Hunter: Finally, the Details of How Proteins Evolve

I disagree. The output is consistent with random genetic change and selection.

Show the math. It will appear just as did @Chris_Falter’s excellent post.

It has nothing to do with the math it is about the mechanism being a credible cause of what is observed. We observed known cellular mechanisms over many cell divisions generating the functions observed.

What we did not see is a new proteins sequences that would be required to build a flagellum de novo.

If a protein sequence evolved relatively recently de novo from non coding DNA, what evidence should we expect to be able to find in closely related species?

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LOL! Offering “science” from Sal Cordova is like offering “science” from Ken Ham or Kent Hovind. :smile:

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To let everyone else in on the “inside” story, as it were:

The research I am referring to deals with the movement of DNA from the chloroplast to the nucleus in higher plants. It turns out that one can assay for this by placing a transgene in the chloroplast genome that has nuclear (eukaryotic) gene expression signals - promoters, poly(A), among other things. If the transgene codes for an enzyme that confers antibiotic resistance, then one can monitor gene flow from the plastid to the nucleus by screening for resistance to the appropriate antibiotic.

Typically, this sort of study is done by linking the nucleus-enable marker gene with another marker (resistance to a different antibiotic) that is expressed in the chloroplast. This is how one can select for trans-plastomic plants that carry foreign DNA in the plastid genome. This second marker has chloroplast (prokaryotic) gene expression signals, and will not usually be expressed if it finds its way to the nucleus.

The process that moves the nucleus-enabled marker to the nucleus also will carry along linked DNA, such as the chloroplast marker. So, if one first identifies plants that have had the nuclear marker move to the nucleus, and then ask how frequently the second antibiotic resistance marker is expressed (again, a simple selection on suitable media), then one can get a handle of the frequency with which the second marker captures promoters in the nucleus. Long story short - this happens often enough that it can be detected in the laboratory. Which means that, contrary to what ID proponents claim, this sort of event is not fantastically improbable.

There are details I won’t elaborate on here, but they speak to mechanisms that are generally in operation in eukaryotes (and not plant-specific). Beyond this, these studies are all very interesting, and have important ramifications for plant biotechnology.


The event in itself may not be improbable because of the specific circumstances and the mechanism that is causing the resistance.

You left out the role of selection, which would have made the existence of Cornelius Hunter far more probable. Certain even. No need to even consider the role of chance.

There is no need to do a probability analysis as the mechanism that created CH is known and deterministic.

I don’t understand your argument, Mung. Could you elaborate? As you explain, please address the widely accepted axiom that prospective probabilty and retrospective probability are vastly different.


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If we can invoke selection then the probabilities just don’t matter.

You wish to discuss philosophy?

Are you sure @mung? That is not the case as far as I know.

That is not true.

This is correct @Chris_Falter. You got it.

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I’ve got to give it to you, Mung, you can google with the best of them.

Readers of this thread will probably find your contributions more convincing if you engage the details. Linking to a 30-page reference article doesn’t help us understand your argument very well. Or perhaps others are different, so I’ll just say I don’t understand how the reference article pertains to our discussion here.



Which would be the mechanisms that ID proponents insist are fantastically improbable. Why do I need to be repeating this?

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My contention is that the science of human sexual reproduction leads to 10375 possible outcomes in the fourth generation. In the mid-19th century when CH’s great-great-grandparents were alive, would it have been possible to use deterministic mechanisms to predict that Hunters named Georgina, Charleze, Ida, Carli, Frangipane, Larry-Boy and (insert 10375 other names here) would not be born in the fourth generation, but the Cornelius we know and love would serendipitously be born?


So you have established that the Darwinian mechanism is responsible for the antibiotic resistance? How many nucleotides are involved in the mutations? What is the reason that given mutation rates and sequence lengths this becomes more probable then other examples. Are the sequence lengths shorter?

Looks like a new challenger for the position of board sealion. :slightly_smiling_face:

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Sure but they all lead to a functional human being if the process is completed. We can eliminate the darwinian mechanism here as we understand it is a deterministic process that creates a new human.

@colewd, please stay on topic. If you’d like to start a new argument, go start a new topic.

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Apparently my summary of the experiments I refer to was a bit too confusing. Unfortunately, I don’t know where to start with these questions. They have nothing to do with what I was describing.