Reaping the Whirlwind: protein function without stable structure


(Raymond Isbell) #523

I’m reading your book, Adam and Genome, and found something on page 31 that needs some explanation. You say, “As before, this level of identity far exceeds what is needed for functional insulin, and strongly supports the hypothesis that humans share a common ancestral population with great apes.”

Can you explain the logic behind this statement? How does identify/closeness of gene sequence support the hypothesis that any phenotype is an ancestor of another?


(Raymond Isbell) #524

Thinking more about your claim that genomic sequence similarity is used as supporting evidence for common ancestry, how does one rule out that the mapping of gene to phenotypic trait is not the result of the avalanche effect we see in secure hash algorithms (one-way functions) where a small change in the input can produce very large changes in output. (Links on Secure Hash Algorithms and One-way Functions are respectively: https://brilliant.org/wiki/secure-hashing-algorithms/ https://en.wikipedia.org/wiki/One-way_function).) I had to study cryptography once during my career, and it definitely made my head hurt.

As I think about your claim that a close match in the genome translates into closeness in the phenome, while at the same time we see huge differences in say apes and men at lower levels (e.g., thought, abstract reasoning, etc), it makes me wonder if the amino acid sequences in proteins resulting from the genome act like a one-way function used in cryptography for secure hashes to specify higher level cell, tissue, organ and high level phenotype function. As you know, in a secure hash, a small change in the input can cause a huge change in the output which is exactly what we see in the differences between man and ape at the phenotypic trait level. Evolutionists focus more on the similarities between them instead of the differences. While the differences may seem modest on the surface, at lower levels, I suspect that the differences are huge. Proteins, tissues, organs and how they work together is something we don’t know much about because it involves command and control (C2) functionality. Does anyone understand how the C2 functions work in the cell? How do they map back to the genome? Much of C2 functionality seems like a synergistic property of all the systems working together. If we don’t understand this mapping, how can we have any confidence that it’s an emergent property that resulted from chance and natural selection?

A final comment. As I write this, I can’t help but think back to the new Scientific American ebook that just came out regarding the science behind debates. They describe an effect call the “Einstellung effect” which is the human brain’s dogged tendency to stick with a familiar solution to a problem— the one that first comes to mind— and to ignore alternatives. It applies to me as well as you guys. I look at everything as an engineering problem. You guys have another method that I still don’t quite understand, and I’m not sure you do either. Every time I articulate the problems I see from my systems engineering perspective, you basically ignore it and its logic and retreat back to your insistence that the cell is different. You account for the enormous integrated complexity found in the cell by using terms like robustness, flexibility, and redundancy. Even after I point out that these terms are really just descriptive of the observed effects rather than the cause. No matter how many times I’ve challenged you, you always come back to the same argument, viz., the cell is different so that engineering logic doesn’t apply.

Thougts?


(Christy Hemphill) #525

You’ve been asked repeatedly to propose an alternative. I don’t remember anything serious being proposed. (Sorry, but the words “design” and “intelligence” doesn’t really count as a viable alternative solution in my book.) Is it still ignoring an alternative if an alternative isn’t there? Are you required to search for an alternative if the explanation you have is completely satisfactory?


(Raymond Isbell) #526

Are you not now exhibiting the “Einstellung effect?” You default back to the same tactic as before. You really should read the SA ebook. It’s an eye opener.


(Christy Hemphill) #527

How? Where is the alternative I’m refusing to consider?


(Christy Hemphill) #528

For the record, I have seriously considered young earth creationist solutions. I rejected them on multiple grounds as unsatisfactory.


(Raymond Isbell) #529

All I can say is read the ebook. It was a eureka moment for me.


(Christy Hemphill) #530

Also, you are ignoring the fact that the majority of people here used to have a different explanation, whether it was YEC or ID, and changed their mind based on evidence and arguments to arrive at the position they have now. So, claiming that we are all people whose minds’ can’t be changed because we cling to what we think at first is simply false. That’s how we got where we are.


(Raymond Isbell) #531

What was your logic in rejecting ID?

My first post this morning pointed out that there must be some threshold for rejecting design when design is the obvious answer. You haven’t interacted with that. There are a serious set of questions that must be addressed.


