Interview with Scott Minnich regarding Lenski LTEE

This was a technical discussion of a paper by Van Hofwegegen, Hovde, and Scott Minnich that covered a series of experiments that refuted Lenski’s claims of LTEE:
https://journals.asm.org/doi/10.1128/jb.00831-15

John Roth of the National Academy of Sciences supported Minnich’s results:
https://journals.asm.org/doi/10.1128/jb.00110-16

Sure, he supports the “results.” All that means is that he believes Minnich accurately reported his observations from the lab, rather than just making them up.

However, how did Roth interpret those results? With my emphasis:

We suggest that the primary message of the paper by Van Hofwegen et al. is that the series of events used to explain adaptation in the short-transfer LTEE (and in speciation) might need to be revised. The amplification model supported by this article has already be proposed as a means of evolving new genes (17) and has been experimentally shown to be capable of generating a novel genetic function within as few as 3,000 cell generations (18). Both of these processes are arguably more difficult to achieve than the ability to activate a single silent gene. It would appear that the delay in the LTEE may not reflect need for a neutral potentiation step but the difficulty of intermittent selection acting on frequent copy number variants. The bottleneck in serial dilutions is hard to traverse when initial improvements are due to an unstable copy number variant that is counterselected during the intervening rapid growth period.

Oh dear. How awkward and embarrassing this must be for you.

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There is no refutation of anything Lenski has said about the LTEE in that article. John Roth pondering the role of contingency in the LTEE isn’t a refutation in any sense of the word. Incidentally there isn’t anything wrong with Lenski’s take on contingency in the LTEE.

Rather, it seems to refute your claim that selection makes no difference to how fast an adaptive trait can evolve.

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Reference 18 is this one:

We had several threads on this forum devoted to explaining the damage control and panic-spawned lies output by the Discovery Institute in response to that paper, since it so directly refuted so many of their claims. It’s also, incidentally, a demonstration of what @colewed claimed in the other thread is just speculation: the real-time evolution of a gene with a novel function through duplication and divergence.

I remember those threads well because I had to go into the methods of the papers and explain to Ann Gauger how she got several simple facts about those experiments completely wrong. Funny.

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novel genetic function is not necessarily a new gene family with no homology to other genes. We can easily make homologs of pre-existing genes. Conserved Domain Database is able to make distinctions between real novelty (as in no homology) vs. homologous changes.

What’s embarassing is you don’t appreciate the distinction.

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If you bothered to actually listen to the interview, you’d realize Minnich pointed out there was no new classes of genes/proteins.

That’s the problem with loose language and definitions. That is also prevalent in the defintion of fitness.

That doesn’t contradict anything John Roth said, nor Faizal’s quotation of him. He didn’t say there were “new classes” of proteins in the LTEE, he said duplication is part of the process by which genes with novel functions can evolve.

Who cares whether that qualifies as a “new class”? It does not matter to the bacterium that gains a novel function by divergence of a gene, that some researcher or algorithm interprets the gene as belonging to the same “class” as it’s parent.

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Are you including under that heading new gene families with homology to genomic sequences that aren’t genes? Or do you demand no homology to anything in the same or any other organism? If the latter, can you provide examples?

Gene duplications can evolve new functions of certain classes, but not other classes. There needs to be appreciation for what real novelty is, that is, something that can be distinguished by tools such as CDART! If one can detect a gene duplication, then that isn’t real novelty is it?

On the left is a human collagen, on the right is a human zinc finger protein. Do any of you think gene duplication followed by mutation will evolved these protein architectures from a common ancestor?

Just because gene duplication can make some novelty doesn’t imply it will make the sort of evolutionary changes required to explain real novelty such as that above, and those which Minnich said were absent in Lenski’s experiments.

Worse for Lenski, his lines were LOSING genes. That isn’t really emphasized enough.

Yes it is. If there is something in the descendant D not found in the ancestor A, then that thing in D that is not in A is novel. Hence it is real novelty.

Compare:

  1. It doesn’t matter that everything else in this sentence is the same.
  2. It doesn’t matter that everything else in this sentence is the same, this part is new.

A novelty. Real novelty.

While on the topic of similar sequences exhibiting novelty, chew on this:

Do they have to?

There are ways of getting lots of divergence (over longer periods of time), and other ways of generating novelty than by small changes accumulating in an already existing gene.

Evolution isn’t a theory that says any particular protein coding gene can be directly converted into any other incrementally. It just requires that some genes can be changed into others, and that there are some ways for de novo evolution of “entirely new” genes.

It isn’t required to, though it can explain really large amounts of divergence too. In fact we know of genes that have diverged below the level of sequence similarity expected by chance, that nevertheless still adopt the same structures and perform the same functions.

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Obviously.

So now Humpty Dumpty is going to make up his own personal definition of “novelty” in yet another desperate attempt to save face.

Don’t you get it? You’re not among your fellow creationists here. The folks here understand basic logic and science. They aren’t fooled by your silly word games.

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Conserved domains and absence of homology which can be discerned by tools such as CDART and even BLAST, etc.

So, do you think these two architectures evolved from a common ancestral form via gene duplications from a common ancestor?

If not, you’ve exactly made my point, that there are classes of novelty not reasonably evolvable via gene duplication from a common ancestor.

BTW, gene duplication that causes a promoter capture isn’t evolution of a new gene. Do you know the distinction. If you bothered actually watching the interview you’d know the difference.

And you responded to my post in far shorter time than it would take you to actually watch the interview and read Minnich’s paper and Roth’s paper.

Perhaps you should be more careful before you respond. Otherwise you’re not really engaging the points very effectively. :slightly_smiling_face:

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Sure.

There is insufficient information there to form an opinion, at least based at my level of expertise.

That does not follow. Even if we grant that those two genes are not homologs, it does not follow that one of them could only exist if it was magically poofed into existence by Baby Jesus, as you believe, or any other similar process by which it comes into being without being derived from antecedent genetic material.

Do you need me to explain further why not?

If it is a DNA sequence that produces a function that did not exist previously, then it is entirely reasonable to call it a new gene. Regardless of whether Humpty Dumpty agrees.

I have read those papers previously. And, unlike you, I was able to accurately and honestly reflect their content. Why is that difficult for you to do, if you have read the papers you cite?

And I have no intention of wasting precious minutes of my life watching a bunch of proven liars lie on video. I’m too old for that.

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Yeah, it’s obvious you’re not speaking from a viewpoint of even minimal requisite expertise. Thank you for the admission.

Those tools cannot detect the absence of either. We know that because we can see statistical significance disappear in domains and whole genes for which we are certain of structural continuity.

So why are you falsely claiming they can?

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And yet, despite your professed expertise, here I am running circles around you and exposing your foolishness with ease. To the point that you simply resort to an ad hominem rather than engaging any of my substantive points.

Imagine that.

And, in light of Mercer’s response above, we have to wonder how much of your supposed “expertise” is just bluff.

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Here’s an example of a family of proteins containing members that have diverged below 5% indentity:
Kinch LN, Grishin NV. Expanding the nitrogen regulatory protein superfamily: Homology detection at below random sequence identity. Proteins . 2002;48(1):75-84. doi:10.1002/prot.10110

On similar sequences producing different structures:

On how to get novel functional proteins by mechanism other than duplication and divergence:

He has none. He just posts pretty figures and frames them in pretentious technobabble, and can copy-paste data into search fields on websites. He has no idea how to evaluate the results and know nothing of the underlying principles.

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Gee. Who does that remind me of…

His pupil, Bill Cole?

Ah, yes, that’s who. Thanks. :wink:

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