Yes, many designed objects do not show IC but IMO, every object displaying a level of IC equal or superior to two CCC warrants a design inference. So what I am saying is that this level of IC is a hallmark of design, in the sense that it is a very strong indicator of design. A sign of design if you will.
Well, assuming you are correct that whatever you are describing there is needed to calculate FI (and I am not certain you are), that would suggest the DI are just blowing hot air when they say evolution cannot produce results of a given FI. If they can’t even calculate it how, would they know this? Although it would finally explain why they have never, ever, not even once applied FI to an actual biological situation to show that evolution cannot increase it.
And there goes another irony detector.
Huh? IC and CCC are two completely different concepts in the Behe Universe. One cannot be derived from the other. It seems your understanding of ID is as abysmal as your understanding of evolution.
A claim that was refuted over a century ago.
The Mullerian Two-Step, or Why Behe’s “Irreducible Complexity” is silly
Except as pointed out, evolution can also produced biological structures that meet Behe’s criteria for IC. Therefore it can’t be a sign of design (re: biology), because IC is demonstrably not exclusive to artificially designed and manufactured objects.
If ID proponents really wanted to come up with a means to detect design and manufacture, then best way is to start with a hypothesis about how a designer would go about creating or modifying biological organisms. Then determine the hallmarks of that process and see if those hallmarks exist in biology.
The two challenges here seem to be, a) getting past the resistance ID proponents have of asking “how”, and b) risking coming up with hallmarks and hypothesis testing in biology that may reveal organisms does not exhibit design and manufacture.
Please show me a case where it has been demonstrated that unguided, blind evolution produced a biological structure that meet Behe´s criteria for IC.
I gave you the previous link to the Behe interview with Dan Cardinale where they walk through Behe’s criteria and then Dan gives examples of biological structures that meet those criteria: https://www.youtube.com/watch?v=nsErbfaq5mc
I understand it’s an hour long video, but if you have a real interest in trying to defend IC here I highly recommend watching it.
edited to add:
Digging through past threads on this forum, it looks like you have previously been engaged on this exact subject in this thread: Creation Myths with Dr. Michael Behe on "The Edge of Evolution"
It interesting to note that presented with examples of evolved structures that demonstrate IC (per Behe’s basic criteria) you, like Behe, appear to then change the criteria.
Which reinforces that IC is a poorly defined and nebulous concept to begin with.
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Does your unsupported opinion count for anything? And “CCC” is something Behe made up, something that seems not to actually exist even for chloroquine resistance in Plasmodium.
Pick a lane.
Said humility befitting a scientist lies in the recognition of one’s own fallibility, the acknowledgement of the possibility of one’s own incorrectness. A scientist has spent enough of their life surrounded by people far more educated than themselves in all manner of areas, and internalized through that experience, that – much though they may have studied – there is for almost every question somebody more knowledgeable, and for almost every guess they’ll make there is a chance it is dead wrong.
The height of arrogance is the idea that watching half a dozen hours’ worth of YouTube sermons, or sitting down in an arm chair for three minutes is all it takes to come up with all manner of gotchas and what-abouts all of the people who spend their lives studying the subject never considered. The idea that confident delivery and flowery jargon is all it takes to get into position to question, let alone undermine, literal centuries’ worth of research, that is arrogance. The idea that having seen next to none of the data, and understood none of the maths, one is still anywhere near adequately equipped not only to meaningfully partake in the conversation, but that there cannot be anything one might have overlooked, that is arrogance. If to the question “How come the entirety of the community of qualified professionals disagrees with basically everything I say?” one’s answer is “They must not have seen all or thought through the facts in such depth as I”, then, respectfully, one has no business lecturing anybody on matters of humility.
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At this point it tells us that there are around 1 to 3 AA changes per protein amino acid position that are tolerated in the human population.
If you look at other proteins with a similar percentage of substitutions in the population it does not indicate how many substitutions will be conserved in the population over time.
Hey @Giltil did you forget the IC stuff and the Cit+ trait? I see you have no response to it.
Anyway:
Really? Because here you seem to understand it perfectly fine. When a sequence of higher fitness replaces a sequence of lower fitness, FI increases.
And here you seem to comprehend that the quantity of information is the product of a probability. In other words, we can simply convert probabilities to bits. A principle you’ve stated yourself previously multiple times.
These are principles YOU have agreed to. You have even suggested them yourself before. The “eminent”, “esteemed”, and “world-renowned” Joseph Felsenstein whom you’ve wasted no opportunity to glaze in similar fahsion when he bothered to reply to your posts, agreed.
