The Mystery of Tetrachromacy

Very inaccurate summary, since I skimmed: Up to 12% of women have an X chromosome mutation that creates a fourth cone. This cone generally overlaps the spectral region covered by the cones sensitive to red and green. The exact area of overlap determines whether or not each woman sees "more": If the fourth cone completely overlaps the region covered by an existing cone, no new information is presented to the visual system and the input is effectively discarded (she sees "just as much" red or green, not more, not less). If, however, the fourth cone has peak sensitivity in the gap between the cones covering red and green, she will she up to 100% more colour than women with normal vision.

That's not quite correct. Where one cone type has a peak response, another may respond with a signal that is only one percent or less of its peak response, but the frequency regions in which hey have _any_ response basically overlap. Given the sensitivity curves, that difference is academic for blue versus red and green sensitive cones, but not quite for red versus green sensitive cones.

What differs is the amount in which having a fourth type of come allows one to get rid of metameries (https://en.m.wikipedia.org/wiki/Metamerism_(color), a term that the article surprisingly doesn't mention)

If your fourth come type has a response curve that is very similar to one of te 'normal' three, there should still be _some_ effect, but it will be hard to devise an experiment that shows the ability to discriminate additional colors.

But given the impact that not having red or green cones with their fairly similar sensitivity curves has, I suspect having a fourth curve, even if it falls between the two, will have a measurable (in the lab) effect on one's ability to discriminate colors.

First thought:

The usual pattern is that only one X chromosome gets transcribed in any given cell.[1] This keeps the dosage of all those proteins correct. Otherwise there would need to be a separate set of dosage controls for XX and XY people.

The inactivation occurs pretty early in life, and when cells replicate they keep the inactivation. This results in macroscopic regions of the body with consistent inactivation. Usually this isn't noticeable, but in cats coat pigment is on the X chromosome, and heterozygous cats often show "tortoiseshell" or "calico" coloring. The patches of contiguous color there are larger than a retina.

So it seems entirely likely that all the cells in a human woman's retina would use the same X chromosome.

On the other hand, that predicts half of het women would be colorblind, which isn't observed. So maybe not so simple...

I have a second thought about downstream neural hookups and the mechanisms for those, but it'll have to wait for later.

[1] https://en.wikipedia.org/wiki/X-inactivation

The key is that which X chromosome is deactivated is not the same in all cells.

It does occurs fairly early in the development process (a stage called gastrulation), and the deactivation does persist for all cells that descend from a given cell present. But critically, it's late enough that a retina could conceivably possess cells descending from two different "lineages".

You can actually visibly see the "resolution" of the deactivation by looking at tortoiseshell cats. Each blotch of orange/black represents one cell present at the deactivation stage.

Maybe because people kept telling her that she must be tripping?