Intelligent Design and Common Descent

Science
Design

#249

From the Wissler et al. (2013) paper:

What evidence do you have to refute their findings?


(Bill Cole) #250

The lack of a model that demonstrates how these mechanisms generate the functional sequences we are observing.


(S. Joshua Swamidass) #251

@colewd we just gave you demonstrated mechanisms. Either engage what others are writing or confine your posts to the chatter category.


(Bill Cole) #252

This is not my point. I will table this for now .


(Dr. Patrick Trischitta) #253

@Agauger Thanks, I read the piece and I fairly good understanding on what you are saying. I do have questions. But instead of asking questions to you now, I am going to step back and watch the interaction you have with the experts here. I will probably gain new insights that way and have even better questions to ask you.


#254

I just gave you one of the the models: non-deleterious frame shift mutations.


(Bill Cole) #255

Thanks. Lets table this for now as I think this discussion folds into Ann’s arguments.

How rare is functional space inside total sequence space?


#256

It would appear that it isn’t as rare as ID/creationists claim. There are thousands of thousands of examples of just a few mutations producing functional proteins from previously non-coding DNA. We have both the functional and non-functional sequences and the mutations that differ between them. So why aren’t these examples of mutations that produce function?


(Ann Gauger) #257

@swamidass @T_aquaticus

We are observing functional sequences which look like they could be the product of those mechanisms, based on sequence similarity and location. Fine, what I have asked for and what Bill is asking for, is demonstration that those mechanisms, acting on other random sequence, can produce functional product. We are not the only ones to think such work is important. Here is one approach and 2 reviews that describe some of what is being and needs to be done…

https://www.nature.com/articles/nature11184



(Ann Gauger) #258

I wonder if you are talking about pseudogenes here. They are an example of gene death, not gene birth.

Thousands of thousands and only a few mutations? If they are not pseudogenes can you cite a paper or two?


#259

We have the functional and non-functional DNA and the sequence differences that separate them. Those differences can be produced by substitutions, genetic recombination, and indels, all of which have been observed happening spontaneously in living populations. How is that not a demonstration that these mechanisms can produce new genes?

From what I am reading, they all feel that mutations are the source of de novo genes. All they are curious about is the order that the mutations occur in.


#260

I am referencing the paper on orphan genes found in the ant genome. For example:

There is significant sequence homology and a frame shift. That’s just a few mutations, and it produces a new gene.


(Ann Gauger) #261

@T_aquaticus

We know that these sequences exist and there are certain statistical statements that can be made about their properties, phylostratigraphy, mutational profile, sometimes function, and structure. These are the success stories. Saying we know what kinds of mutations produced them is not the same thing as saying it is likely that functional coding sequence comes from non-coding sequence.

An experiment: Neme et al have tried it, though I am not sure with great success. Make a library of random sequence. Put it in an expression vector for what ever cell type you choose. Choose a phenotype or types to select for. Go. (This is a poor design. You restrict the possible functions.)

All right. Take an identified de novo gene that is expressed and has a known function. Mutate it to return it to its unexpressed state (preserving expression itself). Put it in an appropriate cell type. What happens?l

Still not satisfied? Neither am I. But I hope you can see the question I am asking. Is random mutation, drift, and selection enough to produce what we are seeing?


(T J Runyon) #262

So, basically the designer made it look just like evolution happened?


#263

That seems to be a built in excuse for rejecting any example given. It is unlikely that anyone would win the lottery, yet it happens all of the time.

Nature has already done that experiment. We have species with the non-functional DNA and the functional DNA.

What I see is people struggling to find excuses to reject the obvious mechanisms that are producing de novo genes.


(Ann Gauger) #264

No. You are thinking it’s due to evolution, meaning random mutation, drift, and selection, without checking whether the mechanism is capable of doing what we say it is.

There is a reason biologists used to say getting function from random sequence was rare. Now we say, oh no, it isn’r rare because we see these sequences. But there is a step missing. What is responsible for those sequences? What if the biologists of the pre-genomic era were right?

Then what is the explanation?


(T J Runyon) #265

This doesn’t really answer my question. You said it seems like these functional sequences arose from the proposed mechanisms. So it looks like what we would expect if it did arise naturally. But you think it hasn’t been demonstrated so design is on the table. If it looks like what we would expect on evolution then the designer seems to design things that way.


(Ann Gauger) #266

@T_aquaticus

I am not struggling to find excuses for anything. It is a legitimate question that should be answered. If it weren’t, why are people putting time and money into doing the work?


#267

Are these mechanisms able to produce substitutions, indels, and recombination events? YES!!! I have checked to see if they are capable of producing all of those types of differences, and they are.

What is responsible is substitutions, indels, and recombination, exactly what we see happening naturally in every single living population.

You seem to be stuck in the Sharpshooter Fallacy. Let’s look at the mutations I have, according to papers that have measured the mutation rate in humans. There are about 50-100 substitution mutations in every human. The chances that those mutations will occur at the exact bases they do occur is 3 billion to the 50th power, or 1 in ~7 x10^473. The chances that those 50 substitution mutations happened at those exact bases is astronomical, YET IT STILL HAPPENED!!! Do you understand this?


#268

The answer is substitutions, indels, and recombination.