Taken together, we can take the probability of beneficial mutations (which would be mutations that change a lower fitness sequence into a higher fitness sequence), compound their probabilities as they accumulate, and then convert the total probability into the change in FI of this series of events.
That’s it. That’s the principle. Simple, really.
No, they’re not. That’s exactly what cumulative selection ensures that they aren’t. If you allow us to keep successful die throws, we can pile up towards extremely improbable outcomes. We’re never going to get 25 simultaneous beneficial mutations in an E coli cell. But that’s where population size and natural selection comes in. We can accumulate them over generations.
That’s deeply confused. The probability of any single, arbitrary mutation being beneficial, is not to be confused with the probability that a beneficial mutation will occur in a population of sufficiently large size.
That response seems almost delusional. Are you in denial that it happened? They really did accumulate 25 or more beneficial mutations, independently, 12 times in parallel. It happened.
Since you believe each beneficial mutation has a probability of 10-6, that’s approximately 500 bits. Your magical insurmountable barrier.
You complain that nothing is demonstrated by mere assertion, and then you merely assert the things twice and call them both demonstrations. Are you trying to undermine ID or something?
That’s also not necessary. We’re not trying to calculate the total FI of the E coli genome. We are calculating the CHANGE in FI as a product of a series of compounding chance events. We do not begin by first trying to determine what the total FI of a living organism is. It’s irrelevant. What we can calculate is how FI changes over time.
In the present case with the LTEE, we are simply calculating the change in FI due to accumulating beneficial mutations.
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The question was not about whether you could convert this into a kind of ratio, but what it tells us about the bigger picture–I’m sure you haven’t forgotten your claim:
A couple of points regarding vocabulary:
- We have a single word to describe your “amino acid position”: RESIDUE. Try using it instead of writing gobbledygook like
- You obviously don’t understand what fixation means. Try to complete the following sentence:
The only entities that are subject to fixation are ____________, not genes.
So, what does the existence of 4500 known variants tell us in the hopelessly garbled framework to which you have repeatedly referred, Bill?
Except that I didn’t write that, did I?
And you have conveniently forgotten that we established that the calculation of FI you were touting tells us that actin has more FI than one of the most functionally complex proteins known, myosin. You have yet to address that.
We’re really still doing IC?
Okay I know the goalposts have moved on this but by any articulated standard, the novel tetherin antagonism trait found in the VPU protein of HIV-1 group M is irreducibly complex.
It’s a new biochemical activity that involves 4-7 specific mutations, the evolution of two new binding sites between VPUs to form a pentamer, the evolution of a new binding site between VPU and tetherin, we have the ancestral (SIVcpz) and derived (HIV-1 group M) sequences, and we know where and to within about a decade when these mutations occurred.
It checks all the boxes, and the only way to claim it didn’t evolve is to say God, uh, sorry, the designer, actively intervened to cause those mutations to occur.
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This is your claim to make and the discussion goes back to myosin 7. I believe you think this large number of variants means fixation in the populations. According to neutral theory this is true but the reality is neutral theory in the exon coding regions is not a good predictor.
Wow. What did he think he meant by that? Anyone?
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Well, there is the case in which there are two alleles at a locus, one of them a gene and the other not, as for example in a gene duplication. In that case it makes sense to say that a new gene has resulted from a mutation and may become fixed.
It means that a proteins amino acid variation in a population does not strongly correlate with fixation. Just as beneficial mutations do not strongly correlate with the addition of functional information.
That would seem to be quite a different statement, and it still isn’t clear what you meant by that one either. You should know that reading your posts is a constant struggle to dig meaning out of gibberish. It’s possible that if you tried harder you could manage to communicate, but we’ll never know until you make the attempt.
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Nope. I’m trying to get you to focus on Notch2, remember?
Nope again. You just confirmed that you don’t understand fixation at all.
Nope.
The reality is that you don’t know what you’re talking about.
One of four! Congrats. So why do you repeatedly write about genes being fixed?
That wasn’t even close to the case being discussed, although there’s a high probability that Bill will claim it does.
More word salad, back to pathologically avoiding the well-defined word “allele”!
And you can simply point out something you need clarification on. I was writing to John M on a subject we have been discussing for years where he has been trying to make the case for genetic diversity based on tolerated amino acid substitutions in proteins specifically myosin 7.
That has been done many times by many people to no avail.
I would not describe any of our conversations as discussions.
I haven’t been “making any case” for genetic diversity. I’ve simply been pointing out your pathological avoidance of relevant facts.
Specifically, there is no protein named “myosin 7.” That’s a reminder of your inability to dig deeper.