these group of skinny malnourished people gain new genetic information and new mechanism after 100 years is what you meant?

 

[JM2C]

He has expressed an opinion that is not within his field with no research or evidence to back it up.

I’ll take his opinion compare to yours.

And after having said that has been refuted and the claim has been proven false.

Show me the link or links if you have one..

 

[JM2C]

View attachment 10185

Evolutionists do. From a dead, a very dead molecule to man. That's how they summarized evolution and the funny thing is, they are now running away from that argument because they've discovered a new theory, and modern theory of evolution without the classical Darwin’s theory. Poor Darwin!

 

[Parsimony]

The Cit- phenotype, the old species of E.coli, was replaced by the Cit+ phenotype, the new species of E.coli, right?

To digest citrate it needs a transporter protein, right?

How did the bacteria “know” when to switch on the genes for making the proteins that could pull citrate into the cell and matabolize it in the absence of glucose?

Promoter regions.

There is a defective mutant bacterium that makes citrate using proteins all the time even in the absence of citrate. It lacks a control mechanism to shut off these citrate-using proteins. This mutant bacterium contained hidden protein called a “repressor” is broken.

Such a defective mutant is not the focus of the paper I linked. There was in fact a mutant promoter region linked to two or more duplicated CitT genes in the bacteria which caused it to metabolize citrate when oxygen was present. The gene was located and confirmed through testing to do this. Again, did you not read the paper?

“The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions.” -Lenski

IOW, all it needed is a way to get the citrate into the cells, right?

Lenski proposed two mechanisms:

1. 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. The evolved changes might involve gene regulation, protein structure, or both. (Blount, Borland and Lenski)

Did it say NEW MECHANISM AND NEW INFORMATION here? Neither one is evidence for a new system.

It doesn't have to say it directly. It's self-evident that there is a new system in place once you understand what actually happened. There is an increase in information because the DNA sequence was enlarged (as I showed with my computer drive example). The new mechanism was the result of a splicing of two genes to form a new promoter region as well as duplication mutations of another gene. No old genes were modified, but new ones were added and gave the bacteria the ability to do something that it could not do before. That is, by definition, a new mechanism. It's like saying that a fish species that gained the ability to breath air somehow did not evolve a new mechanism in order to do it.

I still want to see you address nylonase and to explain how starvation can make a genome mutate (with a citation backing it up). It's become quite apparent that you are completely ignoring answers that are given to you. For example, when you asked Shad if the genome had changed when the bacteria evolved from Cit- to Cit+, I had already told you several posts ago that it had indeed changed and even linked you to a scientific paper identifying the specific genes that were found in Cit+ that were absent in Cit-. You even asked the same thing of David M. How can a person debate with you if you won't even read their responses?

 

[JM2C]

I still want to see you address nylonase and to explain how starvation can make a genome mutate (with a citation backing it up). It's become quite apparent that you are completely ignoring answers that are given to you. For example, when you asked Shad if the genome had changed when the bacteria evolved from Cit- to Cit+, I had already told you several posts ago that it had indeed changed and even linked you to a scientific paper identifying the specific genes that were found in Cit+ that were absent in Cit-. You even asked the same thing of David M. How can a person debate with you if you won't even read their responses?

in this thread alone I get about 10 to 20 questions from you guys and sometimes I have only 2 to 3 hours to read and respond to those questions. Today I have more time, but just reading those questions is just not enough to answer them all. I have to research everything before answering them.

 

[Parsimony]

in this thread alone I get about 10 to 20 questions from you guys and sometimes I have only 2 to 3 hours to read and respond to those questions. Today I have more time, but just reading those questions is just not enough to answer them all. I have to research everything before answering them.

Alright, I can understand that. If this is getting to be too much for you to deal with, then I'll bow out and lighten your load. Peace.

 

[Monk Of Reason]

I’ll take his opinion compare to yours.

Good thing its not my opinion but scientific fact.

Show me the link or links if you have one..

Already have. You ignored them and never responded to that post.

 

[David M]

Yes, starvation was the cause.

No it wasn't. There were many populations that grew and flourished under exactly the same conditions. The new mutations that lead to the ability to metabolise citrate as well as glucose only occurred in one of the sample populations.

As ti what the mutations were (from Wikepedia E. coli long-term evolution experiment - Wikipedia, the free encyclopedia )

In 2012, Lenski and his team reported the results of a genomic analysis of the Cit+ trait that shed light on the genetic basis and evolutionary history of the trait. The researchers had sequenced the entire genomes of twenty-nine clones isolated from various time points in the Ara-3 population's history. They used these sequences to reconstruct the phylogenetic history of the population, which showed that the population had diversified into three clades by 20,000 generations. The Cit+ variants had evolved in one of these, which they called Clade 3. Clones that had been found to be potentiated in earlier research were distributed among all three clades, but were over-represented in Clade 3. This led the researchers to conclude that there had been at least two potentiating mutations involved in Cit+ evolution. [5]