(Christy Hemphill) #532

To clarify, I believe nature is intelligently designed and that the complexity and the fine tuning in the world point to a Creator. But I think that is something I arrive at via intuition and divine revelation, not science.

  1. Almost everything I read from the ID crowd basically took the form of trying to poke holes in evolutionary theory or cast aspersions on scientific consensus. When I looked into it and referred to experts in scientific fields I learned their complaints often involved shoddy scholarship, quote-mining, and misrepresentation of research. So, I did not find them particularly trustworthy.

  2. I didn’t really find an alternative explanation to evolution in ID, just a lot of “this doesn’t make sense, ergo, intelligent design.” That just wasn’t super compelling to me. As far as I know, ID is still trying to come up with an actual model.


(Stephen Matheson) #533

It is statements like this, which fill your screeds, that reveal the vast disconnect between how much you know (which is very little) and how much you are willing to type.

You don’t know what you’re talking about, and worse, you are busily typing while avoiding questions. To use one of your favorite phrases, it’s like you’re hiding something.


(Randy) #534

Keep up the reading. @Raymond_Isbell, how do you think design explains the vitamin C pseudogenes? Thanks.


(Raymond Isbell) #535

Let’s see…I’m asking questions and I’m told that I don’t know what I’m talking about. Did you not recognize the literary structure of the post or is this your standard response to questions that pose a challenge to your viewpoint?

You folks have asked for an alternative to evolution which you have tried to justify with arguments that note the similarities between genomes of species and conclude that they imply common ancestry. I responded with ID as a good alternative, and even offered a scientific approach to validating it (or ruling it out). I then asked how you rule it out. Interestingly no one has responded to that approach, Instead, you keep coming back challenging me to for an alternative to evolution. Are you not recognizing that I’ve not only given you an answer, but have suggested a way to evaluate that answer using good science.

I make a lot of observations about evolutionary logic and find it wanting as a good explanation for life. I recognize that I can be wrong, so I ask for clarification, yet the response is that I don’t understand biology or I don’t know what I’m talking about. What’s left out are answers to my questions and any substantive interaction with the content of those questions. I asked two substantive questions this morning and received nothing back except “why haven’t you offered an alternative to evolution?” and statements that I don’t know what I’m talking about. My questions again: 1) How do you rule out design? 2) Is the process flow for building life where DNA specifies proteins, proteins organize and enable cell function, cells organize to enable tissue function, tissues organize to form organs and their function, and finally organs organize to enable phenotype traits and function similar to the way a secure hash (one-way function) achieves it’s final output? The point behind this second question is that very small changes in the input of a secure hash function result in very large changes in the output. That’s a fair question. I suspect you don’t understand it, and don’t want to understand it (“Einstellung effect”) because it shows the shallowness of the common descent hypothesis. Am I right?


#536

If I might attempt an answer. No. You have been given the example of a change in a single gene which results in longer legs. With no other changes the body adapts to this change and grows longer muscles, blood vessels, and nerves. In fact there are many DNA changes which result in no changes. So the result of small changes could be none, a large change in phenotype, or a small change in phenotype. It is estimated that ever human is born with about 100 mutations. You also acquire additional mutations as you age. If the process was as sensitive to small changes as your example suggests then we would all be piles of goo. The interesting question is why changes don’t cause a larger number of problems. We do know that some small changes can cause problems, such as our broken Vitamin C gene.


(Dennis Venema) #537

Hi Raymond - glad you’re reading the book.

The logic here is pretty simple - if humans and chimpanzees descend from a common ancestral population, then then the genes both species have in the present day would necessarily be inherited from that common ancestor. DNA replication is a really accurate (but not absolutely perfect) process, so we would expect the genes of the two species to be very, very similar to each other but not identical.

To go back to the language analogy - why are Spanish and Italian so similar to each other? Because they inherited their words from a common ancestral source (Latin). But the process of change over time was in two populations - one leading to present-day Spanish, the other leading to present-day Italian. Because the transmission of a language is also highly accurate (but not perfect) we would expect that these two languages would be very similar, but not identical.

