is that the result of new binding sites, or just an improvment of the existing affinity? in addition, what if we want to change an antibody into something like a globin or insulin in small steps?
ok, so what is your estimation? one in how many mutations in general we can get a new function? in addition, how many of these new functions will also be beneficial?
sure. im talking about new functions.
thanks. but i dont think its realy relevant to that specific case, since im talking about two different genes evolving and not just one. unless you refer to other point?
I wonât call this a lie because I suspect you sincerely believe it. But this is false, and youâve been show why itâs false more times than are worth recounting.
No one has explained why his argument is wrong. The reason is it is not wrong. Itâs a legitimate conundrum with the theory that relies on random variation as the change mechanism. A theory that relies on the predictability of reproduction to give it any coherence without any rational explanation for origin of the reproductive process.
You seem conspicuously unconcerned regarding the dismissive response to the equally serious problems @John_Harshman raised regarding the Apollo missions landing on a moon made of Brie cheese.
Anything is possible. That does not negate the problem he has surfaced. He is over the target and all you guys can do is attack him. Lets call it a day and you guys can argue with yourselves.
Not really, no. Many things actually are impossuble. But this one isnât, because the process has actually been reproduced in the lab, as has already shown in this discussion. Here it is again:
Sure they have, itâs the very first response in the thread that shows what his problem is. Itâs called his assumption.
Of course the subject has come up before, and another problem with these types of arguments is they commit the Texas Sharpshooter-fallacy. As usual the odds of the specific, instead of the general case, is being considered. Instead of trying to determine a rate at which similar events occur, heâs trying to calculate the odds of only a particular one.
Itâs the same stupid argument every time. You guys have nothing else than this endlessly debunked crap about trying to calculate the odds of some particular set of mutations after the fact.
This is brain-drool. Itâs like complaining about plate tectonics for not explaining where atoms come from.
Even if God created the first cell, we still now know beyond any rational doubt that this cell went on to evolve into all life we currently see on Earth. The ultimate origin of the process of reproduction is just not a relevant fact in explaining what is wrong with SCDâs quintillionth repeat of the TSF.
We can create a phage display of a library of antibodies to find ones with catalytic antibody function for beta lactam hydrolase function -
In the present study, we report the construction of a phage display scFv library of size 2.7 Ă 109, from the classical murine strains Balb/C (healthy) and the SJL/J strain (susceptible to developing autoimmune disease), which has previously shown to express higher levels of catalytic antibodies [29, 30]. This library represents four different IgG immune repertoires: (a) healthy and nonimmunized, (b) healthy and immunized with KLHâconjugated penam sulfone hapten, (c) autoimmune prone and nonimmunized, and (d) autoimmune prone and immunized. The repertoires are identifiable via a novel ârestriction barâcodingâ technique, providing the first reported example of such methodology, in order to perform 2D screening. We have used two molecularly different inhibitors of the RâTEM βâlactamase enzyme as targets of selection: (a) a cyclic sevenâresidue peptidic inhibitor [31, 32], and (b) the penam sulfone derivative used as the immunogen [33]. We have selected five antibody fragments having hydrolytic activity on a cephalosporin βâlactam ring with different structural motifs potentially attributed to their catalytic activity. Our results confirm the capability of the two βâlactamase inhibitor targets to efficiently promote the formation of catalytic antibodies endowed with this activity. Furthermore, they provide additional information on the potential structural possibilities capable of holding a βâlactamase catalytic function.
Out of a library of 2.7 x 10^9 antibodies, FIVE demonstrated beta lactamase inhibition ability.
If 1 in 10^9 mutant antibodies have one specific function, beta lactamase activity, then the actual figure for any function is much higher than 1 in 10^9.
@Rumraket posted a link to an extremely helpful literature review on de novo genes.
Instead of just asserting the entire community of biologists are deluded because they (supposedly) overlooked something a simple non-biologist like yourself sees clearly, maybe you should address the evidence raised in the article?
You might find that leads to a productive discussion. You might, Deo volente, even learn something new.
But your current strategy is going to lead nowhere fast; I can guarantee you that.
My current strategy is simply to point out that the group is ganging up on SCD using logical fallacies. Do you disagree? At this point some coherent arguments are starting to surface. If you can find an article that is more than starting with the assumption that evolution was the cause I am interested.
If @colewd and @scd want real-world examples of how only small differences are required to provide quite a few functions-
Figure 2 of the following paper shows the sequences for
Porcine elastase
Bovine trypsin
Bovine chymotrypsin
Prekallikrein
Human plasminogen
Human plasminogen activator
Human urokinase
Bovine protein C
Human prothrombin
Human factor XI
Human factor XII
Human factor IX
Human factor VII
Bovine factor X
It pertains to the number you used to specify the odds of a functional protein evolving thru mutations, a number which you seem to have plucked out of thin air.
The experiment referenced shows that number to be off by many orders of magnitude. So it doesnât matter of one or two proteins are involved.
The problem is it is extremely difficult to quantify ALL possible functions, and as you may have figured out, function is not independent of environment.
Imagine a particular alien species decides to play God and chooses to genetically engineer a lab organism to do X when it sees the sequence AAAAAAAAA, to do Y when it sees the sequence AAAAAAAAT, Z when it sees AAAAAAAAC, etc all the way to GGGGGGGGG.
Another alien species does the same, but instead AAAAAAAAA causes the organism to Xâ AAAAAAAAT Yâ and so on.
And we keep reiterating this for 1 billion species.
Then literally a string of 9 nucleotides alone has 9^4 x 10^9 possible functions!
Function is never independent of environment, whether that environment id ex vivo or in vivo, and of course, nobody can work out ALL possible functions, because the possible number of functions that would have to be checked for is virtually infinite.
It is analagous to asking, how many functions are there of a 1 or 0 bit on a computer are there?
Bill, letâs recap how this conversation always proceeds.
Step 1. You complain about a lack of models for the evolution of X.
Step 2. You are presented with an example (one of many possible examples!) of a model for the evolution of X.
Step 3. You reject the model out of hand for no good reason.
You will, of course, return back to Step 1 again in the future (possibly with a slight tweak to the value of X), and the conversation will begin anew. This has been happening literally for years. You waste peopleâs time, never learn anything, and fail to deal substantively with good faith efforts to correct your repeated misstatements.
Whether you mean it to be a or not, this behavior is a form of trolling and should be treated as such.
With all the respect that is due to you Dave my reason was to point out that there was a personal gang attack agains SCD. Although you objected to the most egregious abuse you followed up with this.
Do you honestly this this is inviting to SCD to continue the discussion? The word âTrollâ is a label and as such its use is a logical fallacy.
Here, we develop a novel statistical method to detect positive epistasis between pairs of sites in a protein, based on the observed temporal patterns of sequence evolution. The method rests on the simple idea that a substitution at one site should rapidly follow a substitution at another site if the sites are positively epistatic. We apply this method to the surface proteins hemagglutinin and neuraminidase of influenza A virus subtypes H3N2 and H1N1âŚIn particular, using sequence data alone, our method identifies epistatic interactions between specific sites in neuraminidase that have recently been demonstrated, in vitro, to confer resistance to the drug oseltamivir; these epistatic interactions are responsible for widespread drug resistance among H1N1 viruses circulating today.
I wonât call this a lie because I suspect you sincerely believe it. But this is false, and youâve been show why itâs false more times than are worth recounting.