It is based on population growth over time.
It’s already in the discussion. I surprised you cannot see it.
This is the sequence problem waiting problem challenge that exists in populations. Genes/proteins are made of sequences and populations have a waiting time to fixation. This is why there is no current model that explains the gene patterns in primates.
Your opening statement was categorically false.
So, the answer is no, then. You don’t know what the LTEE is.
You have not linked a single paper, so either you forgot to link your experimental evidence or you’re admitting that you have none. The only thing you linked was a critique of Axe (2004), which… needless to say, does not support your point.
Yes.
Yes, which is 4Ne for neutral mutations according to neutral theory.
The fact that genes are made of sequences, and mutations have a waiting time to fixation, is why there is no current model that explains gene gain and loss? First of all, it’s categorically false that there are no models of gene gain and loss, we’ve already provided multiple mechanisms to you that can explain that. You’re just ignoring it.
Second, why does the fact that genes are made of sequences and that mutations have a waiting time to fixation provide a challenge to gene gain and loss? That’s frankly idiotic. You have not provided a single piece of experimental evidence showing that genes cannot be gained or lost, whereas I and others have provided many papers showing that functional proteins are not rare (at all) in sequence space and, as a consequence, that there is no real waiting time problem.
There are a thousand people on this forum experiencing deja vu now. Many have been just where you are standing. There is no visible end. You will explain this again, he will respond with a variety of non sequiturs and distractions again, and in a while someone else will have this argument with him, revealing that not one word of anything you said was absorbed.
This type of experience is not uncommon with ID proponents. But it is rarely experienced in so pure a form.
As I pointed out in the other thread, conversations with Bill tend to go like this:
Evolution proponent: A is evidence for common ancestry.
Bill: But what about B?
Evolution proponent: B doesn’t even address A, and even if it did, B is wrong because C.
Bill: But have you considered B?
Evolution proponent: No, B is wrong because C, D, E.
Bill: You’re just ignoring B because it contradicts your model.
I’m mostly just continuing this conversation for the benefit of open-minded people who read this thread now or in the future. I was one such person as a YEC and it’s because of conversations like these that I realized evolution and common ancestry were true. But there probably comes a point when we’ve hashed out the same points enough times for it to become ineffective.
I know what the LTEE is and I have read about it and watched its progress over the years. It is a good simulation of what happens in populations.
It’s in the papers you linked. They are working through the sequence challenge and the Lenski experiment shows the frequency of fixation.
Andrew, there is no model here. If this was straight forward there would be.
The experiments you cited are not showing genes/proteins gaining advanced function only basic binding. The Axe experiment showed the break down of an antibiotic in an organism. Axe’s experiment is trivial compared to many vertebrate proteins where they are binding with dozens of other proteins to perform one or more functions.
The experiments also are not simulating what happens in a population where genes are lost due to drift or negative selection.
For a population to find a new protein it has to deal with the reality it is searching through a sequence and the search will take additional time due to drift, purifying selection and waiting for a gene duplication in certain cases. This is a big challenge for building a model based on a mechanism that is not deterministic. A deterministic mechanism bypasses the search problem.
Then why did you say:
Both of which are categorically false statements about the LTEE. It is indeed in a lab, and it is not primarily about population growth over time.
There’s no challenge. What these papers show is that functional sequences are far, far more common than Axe (2004) concludes that they are. He’s off by a whopping 68 orders of magnitude, at least.
…in a population of slow-mutating E. coli which is under no selective pressure. Yes, that’s bound to be representative of natural populations of multicellular eukaryotes. Do you not see the problem with extrapolating from the LTEE in this way?
That is absolutely false. Two of the studies I cited specifically looked for enzyme catalytic activity (esterase and β-lactamase), not merely ligand binding. And anyway, ligand binding is a valid protein function, so that is a non sequitur.
The point of the experiments was to find the approximate proportion of specific functions in protein sequence space, not to look at the evolution of proteins in actual populations. Unfortunately, actual evolution on this scale (at least in multicellular eukaryotes) happens too slowly to observe it in real time. However, we have seen new functional proteins evolve in real time in bacteria (Okada et al. 1983; Prijambada et al. 1995; Crawford et al. 2007), in viruses (Strebel et al. 1988; Smith 2007), and in maize (Rhoads et al. 1995; Beyer et al. 2022). All in the last century.