*as an aside - no one is saying that chimps are ancestral to humans any more than modern Spanish is ancestral to modern Italian - the idea is that they descend from a common source in the past.


(Raymond Isbell) #538

Thanks Dennis. The book is interesting and becoming a slow read because I’m finding statements on every page that are making me scratch my head and ask, “How does he know this to be true.” The statement above is one example. Can you elaborate a bit? Why does the fact that two organisms on the phylogenetic tree with many common or near common genes necessitate an interpretation that they have a common ancestor? What are the details of this argument? How to you rule out that they weren’t intelligently designed that way? How is it that the “chance/natural selection” process is a more viable explanation that ID? This is actually a serious question and is currently my primary “stumbling block” to seeing the truth of evolution.

On page 33, you say as you compare dogs and humans, Humans, on the other hand, have a diminished sense of smell relative to dogs, and the reason became clear after we sequenced the human genome. Many of our olfactory receptor genes are damaged: they have numerous mutations in them that disrupt their ability to be transcribed or translated. The remains of these genes, however, persist in our genome because of the low error rate for copying chromosomes. Since the protein enzymes that copy DNA don’t know that these genes are defective, they copy them as faithfully as possible, just like any other DNA sequence. As a result, these genes persist for a long time as genetic fossils in our DNA. The historical name for these damaged remains of genes is “pseudogenes” or “false genes." They earned the name because they have many of the features expected of genes but cannot be transcribed and translated as a gene should be in order to produce a protein product.

This prompted in my head the following questions: “How do you know that humans have numerous mutations in the olfactory receptor genes? Could it be that they were designed that way because humans would be overwhelmed with such sensitive olfactory genes. With our much higher developed intellect/emotions, etc. could it be that their “smelly world” would be too much for the human psyche to deal with. Wolves on the other hand are singularly focused on smell since it leads to food and survival which are daily realities that must be dealt with. Wolves don’t have much time to do the social media thing and worry about likes/dislikes so for them the smelly world is normal and they’re able to cope.”

As you answer these questions, be on guard so that you don’t use circular reasoning to frame your answer. Also, be conscious of the “Einstellung effect.” (See the SA article on the science of bias)

McKnight, Scot. Adam and the Genome: Reading Scripture after Genetic Science (pp. 33-34). Baker Publishing Group. Kindle Edition. "


(Christy Hemphill) #539

If you were designing a system, would you intentionally insert a component for a function that would be detrimental to the final system, and then break the component so it didn’t work (i.e. olfactory receptor genes)? Or if you had a prototype the worked well and wanted to design a new model based on the prototype but with some new features, would you intentionally break one of the components so that function didn’t work in the new model (i.e. vitamin C production gene)? I’m having a hard time understanding why anyone would look at broken genes and see it as evidence of good design, unless they were irrationally pre-disposed to insist on design. This Einstellung effect works both ways. :wink:


(Raymond Isbell) #540

No other changes? How do you know that a single mutation doesn’t also result in many downstream changes that contribute to the observed changes you mentioned. That sounds pretty naive, and more like narrative than the result of careful scientific investigation/analysis/testing.

How do you know there are not many changes, but none observable? Again, this sounds like narrative instead of good science.

I think you misunderstand my analogy to the one-way functions in cryptography. The crypto analogy as I think about it also supports the contention by Axe, et al. that a single mutation may have broad downstream results, but only a few lead to viable function. Thus, the ID claim about the rarity of functional protein sequences may be viewed as supporting the crypto analogy.


(Raymond Isbell) #541

This is a common tactic for evolutionists, viz., they employ the argument that since humans with their incomplete understanding of the cell see it as a bad design, clearly God would not do it that way. Are you saying God wouldn’t have done it this way so evolution must be true? Really? Just asking that question would make me go back to the drawing board. When is man’s assessment of God’s way of creating and sustaining the world a good criteria to use for deciding how God does it?

Let’s get away from these meta-arguments and stick to scientific ones.


(Christy Hemphill) #542

This made me laugh, because pretty much this entire thread is you employing the argument, “since I as a human engineer with my incomplete understanding of the cell don’t see how this biological system works, clearly it wasn’t evolution.”