If the evidence is so strong, you should be able to explain how many there are and what taxa they are. Yet you can’t even attempt such a thing. Doesn’t that tell us something about your ideas?
Are you referring to Andy Devine, beloved character actor of 1950s Westerns? Incidentally, that link doesn’t go to the diagram, which we’ve been over many times and which you still don’t understand in the least.
He’s referring to the Venn diagram of four species (a human, a mouse, a chicken, and a zebrafish), showing the number of orthologs shared among the various combinations of species. His interpretation of that figure is, to say the least, idiosyncratic. Here’s a clue: he got it from Sal Cordova.
By Behe agreeing that his model’s parameters were unnecessarily restrictive:
Our paper (Behe and Snoke 2004) contains one simple result. When reasonable parameters are used with our model to estimate actual time scales or population sizes for the evolution of multi-residue (MR) protein features, they are unrealistically large. This implies that the model we chose, which is restricted to point mutations and assumes intermediate states to be deleterious, isn’t a plausible evolutionary pathway.
Behe goes on to wave his hands by pointing out most mutations are deleterious:
Experimental studies contradict Lynch’s assumption of complete neutrality as a rule; the majority of amino acid substitutions decrease protein function.
But experimental studies also contradicts Behe’s assumption of complete deleteriousness as a rule, some fraction of amino acid substitutions really are neutral, and those mutations really do contribute to protein evolution.
If all mutations were deleterious as Behe assumes, how’s this possible?
Yep, it’s that damned Omicron variant spike protein again, taking a gigantic dump on creationistic apologetics by having accumulated more mutations in the span of a year than the carbage models of apologists like Michael Behe and John Sanford thinks could happen in the entire history of the universe.
Yeah, that’s how gene duplications evolve into new genes. That’s how for example the nylonase enzymes evolved by duplication from pre-existing beta-lactamases. There are bacteria in existence right now breaking down the waste products of nylon manufacture with mutationally diverged enzymes having acquired new functions through a process Michael Behe’s garbage model says can’t happen.
Behe has a model with unnecessarily restrictive parameters that says what happened in nature can’t happen. And yet it did. What does that say about Behe’s model? That it’s garbage. He even admits it, and yet you come here citing his paper as if it supports your delusions about whether new genes can evolve.
You understand that omicron is less virulent then pior versions. This is with less then 1% or the AA’s being substituted. Sanfords predictions are supported with this evidence.
Feel free to use those procedures for any other item you choose. Are you aware that these have never, not once, been used in a real world situation to differentiate design from non-design. Not once, Isn’t that odd?
I think that is a very weak argument but maybe that would take us too far off topic to pursue that discussion here.
I was not here referring to the argument from reason. But we seem to arrived at a poossible point of agreement: “Design” refers to that which cannot arise naturally, i.e. without the intervention of a human being, or similar “intelligent designer” if such exists. However, that does not mean we agree on how this can be determined or detected.
Stay tuned…
That’s the definition of design, not the method by which we detect design. My position is that we can only know that if we first know how a particular thing is produced, and whether it can arise thru natural processes. We do NOT know it thru the methods that ID uses.
To choose a specific example: The bacterial flagellum is not considered by practically all competent scientists tp be designed because it is not produced by human beings. It only comes into existence thru the natural processes by which bacteria reproduce.
That is just an opinion, not something that is known.
It occurs to me that an explanation for the many genes shared among the three amniotes only could involve the process known as diploidization: after a whole genome duplication, in which every gene is represented by two copies in each gamete, a random one of those genes is frequently lost, and if not the two probably diverge. Since teleosts had an extra round of genome duplication, diploidization should have cause many previously shared orthologs to be lost or transformed so as to be considered paralogous.
And what I am saying is that this is a very blinkered view of what evolution is and does. Me winning the lottery as one out of hundreds of thousands of players is such an improbable event that it must have been caused by God. That is the entirety of your reasoning, and I hope we can agree that it is fallacious.
Would the moderators consider splitting off the posts where people engage in the equivalent of banging there heads against a brick wall, i.e. explain to @colewd his misunderstands of Ewart, the flower, and Lynch/Behe for the millionth time? It might make it easier to follow the parallel discussion occurring with @lee_merrill.
why such a fossil will falsify evolution? we can just push back the origin of that species. in addition, do you think that a reproducing watch is evidence for design or a natural process?
true. but i think that we can get a number which suppose to be close to the real number. for instance: what do you think is the chance to get a new anatomical trait which suppose to be the beginning of a new organ? also see my question above to paul.
And Lynch’s model claimed that mutations to genes were neutral which is also false so both models are not perfect. What we do see however is that a 2 mutation adaption takes a long time (thousands to millions of years) to fix in a population and the Howe diagram shows thousands of unique genes in 4 different vertebrate.
Do you see a problem with a model which claims that change is random until it is fixed in a population by either selection or drift.
As I said above, I think that analytical probabilistic estimates of evolution are misguided. How would we even go about answering this question, which is so vague as to be essentially meaningless?
It has but it has also lost virulence. Loss of virulence is loss of function. This is what sustained random change does to a sequence. If you want to prove this buy a scramble game organize a word and change out the letters randomly. I predict that most often you get an unrecognizable sequence of letters.
The other problem with the omicron argument is that it is showing variation in a single population and not fixation.
Virulence isn’t fitness. It’s how sick the infected become due to damage caused by the infection. Damage caused by infection =/= ability of the virus to replicate and infect new hosts.
We expect selection against virulence because sick people are less likely to spread the virus because they themselves and those around them take precautions.
No, Sanford’s predictions (to the extend that they can be distinguished from those of established epidemiology) are that the virus should go extinct due to accumulation of deleterious mutations all the way down to a level where the reproductive output of every viral particle falls below 1, which then leads to population decline until literally 0 viruses are left in existence.
This isn’t happening.
That virulence should decrease isn’t Sanford’s prediction, it’s a prediction of established models of epidemiology, and does not support his contention that the virus should be going through population decline and then extinct. It isn’t going extinct, it’s doing just fine. It’s done the opposite of going extinct, it’s actually adapted itself to the human population.
The Omicron variant did not lose its virulence. It seems to have experienced a reduction in virulence. Reduction and loss are two different terms.
Also explain how virulence is a function of the coronavirus or any other pathogen?
The Omicron variant is the fittest hCov19 strain thanks to the barrage of mutations that produced it. Do you even know what fitness, in an evolutionary context, means?
