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This is fairly typical for genetic studies. We can observe an association, without understanding the causal relationship. Those of us who take the molecular biology/biophysical view of genes and proteins have been watching the geneticists slowly discover that "the allele of a gene that codes for" mental model is very limited; at least they're starting to pay more attention to the regulatory changes and indels and structural rearrangements, even if they don't have the tools to explain the underlying mechanism.

Like most hair/skin coloring, it's related to melanin production, regulation, and distribution.

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Very often the appropriate lens for genetic expression isn’t traits, it’s tools - a gene knockout isn’t “blue eyes now”, it’s “socket #6 is missing from the kit,” which is why you’ll see blue eyes and a bunch of other unrelated stuff.

(With love to my blue-eyed friends in the thread)

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Yes; the molecular biologists have been pointing out this for decades. Trait-based genetics really set back the mental model for understanding complex phenotypes (the ultimate phenotype being the molecular structure of an entire human being over time). It's been an uphill battle to fight the long-term insistence of genetics professors that we just need to do a few more association studies on larger genome populations and all of diseases will be cured.

But I don't know how well a gene knockout maps to a single tool missing (in terms of analogy); due to the intricate, complex, functional history of evolution, many genes play multiple roles (a wrench can be used as a hammer), and many phenotypes are resilient to loss of one or another tool (can't find wrench? Use this hammer instead!) Understanding those details at the molecular level and relating them to the full human phenotype has been a major interest of mine for decades, but I can't say I really understand anything about it.

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Tool blueprints, I might suggest. (I.e. genes are blueprints for tool proteins/enzymes/etc.)

Though with the weird proviso that every so often, each cell opens up its cabinet of blueprints and just 3D-prints up one of every tool it has a blueprint for, unless sees a sticky note on the blueprint telling it to skip (silence/suppress) printing one of that tool for now.

(And, if anyone is wondering, this strategy of "just always print all tools unless otherwise specified" works because these tools are mostly very flimsy, breaking/being consumed quickly after just a few uses, sometimes as little as one. So there's a constant need for new prints of most of these tools. The ones that are more durable, the cell has to be more careful to not overproduce.)

I say that "tool blueprints" is a useful model, because it makes it more intuitive that e.g. for the important stuff, the genome keeps a pile of duplicate blueprints for the same tool; and then also keeps some machinery (autosense suppressors) to add and remove notes to those blueprints on observing that there's "enough" or "not enough" of the tool floating around inside/outside the cell. Which allows "having N redundant tool blueprints" to work just like "having only one tool blueprint" does, rather than drowning you in printed tools; yet also ensures that if something scribbles over one of the blueprints, everything "just keeps working", since the machinery will just end up unsilencing the other blueprints more often. (And also, as a bonus, allows the "corrupted" duplicate blueprints to act as forks of the parent blueprint, gradually being redrawn over N generations of mutations into a working blueprint for a new tool, much more quickly than a new tool blueprint could be mutated into existence from scratch, and without losing the ability to produce the original tool in the process.)

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Oh, and to be even more pedantic, it's probably best to think of genes as tool part blueprints, since several proteins might need to come together and link up to make a functional tool; and since a single part might end up being consumed in the creation of several different tools. (But that doesn't really add much to predictive intuition, unless you're trying to predict the precise failure modes of any particular tool's production under a point mutation of a single part. You can mostly forget about it.)

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See, this is the dicsussion I didn't want to have. I don't really care about the analogies, I care about the mechanistic details in a holistic way, and I've concluded that no human alive is smart enough to understand that, so we need AI to help us make forward progress on complex phenotypes now.
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Yeah but there's good reason for an investigation here, in particular:

  Arhgap36 is known to cause developmental problems in other animals when it is over- or under-functioning.
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Said every scientist who wanted more grant funding.
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The color is genetic. The behavior is due to them not having a soul. While there is an obvious relationship, it's not direct but mediated by the color.
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The behavior is because of having one orange brain cell.
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