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From Annenberg Learner:

Because the X is inactivated randomly in cells, one cell could have the maternal X inactivated, while the adjacent cell could have the paternal X inactivated. This causes a pattern of gene expression called mosaicism, which occurs when different alleles of X-linked genes are expressed in different cells.

However, this seems at odds with colorblindness being more likely in males. From Wikipedia:

The genes that produce photopigments are carried on the X chromosome; if some of these genes are missing or damaged, color blindness will be expressed in males with a higher probability than in females because males only have one X chromosome, whereas females have two and a functional gene on only one of the X chromosomes is sufficient to yield the necessary photopigments.

Question: If X chromosomes are randomly inactivated cell by cell, shouldn't the fully functional photopigment-producing gene be inactivated approximately half the time? In which case, wouldn't we instead see females with colorblindness with higher frequency as males, but experiencing colorblindness to a lesser extent? (After all, two X chromosomes means two chances for a dysfunctional gene.)

I'm guessing I'm missing a piece of the puzzle here, e.g., perhaps the relevant cells "know" to inactivate the dysfunctional X chromosome, or perhaps it's to do with X chromosomes only being incompletely inactivated.

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    $\begingroup$ @Christiaan. I was thinking the exact same thing about the tags. But it had a part about sex determination in it, and while not what I would consider sex determination it was related to sex-linkage... I agree with your decision. $\endgroup$
    – AMR
    Dec 12, 2015 at 21:45
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    $\begingroup$ @AMR - I just posted in chat. Will ping $\endgroup$
    – AliceD
    Dec 12, 2015 at 21:48

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In heterozygote females with colour defect genes on the X-chromosome, even if approximately half of their photoreceptors are dysfunctional they usually have enough functional cone photoreceptors to have normal colour vision.

From Molecular genetics of colour vision deficiencies:

Due to X-chromosome inactivation during early development, heterozygotes are mosaics for two populations of cones, one expressing visual pigment genes encoded by an X-chromosome that would cause colour vision defects in males, and the other expressing genes that would confer normal colour vision on a male. In support of this, patches of defective colour perception were detected by shining a very narrow beam of red or green light into the retinas of female heterozygotes for X-linked colour vision defects. The majority of heterozygote women (carriers of colour vision defects) have normal colour vision.

This means that – in most cases – for a female to be colourblind, her father must be colourblind and her mother must be either a heterozygote (carrier) or homozygote colourblind. In a male, only the mother's X-chromosome determines whether he inherits the defective genes, so he is more likely to have the colourblind trait.

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