I think this gets into discussing the detail of what a predictive mathematical model is to each of us. I understand your opinion is that I am wrong. The paper you cite assumes the existence of a receptor and a virus protein binding to it. @scd argument does not start with these working assumptions.
@scd made no mention of working assumptions.
Why are you assuming that he (does or doesnât) assume?
Also, there is a difference between abiogenesis and evolution.
By the way, our mineraloid and glucocorticoid receptors evolved from an ancestral fish DOC receptor.
No. His argument started with the assumption that the odds of a functional combination of two proteins evolving are 1 in 10^18.
He therefore concluded that, according to his model, the odds of such a protein combination evolving are 1 in 10^18.
Boy, he really must have done a lot of difficult math to figure that one out.
Another member also proposed a hypothesis based on the assumption that ihe moon is made of Brie cheese.
Both hypotheses are jokes. But in only is the person making the hypothesis aware of this.
We also can assume that from his argument that the evolution of the binding of the proteins are independent events. @scd do agree?
If the two of you are going to assume no existing life, then say so.
As has been pointed out over and over, abiogenesis =/= evolution.
If there IS life, his numbers are absurdly wrong, as the existence of life in a suitable environment given sufficient time has a probability of 1 of evolving receptors and ligands.
Even with 1 billion mutations that is just 20 million offspring for humans. Easily achievable.
What @scd is trying to argue is that you need two very specific neutral mutations to occur at once in order for there to be a beneficial adaptation in all cases. This ignores the possibility that a single mutation would be beneficial on its own, such as a mutation to a hormone catabolism pathway enzyme producing a beneficial change all on its own. You could then have modifications to the protein that binds the hormone that also increase fitness.
In yet another example from the opening post, venom sacs could have served a different purpose before venom evolved. Non-venomous snakes have oral glands for producing saliva and mucous, so it isnât hard to see how these same glands could also produce venom, and then become more specialized over time.
IOW, the only problem is @scdâs ability to understand how exaptation works.
If you are arguing that you absolutely require mutations in both proteins before they will bind to one another, then you are wrong. You potentially only need mutations in one of them.
Please explain, in detail, the mathematical analysis you did to determine this alleged lack of viability. You can start with the paper cited by @Rumraket above.
Absolutely. Incredibly high-affinity ones, too. Are you aware of the typical Kds?
Thatâs precisely what antibodies provide. They evolve from random variation and selection in about 2 weeks.
Does it? Because itâs very clear that you have no predictive mathematical model to present or discuss.
I do. Your view of what is and is not a fallacy depends on your awareness of empirical data. Someone who argued 200 years ago that 280 people could gather into a powered vehicle and travel from one coast of the continent to the other in just 6 hours would have been treated as a raving lunatic. Now there are dozens of non-stop flights every day, and no one considers it fallacious thinking.
So my recommendation continues to be that you become a student of the work that biologists have done in building theories that are supported by empirical data. Relying on analogies to cars, factories, motorcycles, mousetraps, etc. will not get you or anyone else to a place where you can render sound judgment.
The paper that @rumraket already provided a link to in this thread is founded on genetic phenomena which are observed all around us today. In other words, processes that are observed today are inferred as explanatory factors in biological history, just as todayâs plate tectonics are inferred to explain the congruence of the western Africa coast and the eastern South America coast.
If you do not think that genetic transformations that are observed today can be reasonably inferred as causal explanations for natural history, then thereâs no science to be discussed. But I donât think you reject scientific investigation into natural history. Or am I mistaken?
Best,
Chris
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im of course refer to your objection to my calculation.
there is if only one in 10^9 mutations is functional.
do you have an example of a specific hormone that function with and without its receptor?
the same question above.
i dont think its the case, since im talking about any function, and not just about a specific one.
indeed. this is why i asked for your estimation.
how exactly? the article is talking about many ways to get a specific function from the same starting point. but it doesnt tell us much about the chance to get a new function.
i think we can get some idea about that number. for instance: do you agree with me that the assumption that one in about million births we can get a new function (and i mean any new function) such as a venom, or a venom sac or a stinger?
(image from Bee stings and stinger removal: have we been doing it right?)
i think this is very generous estimation since we never seen such a thing evolving, even though we watched billions of insects (in or out of the lab). do you agree with that?
im talking about two genes\anatomical parts which depend on each other. so they are neutral in themselves.
if the snake start to produce venom, isnt that a problematic situation without a self resistance?
The phrase âmay waysâ is the give away. You might also want to clarify in your mind the difference between a âspecific functionâ that did not exist before, and a ânew function.â
What I was saying is that a hormone doesnât require a brand new receptor. A modified hormone can bind to an already existing protein.
Would you agree that these features would more than likely be modifications of systems that already exist, and that venom could be beneficial without a specialized venom sac?
Again, you are ignoring exaption.
You are already shifting the goalposts.
To me, itâs a mathematical model that can be used to make predictions by using appropriate equations and parameters.
To you, itâs a magic phantasm that bolsters your opinions.
Letâs take a look at a paper which directly addresses the hormone-receptor question in the opening post.
Here is the problem. Most vertebrates have two hormone receptors that originated from a gene duplication deep in the vertebrate tree:
mineralocorticoid receptor (MR) : binds to both cortisol and aldosterone, but is associated with aldosterone because it resides in tissue that quickly clears cortisol.
glucocorticoid receptor (GR) : binds to cortisol
So the question is how could aldosterone evolve without a receptor to bind it? Without aldosterone, why would a receptor evolve to bind it?
To answer this question, Bridgham et al. (2006) reconstructed the ancestral protein from before the gene duplication. They could do this because the agnathan branch split off before the gene duplication.
So what did they find when they expressed the reconstructed ancestral gene? It was able to bind aldosterone, even though aldosterone had not evolved yet.
So just as I said, a new hormone can bind to an already existing hormone receptor that had evolved to bind other hormones. As the paper states:
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Didnât we JUST GET DONE hashing this one out with Kleinman already?
I donât think universal common descent is a reasonable inference at this point. How much ancestral connection there is between species is open up for debate. The discussion of primate ancestry is certainly up for debate as is rodent common ancestry etc.
Subtlety is lost on you, apparently. Are you familiar with the acronym âGIGOâ? That describes your âcalculationâ.
How would you debate it?
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Getting people to think scientifically is worthwhile.
@colewd, if you were a scientist, which all humans generally are to some extent (even babies when they try to eat everything or grab everything are scientists in a sense), how would you go about proving (or providing evidence for) or disproving (or providing evidence against) human-primate, human-rodent common ancestry?
Are there any testable hypotheses you might try and test?
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Getting Bill to think scientifically is more quixotic than worthwhile. But good luck to you. They might be giants.
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