My guess is you’ll try to invalidate this by saying that bacteria, viruses, and plants are somehow exempted from the sequence and waiting time problems. Or you’ll regurgitate some DI article that ‘refutes’ these claims but has already been debunked. That’s the route that most ID/creationists seem to take.
You have not provided any quantitative reasons, based on experimental evidence, for me to believe this. Meanwhile I have provided much quantitative, experimental evidence that shows that these are not actually problems. Until such a time as you provide real evidence for your baldfaced assertions, I see no reason to take them seriously.
Looks like word salad, but I’ll try my hand at understanding this. Do you mean that a deterministic mechanism of evolution would somehow be unaffected by the claimed sequence and waiting time ‘problems’? Do you not realize that the laws of physics are deterministic? Do you not realize that an intelligent designer would not be deterministic – assuming you believe in libertarian free will, which I presume you do?
Even if we bypass the fact that this is a baldfaced assertion with no evidence to back it up, this doesn’t even support ID. You are not even wrong.
Note also that nothing so far is relevant to the supposed subject of this thread. But that is Bill’s most basic and persistent misunderstanding.
Yeah, very good point. @colewd, can you provide evidence that all organisms do not share common ancestry? Not evidence against unguided processes working in tandem with common ancestry, but evidence against common ancestry itself? Note that your gene Venn diagrams are not evidence against common ancestry; even if unguided processes cannot cause gene gain and loss (although they can), this does not have any bearing on common ancestry itself.
Fascinating new paper. Makes many of the same points and referencing the same research we’ve been trying to get across to people like @colewd around here for years.
Will it help? No. 
What an idiotic point. Creationists need to get over their insanely stupid and ignorant understanding of the Lenski experiment.
In the Lenski experiment they didn’t evolve nylonase enzymes(which evolved by duplication and divergence in nature) because the waste products of nylon manufacture wasn’t present in the Lenski experiment. They also didn’t evolve resistance to chloramphenicol (which bacteria in nature have). And they also didn’t evolve the ability to degrade D-arabinose (which bacteria in other experiments have), or innumerable other organic compounds not present in the growth medium.
The environment used in the Lenski experiment is literally the simplest one possible that allows growth for E coli. They use minimal medium, it has only and exactly the smallest known compounds that E coli needs to grow and divide, and the temperature is kept constant at the optimal level for growth. It has nothing else. The bacteria experience no condition in that experiment they don’t also experience in the mammalian gut. That means whatever they could possibly adapt to in that experiment they have had hundreds of millions of years to adapt to in nature. It selects almost exclusively for growth rate, which most strongly favors genome reduction since this is the primary bottleneck to speed of replication.
You are aware that in natural environments you also have to do stuff like survive periods of dessication, starvation, cold, heat, predation, pollution, radiation, viruses and other forms of predation, etc? And that in natural environments you encounter many novel compounds of much greater complexity, and that all the conditions fluctuate up and down in degree, and some come and go?
Experiments that select for novel genes are known. Simply make a novel environment containing conditions not before experienced by E coli. One of those is a citrate only carbon source environment. Now suddenly genes that favor metabolic processing of citrate are selected for. Massive gene duplication numbers are favored for genes that affect citrate metabolism. I’ve cited the paper to you before numerous times. In several replicate lines the bacteria evolved hundreds of duplications, with some lines increasing their total genome size by 15%.
Please get your synthetic and volitional dementia under control.
Nobody gives a fork about what you consider “advanced function”. If the function is new and is conferred by a protein sequence that is at all different from whatever came before it, it’s a new gene with a new function.
No it didn’t. Axe never characterized any chemical reaction in his experiment. All he ever did was observe whether colonies formed on agar in petri dishes.
You don’t even know or understand the supposed penultimate pro-ID experiment. Is there no subject upon which you will not make a fool of yourself?
Why would you compare an experiment to a protein? They’re two entirely different things. One is a material biological object, another is a process constructed to aid observation.
