The problem is that the “above” only repeats the exact same problem I described in my last post:
Any time you focus on “specific” historically-contingent events you are commiting the Texas Sharpshooter Fallacy.
Evolution in general, and/or Natural Selection in particular, need not have converged these two specific groups of organisms, on this specific function – they could as easily have converged two completely different groups on a completely different function. The correct probability calculation is that of the probability that no two groups would, a priori, converge to any common function. Have you calculated this?
I don’t believe that we can. It is very likely that the probability of achieving that function will be greater even on a single trial. We are not dealing with purely random probes into sequence space,
That’s assuming that all functions are that rare in sequence space.
Beta lactamases seem to have evolved more than once. Do you wish to claim that your designer is deliberately creating antibiotic resistant bacteria?
it will not change the big picture so much. if a specific function occurs at least few times then it doesnt realy matter. in addition, how many different functions exist in the same group? a million? so at best you can reduce it by million fold. which still give us a huge number.
no. some functions might indeed be common in sequence space. but not so with multiple protein system or complex proteins.
since evolution has no goal it should be similar to a random search. take this simple analogy for instance: suppose that we need to get the number 777777777 (which represent a specific function for instance) from say 333333333 (which represent other specific function). can you do that by small steps without knowing the target?
Yes, that was one of my points. Your figure only concerns AroQ mutases, and there are many other potential functions proteins can have, obviously. As others have pointed out; taking that figure regarding ONE specific function (AroQ mutases) and treating it as if it applies to ANY specific function, this is committing the Texas sharpshooter fallacy.
Furthermore, we weren’t talking about proteins that need “3 binding sites”. We were talking about how likely it is for a protein to have ANY function. ATP binding is one example that seems relatively common among a random polypeptide library. After this example was provided to you, you engage in an ad hoc rationalization to argue this example isn’t enough to your satisfaction, and we need to show the evolution of 3 binding sites instead. What is up with you people and your inability to keep your hands off the goalpost?
However, it is actually worse. We originally weren’t even talking about how likely it is for a random polypeptide to have any function. Initially @Rumraket was talking about how likely it is for mutations to be beneficial - or specifically - the likelihood that one protein can acquire other functions via mutations. Which is distinctly different from asking how likely it is for a random polypeptide to be functional. If you can’t tell the difference, excuse yourself form any discussions on this topic until you can.
Uh…yes…that is my point. You can’t say “it looks designed” as a reason to conclude “therefore it is designed” with anything, not even with things such as watches, gears and motors. The reason for how we know these are designed is from our background knowledge, not from whether or not they “look designed”.
Whenever you respond with something like this, as if it goes against my point even when they don’t, I can’t help but getting the impression that you keep missing the point.
Regardless, you say that it doesn’t look designed to you, which already is a tacit admission that “looks designed” is entirely subjective. Furthermore, it is also missing the point that this structure does look designed according to a lot of people. The Giant’s Causeway even has been regarded as the making of giants in mythology. So does the fact that it “looks designed” means that it (likely) is designed? The answer is obviously no, which is one example for why such reasoning is flawed.
Not to mention it seems to completely dismiss the idea of an attractor in the space of functions. A function really can be extremely rare, but there is some force or bias in a random walk in the space that generally pulls things towards them. So things can begin with very simple and rudimentary functions that are much more likely, and these be combined in new ways and therefore serve as stepping stones towards more complex functions.
Then define “specific” in this context, with examples showing that all other functions have been tested for and not been detected.
If you try to do so, you’ll find that such specificity does not exist in biology. This is why every drug has side effects and is predicted by evolutionary theory. An omnipotent Designer, however, by definition would have no problem designing truly specific proteins.
I see the Texas Sharpshooter fallacy, fueled by a lot of misunderstanding.
There you go with the ‘I’m committing the Texas Sharpshooter Fallacy’ word again.
How do you know it’s only a million, not a trillion or several higher orders of magnitude? Have you counted?
How do you know that the odds against any specific example of convergent evolution are 1 in 1030? Who calculated this? And it seems absurdly unlikely that they would all have the exact same probability.
This ‘argument’ fails on so many levels that it seems absurd to even call it an argument.
This says that your evidence does not have broad significance. What is missing is a general purpose model which is missing from all these papers. @RonSewell posted several interesting papers on anti freeze proteins in arctic fish. The problem with these papers is evolution is assumed and the most probable pathway is chosen.
