You do need some math. Thus far you have only given the math for a 70 aa peptide binding to ATP which isn’t even a protein. Where is the math for the probability of two proteins binding to one another?
Just from my own experiences, non-specific protein to protein binding is a massive problem in many situations, especially in protein purification. In fact, your own immune system depends on random proteins binding to other proteins. During B-cell development there are DNA modules that are shuffled together to form the unique antibody that a B-cell lineage will produce. You have millions of different B-cells lineages in your body right now, and those random arrangements of sequence end up binding plenty of antigens and protecting you from infection.
I will concede your point is true for single substitution mutation. What you have described is phenotypic plasiticity.What happens when a series of specific mutations are required? Single substitution mutations obviously do not lead to speciation (else we would have seen it in humans by now, if all possible single substitution mutations exist in the human population).
Isn’t this speculation? Most likely the zygote wouldn’t develop into an embryo.
Not without actual evidence. If you can substantiate your claims, it would help.
After all my kidney cells and brain cells have the same genome, but have entirely different phenotypes.
You are excluding all of the possibilities before that point.
That is true of many protein-protein interactions. The fact stands that random shuffling of antibody genes results in many, many antibodies that are able to bind to other proteins.
Again, it does not matter you are observing 5 proteins binding together and performing a function. Is like observing a table of people playing poker and seeing 4 straight flushes dealt.
Yes, we know this. The challenge again is the size of the total sequence space compared to these possibilities. You failed to mention hypermutation which is a cellular mechanism is involved.
Phenotypic plasticity does not involve a change in DNA sequence. For example, when you tan it isn’t due to mutations occurring in your genome. Rather, it is due to a change in gene expression of genes that you already have.
The same thing that happens when a series of numbers are needed to win the lottery.
I also don’t see how substitution mutations can not lead to speciation. I would fully agree that indels and recombination are also going to play a part, but substitutions are going to be in there as well.
It is an educated guess, not total speculation. Humans and chimps share a lot of DNA, and all you need is the initiation of embryonic development to go smoothly. After that point the chimp proteins and RNA will be diluted out and replaced by the homologous molecules from the human genome.
It is interesting to note that scientists are trying to resurrect an extinct frog by putting its genome into the egg from a different frog species:
So what do you think is responsible for the physical differences between humans and chimps?
That would be the Sharpshooter fallacy again. You are trying to claim that there is only one solution, the solution we see.
What challenge? You have tons of antibodies from random shuffling that bind other proteins. You also mention mutation of those antibodies which increases the specificity and avidity of binding which argues against your claims. Hypermutation should destroy binding according to your claims, but it actually improves binding.
I have personally run assays against peptide libraries and found activity against a wide range of very short peptides, from 3 amino acids up to 10 amino acids. It isn’t as if antibodies are a special case.
Your statement is false. I am simply observing the hand that was dealt. What we see is 5 proteins that can bind and perform a function. Not a fallacy at all.
Please explain this claim.
This is a vague answer. Looking at a vertebrate proteins what percentage would bind with less that 10 amino acids? Are we forgetting proteins that are the result of two or more proteins binding together?
What you are ignoring is all of the hands that could have been dealt. Using your analogy we would conclude that all of these lottery winners are a miracle because we are ignoring all of the outcomes where other people would have won.
Once an antibody binds to an antigen the B-cell expressing that antibody is turned on by a T-cell. This causes the B-cell to rapidly divide and pump out antibodies. During this rapid expansion of the B-cell lineage there is also an increase in the mutation rate within the antibody. Any mutations that increase the avidity with which the antigen binds to the antibody on the surface of the B-cell results in the B-cell getting an even stronger signal to keep dividing and keep pumping out antibody. This process of mutation and selection increases the effectiveness of the antibody over time. Your immune system actually takes advantage of evolutionary mechanisms.
Probably the vast majority of proteins interact through a very limited number of amino acids. Most protein folds used for binding are only a few amino acids long and can only fit a small portion of another protein. You can check out protein binding motifs here:
The hands that could have been dealt are not relevant to the analysis. I am observing the hand that was dealt and determining if it was fairly dealt from a properly shuffled deck. With four straight flushes my analysis is easy.
