Why are We Disagreeing with ID?

This.

Consider the space of all possible nucleotide sequences. Simply picking some long genome sequence at random and then working out (if we imagine we can do this) what sort of organism some randomly picked nucleotide sequence is going to result in.
I think we can agree that randomly and blindly picking a genome sequence that corresponds to a highly anatomically streamlined fish is unfathomably remote. In the space of all possible nucleotide sequences that vast majority must either be nonfunctional, as in not result in a viable form of life at all, or at the very least result in something very, very different from a highly streamlined fish.

Yet it should also be very clear that in so far as we have an organism that can live and swim in water, it is essentially guaranteed that under natural selection this species can and will evolve ever more streamlined body morphology. So the real question isn’t whether it is likely to pick a streamlined fish from among all possible genomes, that’s just not how anything evolves. The real question is what is the probability that a mutation occurs that affect body morphology in a way that reduces aquadynamic drag, in a member of the species? Given that these obviously occur in large quantities every generation (the drag coefficient of fish is a variable and heritable trait in any population), one can move gradually towards extremely rare genotypes.

This is the power of cumulative selection, and why an attractor in a space can vastly affect the probability of obtaining something that is a priori very unlikely.

It is an entirely reasonable and interesting question to ponder what that attractor might be in protein sequence space. It doesn’t actually have to be(and probably isn’t, in many cases) a persistent selection for a specific function. If certain functions are extremely rare in protein sequence space then you obviously can’t select for those functions right out of the gate, but you can select for something else that might lead to such rare functions as an unavoidable byproduct. Some of the rarest functions in protein sequence space might in fact have begun long after the protein’s first origin, as spandrels that resulted as a byproduct of some other selection pressure, such as the long-term consequence of selection against the inherent aggregation propensity of polypeptide sequences.

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You might think that, but we know it’s not true.

Two proteins can have different functions and different sequences but very similar structure.

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well, take the motion system as example. can you as a designer made a motion system that is base on a single part? i mean, can you add a single part to an object (that cant move) and it will start to move from A to B on its ownf?

i guess that any new and different bump that serve a new function might be a good start.

ok. so i will say that the average rate to get a new anatomical trait is one in about 1000 births, and probably more then that. why? because we have seen billions of living creatures (human population alone is about 8 billion). and as far as im aware only in rare case (if any) we see a new function. let alone a begining of a new organ. so i think that a rate of one in 1000 births is very generous and even contradict empirical reality.

i refer to the cases that its true. which is a lots of cases.

Obviously then your answer is “no”. So in that case “we know” is not really applicable - it’s just an assumption in a purely fictional example with no apparent relevance to anything that actually happened.

First, do we need a new organ? To what purpose? Why should we expect a new organ in any event?

Billions of years of evolution, and humans have wound up with 78 organs give or take. That is compatible with the development of organs being exceedingly rare, so we would not necessarily expect to witness that.

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Why not a “new and different bump” that has no new function whatsoever? Can you provide some reason that this could not be a step in the evolution of what will eventually become a “new organ”?

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We don’t know that humans or some human-like creature didn’t make nature. While unlikely, that would be impossible to prove. We accept human design where we have material evidence that human design is feasible. We have material evidence supporting design-by-evolution, but no material evidence for any other. (That’s OK, we should not expect material evidence of immaterial designers).

More, concluding some unspecified"other designer" causes problems. Literally any other possibility can be concluded, including silly things like Flying Spaghetti Monsters. I do not mean to mock, but this puts the idea of God as the designer on equal footing with FSM. None of the more theologically-minded people I have discussed this with find this idea acceptable. Reason include mockery of God, “putting the Bible on a pedestal of science,” and more.

Still more, if you hadn’t noticed - science has left the building. The possibility of a supernatural explanation, based on a lack of material evidence, if simply a no-go for science. If you are not content with the theology you have, I really don’t think try to “science it up” if going to help you. IOW, it’s OK to have faith, but it is not reasonable, or helpful, to pretend that science backs up one’s faith.

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Trivially. One example would be adding a connecting rod between two gears, one linked to an engine and the other to a set of wheels. The object would not move previously because the engine wasn’t connected to the wheels, but now it will.

Had you thought about your question at all before asking it, you might have come up with this example yourself.

No you weren’t. You were referring to an analogy involving strings of numbers, not to any actual cases.

That is not how it works scd. You plucked “one in about 1000 births” from thin air without evidence, so per the aphorism I quoted to you before, I can simply dismiss that claim without evidence. The need for this evidence is a large part in why I asked you for “your probability calculations”, so that your calculation would, of necessity, include this evidence.

I would also note that you ignored my point about the wide range of probabilities, by continuing to treat all functions as being of equal probability.

The first step is for you to decide which evolutionary convergent function you wish to calculate the probability for.

The second step is to decide what evolutionary starting point you wish to choose. Do you want to give echo-location to a mouse, for example? The starting point will make a very large difference, as for example the aerodynamic properties of feathers gave birds a considerable leg up over mammals in developing flight – with the result that bats need to keep flapping their wings all the time in order not to drop out of the sky.

