It may seem strange but random chances to sequences is the raw material for every evolutionary innovation. Of course, most of the changes are bad or neutral, but occasionally they are spectacularly creative. For a simple example, one need only look at the emergence of lactase persistence - the ability to process lactose through adulthood - in human populations. Mutations to accomplished this appeared in THREE different human populations (and we know they were separate emergences because they are different mutations) not long after humans began to domesticate goats, sheep, and cows. The random mutations are always happening. But when a potentially beneficial mutation happens in the right place and the right time⌠you get adaptation. 
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Changes are not breaks, theyâre changes. They encompass both breaks and novelties, and sometimes breaks can facilitate novelty. An example of the molecular level - a couple of nucleotide changes in a short transcription factor-binding motif can change the binding affinity of that site from transcription factor X to transcription factor Y. This changes the regulatory network, so Gene A might go from being expressed in tissue B to being expressed in tissue C, for example.
Again, this could be deleterious, or it could be beneficial and produce interesting novel features (usually in concert with other similar changes to other genes).
Whats the right way?
I donât think the current paradigm explains new features. I think it explains genes being passed from one generation to another. New features require new functional information. This information lives in very large sequence space so any change is exceedingly more likely to break it down then generate new information.
Too strange
Can you cite an example of this?
None of that is particularly contentious, weâd just argue that though the sequence space is large, itâs so large as to be innaccessible to the natural process of evolution. I also think fitness landscapes are surprisingly smooth when you take into accout their hyperdimensionality. Have you read Andreas Wagnerâs book?
An example of changes in transcription factor binding motifs changing the transcription factor that binds to the motif? I thought that was self-evident. Do I really have to give an example?
Yes. A couple of years ago along with Shapiroâs book.
What did you get out of it?
He had an explanation for the arrival of complexity that involved metabolic networks. I thought it was interesting conceptually but did not address the problem we are discussing which is the arrival of large functional sequences.
Yes. Eukaryotic transcription factors are very complex and I am skeptical you can swap them randomly and not have a catastrophic event.
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Instead of looking at it as changes to a sequence, look at it as beneficial changes to an organism and its descendants.
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The source of that change is?
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Pragmatism.
Yes, there are random changes. But it is pragmatism that makes use of the changes that work well.
I think @colewd was asking how you get changes in the organism.
Once a change is made, pragmatism, aka natural selection can kick in⌠not before.
The only pragmatism I see to random changes in the cell nucleus is purifying selection.
This issue is what I was getting to above and Iâm still confused about it. This could be a sidebar or maybe you donât even wish to engage, Neil, but, to me (admittedly from the outside, looking in) the beneficial changes to an organism are a description of what we see. As such, they cannot also be the cause or explanation.
When Dr. Lents would describe the mutations, he would also speak as to their acceptability(?) Is it not circular in terms of an explanation to define the mutations as being either neutral of beneficial, but also to point to their being beneficial as causal? Every time I read this kind of statement, it doesnât feel right to me. But I could be misunderstanding.
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So you agree that transcription factors can be âswappedâ by mutations, youâre just skeptical that it could happen and be anything but a catastrophy?