As in biology we are observing a sequence of DNA that generates proteins and I am determining if they could have been formed by a random process. The analysis is whats being observed and estimating if the null hypothesis (randomly generated) is viable. With a fully functional cascade of a light sensitive spot and detection my working hypothesis is that the null hypothesis is falsified. I think it is unlikely that what we are observing is the result of a random process.
I think this a valid observation for some proteins but not the vast majority. This ignores proteins made up of several transcribed sub units. Doug Axe’s work was an example of this. It also ignores proteins that bind to several other proteins which is common in the cell nucleus.
Yes but you don’t have evidence. I posted a discussion here between Dennis Bible,Lynn Margolis, Dawkins etc. Lynn Margolis asks Dawkins to give one exMple where speciation has happened by random mutations (meaning substitution mutation). He couldn’t give one. All he could hide behind was “parsimony”. Your intuition is not worth much without actual evidence.
That’s the whole point. You might be right. Buy we can’t know till there is actual evidence.
Embryonic development is a complex process. Read up on cross species NT (Nuclear transfer). The embryo does not develop in most cases except for very close species.(which would be expected from examples of cross breeding between tiger and lion etc).
The entire system. End of the day gene expression can cause far more difference than point mutations.
We have examples of organisms that look identical while having very different genomes. And organisms with identical genomes can present different phenotypes. For example identical twins don’t show identical propensity to diseases.In honey bees, the queen and female workers share the same genome. Yet phenotype is different. And in our own bodies, the kidney cell has the same genome as the neuron… yet totally different phenotypes. There is much more going on into what makes an organism that just the genetic code.
There are well known cases of genetic drift causing a new species in a single generation. Add more time and it’s difficult to imagine it wouldnt cause new species. @Ashwin_s a few quote mines plus some personal ignorance isn’t an argument. You are very far from your area of training in a very complex area. If something doesn’t make sense the default explanation is that you have more to learn, not that evolutionary science is failing.
If something an expert says doesn’t make sense in an area that we don’t understand , the logical alternative is to get a second opinion. Listen to what other similar experts say. For example, if you want to build a house and what the architect claims doesn’t make sense, you get a second opinion or even a third opinion. It’s one way how people judge truth claims they cannot personally verify .
What you call “quote mining” is just me taking @T_aquaticus and even your versions of what the science says with a pinch of salt. I am seriously listening to other voices/opinions and understanding what they said. For example what I quoted about Lynn Margulis was after listening to a 4 hour video discussion. That’s not quote mining.
Take your stand that neo Darwinism was disproved decades ago. It seems wrong because even a rudimentary Google search will show us scientists (even excluding ID/Creationists scientists) routinely discussing it and even debating it.Obviously you are communicating the truth as you knkw it…And people still talking about Neo Darwinism are also communicating the truth. Maybe you mean different things by the word.
What I understand is that biologists are so specialised that different biologists tell different stories about evolution using the same words with different meanings. When I read people working on protists, they speak from a totally different paradigm.
Pls note, I don’t think evolution science as failing. I just think communication of the science is in bits and pieces… all over the place.
And hence I need to listen to a mosaic of voices to piece things together.
So if I come across qualified scientists in the main stream disagreeing with you or anyone here, I will point it out in good faith for a transparent discussion.
You are pointing to comment by Dawkins. He is not the fount of all knowledge. It just takes one example to show a case where drift is causing speciation. We have more than one.
Yes. And if they mean positive selection dominated change, they are working from a falsified theory of evolution. We have ample evidence that panadaptionalism is false. What exactly is your point?
This is happening because you cannot explain biological change in way that makes sense without some kind of teleology/directionality. Whenever the explanation requires this , biologists seem to resort to selection as the only option available, even as they repudiate panadaptionism.
How do we avoid this in explanations except in cases where it has been thoroughly established empirically?
You can’t have it both ways. Perhaps explaining how and up to what extent NS plays a role will help. Or how exactly panadapgionism is repudiated and what usages of NS as an explanation are not supported by science would help.