Lenski addressed this paper several years ago
From the Intercept article you cited:
None of the viruses listed in the write-ups of the experiment are related to the virus that causes Covid-19, SARS-CoV-2, closely enough to have evolved into it.
So I’ll go with what the article actually says and recommend that you do the same, @DaveB.
The PubMed article is certainly interesting, but given that the Wuhan Institute research was documented not to do anything remotely close to the recombination events that gave rise to Sars-Cov-2, the article gives exactly zero support to any theories involving Fauci or the Wuhan Institute.
What we are left with is 100% pure speculation:
You will have to forgive me for not counting this as evidence, but I don’t.
That leaves us in our original status, as far as I can tell:
Authorship list for the Rapid Evolution paper:
Van Hofwegen loves sharing his passion for God’s creation with students and colleagues. Sharing these research interests, motivation, and excitement with students greatly enhances what they are learning in the classroom. He is especially committed to partnering with students in their development as Christian disciples and scholars who seek to advance God’s redemptive work in the world.
So far as I can find, this paper in Van Hofwegen’s only publication in a mainstream journal. He has interviewed with Jonathan Witt of the Discovery Institute and appears to be a supporter.
Scott Minnich may fairly be described as an ID activist and features as a poster child for suppression, having testified at the Dover trial, and engaging in questions concerning the Lenski experiment and bacterial flagellum.
Carolyn Hovde Bohach is a colleague of Minnich at the University of Idaho. I cannot find anything at all directly concerning her views on origins.
I described the mutation in an earlier post, but here is a graphic of it. The mutation creates a new section of dna which places a copy of an existing citrate transporter gene downstream from a copy of an existing promoter which is active when oxygen is present.
E - Wikipedia.coli_long-term_evolution_experiment#/media/File:Novel_rnk-citT_module_and_citT_expression-_actualization_of_Cit+_trait_in_LTEE_population_Ara-3.svg
The expression of the existing transporter gene is what is being switched on. Once the transporter is produced, the E. coli can take in citrate as food.
The key is “when the right conditions occur.”. As the Minnich paper states: “We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event”.
In other words, the way that the LTEE was set up prevented the right conditions from occurring. Perhaps procedures weren’t followed correctly for the one strain that developed the mutation.
In any case, Minnich showed that under the right conditions, the mutation happened repeatedly and in a short amount of time.
You have not answered my question. I repeat, what “mutation was consider[ed] new and unique”?
Stop saying nonsense please. The citT gene can always be expressed regardless of oxygen levels. However, in the presence of oxygen, there is marked repression of citT expression preventing effective uptake and metabolism of citrate as a carbon and energy source. I repeat, the trait can always be displayed, but it is effectively suppressed under oxic conditions. The E.coli lineage which could take up citrate at physiologically significant levels under aerobic conditions bypassed this suppression by having a duplicate of its citT gene placed downstream of a constitutive promoter. This “switched on” narrative of yours is probably a product of you getting information about the LTEE from a creationist or ID source and it is BS.
Clarifying a few things here should prevent misunderstanding this comment. When it said that the expression of or gene cluster such as the citT operon is repressed, it doesn’t mean that the operon is fully turned off. It just means its expression has been been dialed down to levels of no consequence to the cell. Similarly, when the expression of an operon is induced, it doesn’t mean the repressors have all been tucked away into some corner: it really means the level of repression is too low to be of significance to the cell. Its a matter of the level of gene expression.
Or maybe Minnich screwed up in his methodology. Given the respective CV’s of the two groups, that is by far the more likely scenario.
In any event, it’s difficult to see just what Minnich thinks this would demonstrate even if he were correct. If undirected evolutionary processes are MORE likely to produce this particular complex adaptation than Lenski’s study would indicate, exactly how does that support Minnich’s belief that evolutionary processes cannot produce complex adaptations?
