From Panda's Thumb: The Evolution of T-URF13: Does Irreducible Complexity Count or Not?

Well, the probability (before the fact) that someone will be born in each generation is pretty high, and the probability that a person born in my generation will have a genome is 1. Now you are remarking that someone won the lottery, which is highly probable. We have to distinguish it from the probability that a given person will win, these are two different events, with different probabilities.

There were two components involved, though, right? “Data show that T-URF13 has arisen by rearrangements involving recombination events from two different fragments of the mitochondrial gene coding for 26S rRNA (see Fig. 2–4).” So this will not produce all of the above that you listed.

Coronavirus genomes recombine. Do they have any of those parts that you claim are required?

5 Likes

And the probability that a bacterium will divide and pass on mutations is also 1.

I haven’t made a lottery analogy, no. I used your personal history as an example of a (from the perspective of the past) very unlikely outcome of 10 consecutive generations of 100 mutations. Stick to arguments I actually make. I make that analogy to your own history exactly because it makes your mistake all the more obvious.

Yes it will, and it did.

You are confusing the number of attributes and functions of the gene that evolved, with the number of parts from which that gene derives.

A gene can originate from two parts of another gene(in this case two fragment of 26S rRNA), but the resulting gene can have many more functions than the number of parts that it derives from.
So the fact that T-URF13 seems to derive from only two fragments of 26S rRNA doesn’t mean it can’t result in a protein that has multiple protein-protein binding sites and is irreducibly complex.

If you actually bothered to read the link provided in the op, and the references it makes, you would understand that T-URF13 is a protein that oligomerizes to form a membrane pore complex. You need to understand what this word oligomerizes means. It means when the gene encoding the T-URF13 protein is expressed multiple times there will be multiple copies of that protein present in the mitochondrion. They self-assemble into a larger structure that sits in the mitochondrial inner membrane and forms a pore complex. They form an oligomer of T-URF13 proteins. They stick together because the T-URF13 protein has multiple protein-protein binding sites. It must have at least two to be able to do that.

This is the basic idea:

3 Likes

Except he is not consistent on that. He flip flops back and forth between a broad and a restrictive use of the term “Darwinism” as suits whatever point he wants to make at a given moment.

I think he does this so he can get away with lying and not be sent to Hell by his god, but that’s just a guess.

3 Likes

If it was deterministic then we would see the same protein evolving independently in many different lineages of corn.

3 Likes

That’s exactly the mistake you and other ID proponents make. You look at one adaptation and then calculate the probability of that specific adaptation evolving instead of looking at all of the possible adaptations that could have evolved.

5 Likes

How would any possible adaption build a functional living organism?

Why would it have to? Nobody says it does. What we say is that when life exists, how you get new functions is by the emergence of any possible adaptation.

In the case of antibiotic resistance there are innumerable ways to develop resistance. One mechanism is to adapt an existing enzyme to accept a new substrate (how TEM1-beta-lactamase evolved). Another is to gain a novel small peptide sequence that inserts into the bacterial membrane and depolarizes it so the cell takes up much less antibiotic.

Abstract

Resistance to antimicrobial agents has become a major source of morbidity and mortality worldwide. When antibiotics were first introduced in the 1900’s, it was thought that we had won the war against microorganisms. It was soon discovered however, that the microorganisms were capable of developing resistance to any of the drugs that were used. Apparently most pathogenic microorganisms have the capability of developing resistance to at least some antimicrobial agents. The main mechanisms of resistance are: limiting uptake of a drug, modification of a drug target, inactivation of a drug, and active efflux of a drug. These mechanisms may be native to the microorganisms, or acquired from other microorganisms. Understanding more about these mechanisms should hopefully lead to better treatment options for infective diseases, and development of antimicrobial drugs that can withstand the microorganisms attempts to become resistant.

For each of these basic mechanisms of resistance, there are numerous ways of achieving them.

Looking at the life of any given organism more holistically, any change that raises survival and reproductive fitness are the resource of evolution. That means anything that has the potential to kill the organism or reduce it’s reproductive output is something to which an adaptive response is possible.

This is where the hard pivot to Theology starts.

The same way they do now.

On the contrary. You’ve been doing theology from the very start. Creationism isn’t science at all, just religion. Your attempts at science all rely on theological axioms that you refuse to examine — and you’re probably incapable of examining them.

It has to because complex adaptions require interaction. If evolution is true (small gradual steps) specification increases with the addition of every new component. This is why Behe’s argument is so powerful.

When you bring in micro evolutionary evidence to support macro evolutionary changes you are using an apple to explain an orange.

Then again, the probability (before the fact) that someone will be born in each generation is pretty high, and the probability that a person born in my generation will have a genome is 1. Someone being born in 10 generations is fairly likely, so my presence is not that remarkable.

I find it unlikely that all this function came about by simply combining two parts, the parts must have had pertinent function before the combining.

But the adaptation evolving has a probability of interest, and if it’s small, it means that probably that adaptation didn’t evolve. Certainly the probability of all adaptations evolving is of interest too, but this is a herculean task! So we stick with what is more doable.

But we’re not just talking about just any imaginable history of ancestors, just like we’re not just talking about any imaginable history of mutations. We’re talking about the specific results of each: You with your genome, and the flagellum.

Just like you are the result of a very unlikely series of mutations, as each of your own ancestors have their own unique set they passed on, the flagellum is a result of a very unlikely series of mutations, as the bacteria had their own unique set they passed on.

So this is what it comes down to, then. T-URF13 doesn’t count because ID-creationists simply refuse to believe what happens in reality.

Then your problem is your own intuitions are not a reliable guide to biochemistry and physics.

3 Likes

That’s the Sharpshooter fallacy.

Yet again, the very definition of the Sharpshooter fallacy.

3 Likes

But these two are not comparable, yes, the probability of mutations in every generation is high, but the probability of those mutations producing a flagellum is low, whereas the probability that 10 generations of people will produce a person is high.

No, I believe what happened, I only say that it’s unlikely that two parts came together, which did not have some of this function, and produced this function.

How so? Forensics engages in this type of reasoning all the time: if the probability of this incident happening by natural causes is low, then we conclude it was not due to natural causes.

My argument is not about just any person, it’s about you specifically. Of all the possible people that could in principle have resulted from 10 generation of reproduction, it’s you. Your genome, your characteristics, your set of 10 generations of ~100 mutations accumulated every generation. We didn’t get just any possible person, we got you.

In both cases we got a particular result among innumerable that are possible in principle. Both results are unfathomably unlikely out of all the alternatives we know could have happened. Picking out the particular one we ended up with and computing it’s odds out of all the possible alternative histories, whether done for you or the flagellum, commits the Texas sharpshooter fallacy. Whatever argument you come up with against the flagellum being the result of a long series of compounding chance events can be applied to your own existence and the reasoning would be the same. If one must fall, so must the other. But that would be absurd, since obviously you exist and have at least 10 generations of ancestors. We can thus understand that the flagellum, like yourself, is just a contingent outcome of the history that happened to occur because those were the circumstances at the time.

26s rRNA doesn’t code for protein. It’s the ribozyme within the ribosome of eukaryotes. The gene fragments from which T-URF13 derive come from DNA encoding a ribosomal RNA ribozyme (the ribosomal RNA called 26S rRNA). It is a gene that codes for an RNA molecule. It does not code for protein. So once again, you’re just wrong to disbelieve it. Your intuitions are failing you and you should take a closer look at why that is.

3 Likes

You are only focusing on the solution that was found instead of all solutions that were possible.

4 Likes