What is missing is a feasible process… Where plants can change gene form by mixing exons through recombination I have not seen this in vertebrates. Mixing exons is a reasonable explanation for some de novo genes. A random walk through many improbable mutations is not a likely conclusion…
In the case of anti freeze genes there is extreme selective pressure but on the other hand the paper 1. suggest a long improbable road to arrive at the point of that selective pressure. While this could possibly happen I think ID is the better explanation for the origin of the arctic anti freeze gene given the current available evidence.
That doesn’t even make sense as a response. You can’t justifiably make any conclusion on probabilities on the information given.
Small steps are very different from completely random jumps to anywhere in sequence space. The distribution of function matters - a lot. So what if a useful function is at 333333332 ? Since evolution has no target it doesn’t care which function it finds.
A better analogy. Let’s say that 777777777 has a specific function X, and 333333333 has function Y. And let’s say you can mutate to be something like 777777377. It retains function X despite the mutation (functional robustness, which is observed in proteins), but it now it does a bit of function Y (functional promiscuity, which is also a property seen in proteins). By continuous mutations it becomes more specialized until it becomes 333333333.
That way, proteins are able to traverse the fitness landscape of the sequence space, while in a non-directed manner, it nevertheless allows for the discovery of new fitness peaks. Here below is a real life example. Take your time to comprehend the illustration.
Duplication events and changes in specificity and activity during the evolution of Saccharomyces cerevisiae MALS enzymes.The hydrolytic activity of seven modern MAL and IMA enzymes and of key ancestral enzymes (prefix anc) is given. The width of the colored bands corresponds to the k cat/K m-value of the enzyme for a specific substrate. For details see Voordeckers et al. (2012).
we can deal with that too. if indeed all biological systems where near each other in sequence space, all of them should be very similar to each other. but we know that this isnt the case. olfactory system for instance is very different from heme synthesis, which is very different from a motion system etc. thus many biological systems are indeed isolated in sequence space, and we cant move from one system to another by small steps.
so you basically agree that motors and gears are the result of design or not?
If proteins can traverse the sequence space over time, that means they don’t have to remain “near each other”. Also, that doesn’t mean that every single proteins evolved from one another. That is not what I am saying ether.
Sure, unless you want to define “motor” so broadly, such that you would call some protein complexes “motors”… which is likely what you were getting at with this… then I would say that SOME motors are designed. We can conclude that THOSE motors are designed, because we have the background knowledge. This isn’t the case for the other “motors” and we can’t conclude they are designed because they “look” designed.
Although, I wouldn’t call any biological system “motors” since such analogies poorly describe biological processes. Organisms are not machines.
so what do you think is the rate of a new biological function? one in a million mutations? something similar to that? one in how many births we can get a new anatomical trait in a direction of a new organ? do you agree for instance that a rate of one in 1000 births to get a new anatomical trait is generous?
the problem is that we know that function A is very different from function B in both sequence and structure. thus we do need to change 333333333 to 777777777.
they need to be near each other in order to evolve from each other in small steps. but its clearly not the case with complex biological system. you cant change a non-motion system into a motion system by small steps. and you cant get a motion system from a random sequence either. so in any case a motion system is isolated in sequence space. and its true for many other biological systems.
do you agree with me that a watch which is made of organic components is still a watch?
The definition of “motor” is pretty broad. The dictionary definition and the engineering understanding of a motor as any transducer which converts a form of energy to mechanical motion agree well enough. While it is analogous to compare the flagella to specifically induction motors or internal combustion motors, I think that it is within usage to term some biological processes literally as motors. This is no concession to ID.
Assuming that you mean “structures that have function A are all very different from those that have function B’ I have to ask if this reflects any real situation. And by that I mean a case where the evolution from function A to function B happened despite the large difference - and happened directly, without intermediate stages that served some other function.
I’m pretty sure we have discussed this before, but I don’t recall you answering the question. If you did, please remind me: What would we expect to see if an organism had the beginnings of what would eventually be a “new organ”?
I think treating all “new biological function” as homogeneous and having the same probability is absurdly silly and simplistic.
I think the probabilities will vary radically depending on things like:
the complexity of the function;
the degree to which the new function can co-opt existing functions (flight is a lot more easy if you’ve already got feathers, for example); and
the number of different evolutionary pathways leading to the new function.
(This is just a few factors that I could think up off the top of my head – I’m sure that there are dozens of others if we look in sufficient detail.)
But that is not my problem – as I’m not the person making claims about how unlikely these functions are. It is the problem of the person who is making those claims to provide substantiation for them. That person is you. So where is your substantiation? Where are your probability calculations for each and all these functions?
Without such substantiation, we get back to:
That which can be asserted without evidence, can be dismissed without evidence.
… and your entire argument can therefore be dismissed out of hand.