There is zero evidence that the cells in the LTEE are able to “actively initiate” the mutations that cause the Cit+ phenotype. Rather all the evidence shows simply that it is the selective pressure, that is the particular environmental conditions, that ensures certain mutations are favored over others. Hence it’s a textbook example of evolution by natural selection.
Short amount of time is totally relative, it’s still trans-generational change that occurred due to spontaneous mutations being subject to drift and selection, over several weeks to months.
Nothing about the fact that something evolves faster under particular conditions, can be meaningfully said to constitute a “programmatic” response, any more than me being able to roll 6 on a die over and over again - if you give me enough throws of the dice - make that a “programmatic” response.
Again, a textbook example of natural selection. Some mutations are favored under some conditions, and not favored under other conditions, so if some particular adaptation is dependent on mutations with particular effects, that adaptation will evolve more quickly under the conditions that favor those mutations over others, since then they can be driven to fixation by their effect on competitive fitness, rather than by genetic drift.
If it really was a “programmed” response to a particular setting one wonders why all the required mutations weren’t immediately instantiated at the very first generation these conditions were encountered. It should have taken at most two hours to evolve then. It does not make sense to describe a transition occurring over hundreds of generations of accumulating mutations as “programmed”.
I think @DaveB must have been referring to the research which shows the rate of mutation can jump in some bacteria when certain environmental stresses increase. IIRC, the DNA repair mechanism seems to be hindered by such stresses, with the result that the ability to find novel solutions for the environmental stress increases. I do not have a link to the research on this issue, but I remember reading a paper or two about it.
Of course, one can readily understand how the coding of the DNA repair mechanism could evolve as an adaptation to severe environmental stress. In other words, this phenomenon is not in the least an enigma to evolutionary biologists, as far as I can tell.
He could have had that in mind, but the specific point where he invokes a “programmatic” response concerns the LTEE, and he’s been talking about the contrast in the speed of evolution of the Cit+ phenotype as it occurred in the LTEE and in the Minnich et al experiment as if this shows the Cit+ phenotype to be something that was programmed. This is an all too common creationist response, and it’s wrong.
I’m not just talking about the speed that the mutation happens, I’m talking about the fact that the new region of DNA that enables the cit+ trait is the same in all cases.
How can that be the result of a random mutation?
Your bias is showing. You could have avoided this if you had read the blog post that was linked to by @Michael_Okoko.
From Lenski’s post:
Let’s begin by saying that it’s great to see other groups working on interesting systems and problems like the evolution of citrate utilization in E. coli .
Moreover, the actual science that was done and reported looks fine and interesting, though we have a few quibbles with some details that we will overlook for now. By and large, the work confirms many of the findings that were reported in our papers cited above:
You will have to explain how a random, undirected mutation can occur over and over.
Is there really a meaningful distinction between “dialed down to levels of no consequence” and fully turned off?
Maybe you can explain it to Lenski.
The inability to use citrate as an energy source under oxic conditions has long been a defining characteristic of E. coli as a species (35, 36). Nevertheless, E. coli
is not wholly indifferent to citrate. It uses a ferric dicitrate
transport system for iron acquisition, although citrate does not
enter the cell in this process (37, 38). It also has a complete
tricarboxylic acid cycle, and can thus metabolize citrate internally during aerobic growth on other substrates (39). E. coli is
able to ferment citrate under anoxic conditions if a cosubstrate
is available for reducing power (40). The only known barrier to
>aerobic growth on citrate is its inability to transport citrate under
>oxic conditions (41–43).
Why doesn’t he say “inability to transport enough citrate…”?
When we toss coins, they keep coming down either heads or tails. That happens over and over, even though the coin tosses are random and undirected.