What experiments are you referring to?
It just has to duplicate one that already exists and then one of the two copies must suffer a mutation that changes the sequence of amino acids. Then a new gene has evolved. There’s now two genes where before there was one, and one of the copies is different from what it’s ancestor was like. Hence new, and therefore a new gene. By any rational understanding of the word new.
Nylonase, T-URF13, VPU1, etc. It happens all the time in nature. Your hurdles are imaginary and of no value or consequence.
Actually in this case Bill is (sort of) right. Axe grew his E. coli on an agar plate with a few penicillins (chloramphenicol and ampicillin) on it. He then observed whether they grew on the plate despite the presence of the antibiotic, in order to estimate whether their β-lactamases were functional (since β-lactamase catalyzes the breaking of the β-lactam ring in penicillins).
This doesn’t help Bill’s point at all, since he’s ignoring the fact that a different experiment tested for the same type of enzyme (β-lactamase) and found the prevalence of β-lactamase within sequence space to be ~1 in 5.4 * 10^8 (Shahsavarian et al. 2017), showing that Axe’s ridiculous number of 1 in 10^77 is off by at least 68 orders of magnitude.
But Bill is right that Axe grew his E. coli in the presence of antibiotics (although he may not understand why).
I know. One problem is we technically don’t know whether growth is only allowed due to activity of the enzyme, or came from some other mechanism (some other spontaneous mutation for example). So the conclusion that growth is due to enzyme activity on the antibiotic is an inference. It’s not that the inference is unreasonable (it seems the most likely explanation for why growth occurs), but the conclusion is still subject to some doubt.
More importantly however, and crucially one of the most significant flaws of Axe’s experiment is that he subjects the bacteria to the MIC(minimum inhibitory concentration) of antibiotic. That means E coli can’t grow without having some sort of resistance already, as the concentration of antibiotic inhibits growth. This prevents colonies from forming in the first place, it does not merely reduce growth rate. This is an unrealistic condition because it does not allow weakly active enzymes to confer a selective advantage to the bacteria. It selects only for large-effect mutants that give high enough-level resistance to allow growth under the MIC. This synthetically reduces the number of mutants that could elevate the enzymatic activity and would give bacteria a growth advantage under conditions of lower level antibiotic exposure.
Axe should have done experiments at much lower antibiotic concentrations, and/or he should have characterized enzymatic activity by purifying the mutants and doing activity assays.
He doesn’t do this, and he uses a synthetically temperature-sensitive variant of the enzyme because these factors strongly inflate the degree to which it seems like “functional” mutants are rare. The experiment was designed to fail. Axe bullshits a lot in the discussion to camouflage this fact. His ID fans are too stupid to understand these flaws in his experiment.
Yeah, Axe’s experiment was pretty terrible. And yet ID proponents will continue to tout it as the perfect proof of ID, ignoring all the other experiments that show that Axe is way, way off. Just yet another example of why ID is religious propaganda and not true scientific inquiry.
Can you provide a citation here? I’m sure you’ve done so elsewhere but I’d like to get a look at that paper. Thanks.
We identified another set of parallel amplifications in six evolved genomes. These amplifications are large and highly variable in extent, but all include at least the fdnI , yddM , adhP, maeA, rpsV, and bdm genes. These amplifications were often present in high copy numbers. Three DM25-evolved genomes have 2–13 copies, and three that evolved in DM0 have 28–59 copies (Table 2). In one case, ZDBp889, the amount of DNA in the amplified region constitutes more than 15% of the total evolved genome (Figure 13). By contrast, the amplifications of citT and dctA contain an average of 4–5 and 2–3 copies, respectively (Tables 1 and 2).
Hi Andrew
Common ancestry explains similarities. The evidence against common descent is easy when you do not invoke God as a guiding force. When you invoke God then the evidence against it is more difficult but there are certain transitions that don’t appear to make sense that reproduction as a mechanism was used. An example is the origin of the eukaryotic cell which is radically different in architecture then the prokaryotic cell.
Wait. If you don’t invoke God, what’s your alternative to common descent?
Are you intending that to be evidence against common descent? You will have to explain why.
