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  1. What causes the difference in their spectral sensitivity of the S, M and L cones. I'm guessing that the opsin or photopigments are different, but haven't been able figure out conclusively from my web searches. Would you happen to know what opsins or photopigments each of cones have?

  2. In Protanopia, the L cones are absent, or their spectral sensitivity has shifted. In the latter case, is it that the molecular structure of the opsin in this cone is different than normally expected, or is it that the opsin is using a different photopigment than normally expected?

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When we talk about spectral sensitivity, we talk about the spectral sensitivity of light-responsive complexes which are composed of

  1. non-protein chromophore moieties that combine with
  2. photosensitive chromoproteins.

In cones, you find a specific kind of opsin (photopsin) which combines with a non-protein photopigment that reacts to light via photoisomerization or photoreduction. Long story short: with light, you change the shape of the protein, and this initiates or boosts signal transduction cascades.

This study on Drosophila photoreceptors and spectral sensitivity-modulating factors is a great place to start, with supporting empirical data.

You'll find that both protein component and chromophore affect spectral sensitivity. For instance, difference between Rh1 and Rh2 opsin are responsible for different spectral sensitivities, as well as differences between the same opsin (say, where amino acid subsititutions are made to recapitulate other photoreceptors' structures and sensitivities, see this example). Likewise, the chromophore affects the overall sensitivity to light spectrum too:

The apparent lack of reduction in sensitivity of the UV-sensitive Rh3 and Rh4 rescue flies may be explained by the simultaneous reduction in UV-sensitising pigment associated with Rh1, which strongly absorbs UV wavelengths in the outer receptors.

This answers your title question.

Protanopia is characterized by missing or malfunctioning L-cone (red) cells. The cells are absent/malfunctioning, so the pigment genes specific to the L-cone have no 'place' to function, or are themselves absent from the retina (no expression).

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