Scientists Catch Jumping Genes Rewiring Genomes

Then why don’t any of the people who directly study them, producing new data, agree with you?

No offense, but what “seems” to be true to you does not appear to be based on any understanding of biology.

From what I can see, you don’t appear to be engaging with any of the actual findings of the paper, so it’s hard for me to understand how to help clarify anything.

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Why does a primer in PCR stick to a specific DNA sequence, instead of just any sequence?

How is that even a question? There are different cells, they have different mutations, some therefore reproduce better than others. If you starve to death, the reason you die is because something inside your cells fails to occur, but the result is that your die and are no longer part of the population. That’s how selection acts through events that occur “within a cell”. The things that happen inside the cell affects the whole organism.

No, it doesn’t seem like that at all. Perhaps you just have no understanding of physical organic chemistry? Did you ever take a course in organic chemistry? Try to first understand my question about primers and PCR. You have to understand that there are good physical and chemical reasons why a DNA primer binds a particular sequence instead of just randomly anywhere and everywhere. Same holds for why particular molecules like transposons insert in DNA, instead of just “randomly doing things”.


That’s fine, maybe I just don’t get it in my layman’s understanding of what’s going on. I’ll try to keep learning.


Because it’s designed, of course.

@thoughtful the word “architecture” is neutral with respect to design. I think you were reading into it meaning that wasn’t intended.

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What about shotgun primers?

I don’t think I read anything into it. Certain words will reinforce the worldview I already have, as it seems common sense to me to think of architecture in terms of design.

Somebody’s got to design the shotgun. Isn’t that how it goes?

You seem to be embracing your misunderstanding, rather than correcting it. That strikes me as non-ideal way to learn new concepts.

If you’d like to learn more about what geneticists mean when they refer to “architecture”, you could do worse than this review paper (warning: direct link to pdf):

Genetic architecture: the shape of the genetic contribution to human traits and disease

Here’s a relatively concise definition from the paper:

Genetic architecture refers to the landscape of genetic contributions to a given phenotype. It comprises the number of genetic variants that influence a phenotype, the size of their effects on the phenotype, the frequency of those variants in the population and their interactions with each other and the environment.

The term applies just as well to traits that we can see evolving in real-time (e.g., the timing of flower development in plants at the edge of their range, or the ability of a microorganism to grow on a particular food source) as it does to more complex phenotypes. Its use simply doesn’t imply anything about design.

Sure, for an odd definition of “design” that includes picking random sequences.

Well, I appreciate the criticism. But I wasn’t able to glean from the earlier comment that the word was a scientific term, so I didn’t know it was a concept to learn. But thank you for explaining how it is used.


Architecture is really neutral, and just means “how things are laid out or distributed” or the “structure” of an entity. For example, we can refer to the “architecture” of a pile of sand deposited by the wind, which is clearly different than the “architecture” of a puddle. Or the architecture of a glacier, or the architecture of Mt. Everest.

You wrote,

Of course, God created all things, and in this sense he designed the pile of sand, the puddle, the glacier, and Mt Everest. But the mere fact that we refer to all these things (anything really) with the term “architecture” is not what would make anyone think this.

The point also is that what the ERVs are doing is not precise. The vast majority of ERVs don’t do anything useful. A few of them do something interesting, so it is not really accurate to say ERVs as a whole are acting in precise ways. Given how many ERVs there are doing nothing particularly useful, the chances that a few are doing something precise that is useful is quite high.

One way to think about it is as shots at a basketball hoop. An unskilled player throwing a ball into the air is very unlikely to score a point. But what if you do it a 100 times? 1,000 times? Or even 1,000,000? Well, at some point, it starts to become very likely that a few of those random throws are going to sink a basket.

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Having looked at the paper again, I think this is actually a better description of how “architecture” is being used than my comment above about genetic architecture. The paper is more about architecture in the sense of “what is the structure of the protein”. Genetic architecture is a related, but slightly different concept.

Is this an argument from the absence of evidence? How many have been tested? How do we know they don’t do something during fetal development (as it seems the ones that have been identified do).

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No. It’s an argument from the biochemistry of gene-regulation and the sequence-properties of most ERVs. Many ERVs are actually actively silenced, as in permanently shut off by silencing proteins that prevent their activity. This is a defense mechanism.

And many others are too mutationally degraded to function. And then the majority of the few that do have some activity, their activity levels are at the level of background noise, the kind of activity that is physically unavoidable at the molecular level. And this is even without using lack of conservation as another argument against their function.

Oh and of course, be wary of hasty generalization fallacies, which usually take the form of “some - therefore all” in molecular biology. Just because some ERVs are functional doesn’t mean all ERVs are functional. The fraction of total ERVs known to have function is tiny (estimated to be <0.1%), and the vast majority belong to the categories I mentioned above.


Exon shuffling and gene regulatory networks are observed in action in the present, so I do not understand why you make the distinction about origins. But if you insist on it, then please note that gravity and the standard model of particle physics (which are forces observed in the present) play a key role in origins models for stars, galaxies, and even the entirety of the universe.


Just as physics observed in the present (gravity, the standard model of particle physics, etc.) play critical roles in understanding the origin of stars, galaxies, and the whole universe, biological forces observed in the present (exons, gene shuffling, etc.) play critical roles in understanding the evolution of all life in which those forces have been present.

This definition would include common ancestry for all prokaryotes and eukaryotes, but it would not include pre-biotic metabolic functionality prior to the first cells. Such functionality is not thought to have had DNA replication. The theory of evolution does not depend on the origin-of-life hypotheses.


Just as there is no scientifically meaningful design claim for physics forces and their roles in stellar evolution, galactic evolution, and C-lambda, there is no scientifically meaningful design claim for biological forces and their roles in the evolution of life on earth.

It is of course possible to step outside of scientific investigation and undertake philosophical investigations such as fine-tuning, prime mover arguments, etc.


P.S. You really seem to want to hijack this thread into a forum for your design claims, Bill. If you still feel like discussing design and philosophy of science issues, kindly start a new thread.

EDIT: typos

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I was just trying to answer your post. We can leave it at that.

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