The researchers also found that all Cit+ clones had duplication mutations of a 2933 base pair segment that were involved in the gene for the citrate transporter protein used in anaerobic growth on citrate, citT. The duplication is tandem and resulted in two copies that were head-to-tail with respect to each other. This duplication immediately conferred the Cit+ trait by altering the regulation in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk. The new promoter activated the expression of the citrate transporter when oxygen was present, and thereby enabled aerobic growth on citrate.[5]

Movement of this rnk-citT module into the genome of a potentiated Cit− clone was shown to be sufficient to produce a Cit+ phenotype. However, the initial Cit+ phenotype conferred by the duplication was very weak, and only granted a ~1% fitness benefit. The researchers found that the number of copies of the rnk-citT module had to be increased to strengthen the Cit+ trait sufficiently to permit the bacteria to grow well on the citrate. Further mutations after the Cit+ bacteria became dominant in the population continued to accumulate improved growth on citrate. The researchers concluded that the evolution of the Cit+ trait suggests that new traits evolve through three stages: potentiation (making the trait possible); actualization, (making the trait manifest); and refinement (making the trait effective).[5]

So, where is the new information came from again?

From mutations in the DNA of the lizards. But until the research is done the exact mutations remain unidenitfied.

There is no question they have evolved. The question is did they gain new information and new mechanism. According to you ignoranceMeaning you can’t tell the difference between the before and after they were taken to the island, right?

Yes they gained new information and a new mechanism because they gained new a morphological feature not present in other populations. It is easy to tell the morphology changes because they have been reported, the genetic changes will need further work to identify.

Neither one! So, these group of skinny malnourished people gain new genetic information and new mechanism after 100 years is what you meant?

This is just stupid. Malnourished people who move to an area with high food levels do not undergo changes in morphology. Having a higher average body weight, or avoiding growth restrictions is not a change in morphology for the simple reason that those things are a direct result of nourishment levels, lower the nourishment levels and the conditions reappear.

Find some people whose underlying bone structure changed or who developed new physical structures and then you could try making this argument.

 

[Shad]

You are just guessing. Please read the report.

Nope considering the changes are even hosted by employer

Evo-Ed: The Evolution of Citrate Use in E. coli

What change are you talking about or at what generation?

Thought you read the paper. In LTEE population #9 around the 32000 generation

And if you return them into the glucose environment, will they change back into the old mechanism or is the mechanism was there all the time? Have you ever thought of that?

Not quite right as per

Evo-Ed: E. coli Ecology and Phylogenetics

Cit- phenotype changed into Cit+ phenotype, but did the genotype change also?

The groups began to diverge as per the link above and

Evolution of competitive fitness in experimental populations of E. coli: what makes one genotype a better competitor than another? - PubMed - NCBI

 

[gnostic]

You ask for explanation, so Jonathan180iq provided some links that explain mutations, and then you state:

Enough with the rhetoric please. Summarize those links on how you understand them then I would be interested in reading your post.

I don't know if you understand Jonathan's brief explanations or ignored his reply in post 3103 shortly after, and even Monk of Reason chipped in with a reply. Monk have also provided sources via links, in previous reply.

Show me the link or links if you have one..

But clearly you have ignored monk's links too.

You want explanations, so he has provided some credible scientific sources, but you don't want links, but when explained in their own words, you don't want them or you have ignored them, but then you turn everything around, and now you are saying to provide links, but links that you have already ignored previously.

You keep moving the goalpost around, back and forth. You are essentially being a hypocrite - you are making them jump over hoops, and when they do, you say it is not good enough, and make them jump more hoops.

What do you want, JM2C?

Do you want explanations (or summaries) or not? Do you want links or not? Do you want scientific sources or not?

Make up your bloody mind.

 

[Deathbydefault]

Actually, I'm against all pedophiles, regardless of religious or cultural backgrounds.

It doesn't matter if it occur in Afghanistan or here in Australia. Pedophiles are vile, as are rapists.

And it doesn't matter if a man or woman, who commit pedopilia upon boys or girls, but male pedophiles occurred far more frequently than women.

Perhaps, I am bit of sexist that I would recommend castration of men, but not that of women, who commit the same types of crimes. Jail sentences for women pedophiles, will do.

This reply somehow got lost in my alerts, so I'll give my reply now.

Let me make this clear to you, I am okay with two consenting people regardless of age gap having sex, so long as the younger is above the age of 13 and is physically able, along with mentally capable, to consent.

That is my stance.
If the younger party is below the age of 14, hasn't hit puberty, or isn't physically or mentally capable of consent, then it's a no go.
Otherwise, I am fine with it.

I have recently found out my girlfriend is pregnant.
I am not considered mentally capable of being a father, so I am suggesting abortion.
Of course I will take responsibility if she disagrees and decides to keep the child.

I'm certain I will have no issue with my child dating at the age of 14.
(But, like I said, I am not mentally capable of being a father.
Not in American society anyways.)