Then you have to start looking at evolutionary pathways – not just the one that is most likely to have been the one that happened, but also ones that would have yielded a functionally similar result.

Then you have to calculate the probability of each of these pathways, and sum them up. As probability of the steps will depend on whether each of these steps are beneficial, neutral, or adverse will depend on the environment, the environment will also have to be specified – and may change over time.

Do this for a large number of convergences – both ones that have occurred, and might have occurred, and you will start to develop an understanding on what is or is not likely to happen.

Only then would a general claim along the similar lines to this earlier claim of yours start to become credible:

Until you do this, your claim will have been made without evidence – so it is likewise dismissed without evidence.

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its not an assumption. we know that a motion system needs few parts.

great. so if its so rare to get a new anatomical trait, then a rate of one in 1000 births to get a new anatomical trait is very generous. right?

a new anatomical trait which suppose to be a part of an organ. we do need to start from something after all.

if it has no function then the organ should not evolve, because the small steps are neutral in that case.

in this case the motor has no advantage without that rod. so why it should evolve in the first place? remember that we are talking about a living creature. so that scenario will not work, unless the motor was already in the organism with no function at all.

no. i base my claim on something we do see (or actually not see) in nature. if we check out for instance about 1000 random fish and see no beginning of a new anatomical trait, then we can conclude that the chance to get a new anatomical trait is less than 1000 births. very simple and base on empirical evidence.

if we will see a motor on an empty planet. we cant conclude design base on that motor since we have no material evidence for that designer?

The difference is the artifact is (presumably) constructed by the unknown designer. In biology we know the construction occurs biologically within the biological system. We know that biology can build motors (if we want to call them that).

Also, finding a material artifact makes us suspect a material designer, not an immaterial one. We ask questions and seek answers about this designer - something that ID insists it cannot do.

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Please try to keep track of the discussion. I asked for a real example where a large change of structure was required with no intermediate stages. It doesn’t matter how many parts a “motion system” needs. You need to know what it’s immediate precursor was. The large change is simply assumed.

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and this is what we need to know. i doesnt matter who the designer is. just that he exist.

only if we already have the complex genes\systems to do that.

so if I understand you correctly, you suggest that a motion system might evolved from a simpler system that wasnt a motion system? an easy way to test that is by removing some parts of the motion system and see if we get a different function. but we know its impossible since by removing some parts out of a motion system give us non working system and not a different system. so this cant be done.

Where did you dissect “1000 random fish”? If you didn’t do it yourself, and you cannot point to a peer-reviewed article showing somebody doing this (with proper sampling methodology), then this is not evidence.

For that matter how do you know that the new function involves “a new anatomical trait”, rather than being a metabolic change, or dozens of other changes that would not show up under dissection?

Also your claim demonstrates one of the more pervasive creationist misunderstandings about evolution – evolution involves populations not individuals – so the fact that one of the fish doesn’t differ from the other members of the same population is not indication that the fish haven’t evolved – determining that would require comparing the current population with a population from the distant past.

This all leaves you without even the semblance of evidence.

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Why do you think it is impossible that a series of neutral steps could occur? This is a very common misconception among evolution deniers, and for the life of me I cannot see what is so difficult to understand here.

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I’m saying that your assertion that “a motion system” directly evolved from something very different is in need of support, And your “test” is ridiculous. If the system was very similar the necessary change was more likely a change in one or a few parts rather than the addition of a new part. Further, unless the modern “motion system” is unchanged since it first developed it will be further from the immediate precursor so we can’t expect to recover the precursor through simple changes.

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Then all you need is to find a 289 V8 Small Block on Titan and your all set.

Congratulations on moving the goalpost for detecting design to the very existence of biology. Again, no complaint about your beliefs, only the validity of your argument. You are making a theological claim, not a scientific or logical claim.

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That’s literally how the system works already now. Part of the flagellum functions as a protein translocase, and some bacteria use them as protein translocases. Others use them as receptors/docking sites for extracellular molecules, sensors of local conditions or what have you. They lack the flagellin proteins that make up the filament yet the system still performs other functions.

In addition to motility, flagella have roles in other microbial processes, such as adherence to host cells, host cell invasion, protein secretion, autoagglutination (i.e. clumping or self-adherence of bacterial cells) and biofilm formation [2–6]. For some of these processes a direct involvement of flagella is clear. For example, Campylobacter jejuni flagella are responsible for secretion of several non-flagellar proteins [7–9]. Interestingly, some obligate intracellular symbionts of insects (e.g. Buchnera aphidicola ) have lost many of the genes needed for assembly of the flagellum and appear to use the remaining flagellar assembly gene products for export of bacterial proteins to the host [10–12].

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Well, I haven’t seen more than a few, even by people eager to disprove Behe’s claim.

No, I was commenting on your “boats and planes” claim.

No, the edge is at two new binding sites, I mention dozens because dozens of parts are typical of flagella.

That’s a fair point, how about MotA and MotB? But wouldn’t it still be rather miraculous if the two dozen proteins in flagella somehow assembled (with modification) in a bacterium? The flagellum would not seem to be useful until all the components were assembled.