It isn’t the same, it was different in every single replay-experiment (though 8 of these are similar duplications from the same region), see figure 7 in this paper:
All that means is that this region is likely to be prone to duplication because of some factors intrinsic to the sequences here (mispaired strand slippage, unequal crossover, or stuff like that), but even these specific duplications are not identical. Often times entirely different promoters were captered. See the discussion also:
The Cit+ mutants arose by diverse mutational processes (Supplementary Table 12). Eight have citT duplications similar to the original one, though no two share the same boundaries (Fig. 7). In seven of these, the duplications generated alternative versions of the rnk-citT module; in the other, the second citT is downstream of the rna promoter. Six mutants have an IS 3 element inserted in the 3’ end of citG (Fig. 7). IS 3 carries outward-directed promoter elements that can activate adjacent genes27,45. Two mutants have large duplications encompassing all or part of the cit operon. One mutant has a large inversion that places most of that operon downstream of the promoter for the fimbria regulatory gene fimB , and another has a deletion in citG that presumably formed a new promoter. Also, most of these mutants have stronger phenotypes (Supplementary Fig. 5) than the earliest Cit+ clones in the main experiment (Fig. 4b, Supplementary Fig. 3). In any case, this new function arose in potentiated backgrounds by a variety of mutational processes that recruited several different promoters to allow CitT expression during aerobic metabolism. Thus, these data do not support the physical-promotion hypothesis, whereas the strain-specific differences in growth on citrate conferred by the rnk-citT module provide clear and compelling evidence for epistasis (Fig. 6). However, these hypotheses are not mutually exclusive, and we cannot reject the possibility that some mutation rendered the genome (or the affected region) more prone to physical rearrangements (including mobile-element insertions) and thereby also contributed to the overall potentiation effect.
Here’s supplementary table 12:
Even if it was the same, that could still be the result of random mutations. If the same specific A->C substitution somewhere in the genome is highly beneficial under some specific circumstance, then even though that specific mutation is rare and random (it might only occur once in every 10-10 cell divisions, say), with enough cell divisions you’re bound to get it again and again, and when the organisms that get that mutation find themselves in the environment where it is beneficial, it can be favored over and over again.
He obviously didn’t read the actual paper.
That doesn’t address my concern.
And to this question:
how is this even conceivably intended as an answer?
Not even Minnich questioned that the mutations were random and undirected.
And, again: This new trait only arose in one of the 12 lineages in Lenski’s study after over 30 years. So your claim that it arises “over and over” is simply false.
Yes there is a huge difference with regards to what really happens in cells. The “switch on or off” talk is only an approximate description of what happens in cells. It is a neater but less accurate way of describing the regulation of gene expression.
A good example is seen in the regulation of the Lac operon (the citrate transporter gene is also part of an operon, the citrate operon). The Lac operon allows bacteria like E.coli utilize lactose as an energy and carbon source. In the absence of lactose, a repressor protein binds the operator region of the Lac operon and physically hinders the downstream transcription of the Lac operon genes by RNA polymerase. This hinderance of transcription of the Lac operon genes would also be described as “switching off” the expression of the Lac operon genes.
However, when you do experiments to check this, you find out the Lac operon is still expressed, albeit at a very low level despite being said to “switched off” and this was shown in 1961 by Jacques Monod and colleagues. Look at the graph below and see for yourself.
Look at the section of the graph when the inducer is removed. We can see a very low, but non-zero expression of the beta-galactosidase gene in the presence of stringent repression. This is called leaky gene expression. Leaky gene expression occurs at varying levels for different operons: for example, the lac operon is notorious for this, not so for the ara operon.
Its likely he knows this and uses the approximate terminology just like it is done in chemistry and other scientific fields.
PostScript: I found a much more recent article on the “basal expression” of the lac operon despite being repressed or switched off. Enjoy the graphs!
@DaveB, when we real scientists refer to “reading” a paper, they generally mean the data in the paper, not the words written about the data. The figures and tables come first. Michael’s points are derived from that sort of “reading.”
You’re looking at the words and apparently ignoring the data.
[quote=“Mercer, post:267, topic:14233”]
I hope this doesn’t include me. I have a degree in biochemistry but I don’t consider myself a scientist, yet.