OPN1LW

OPN1LW produces red-sensitive opsin, while its counterparts, OPN1MW and OPN1SW, produce green-sensitive and blue-sensitive opsin respectively.[7] OPN1LW and OPN1MW are on the X chromosome at position Xq28.[11] They are in a tandem array, composed of a single OPN1LW gene which is followed by one or more OPN1MW genes.[11] The locus control region (LCR; OPSIN-LCR) regulates expression of both genes, with only the OPN1LW gene and nearby adjacent OPN1MW genes being expressed and contributing to the colour vision phenotype.[11] The LCR can not reach further than the first or second OPN1MW genes in the array.[11] The slight difference in OPN1LW and OPN1MW absorption spectra is due to a handful of amino acid differences between the two highly similar genes.[8]

The LWS type I opsin is a G-protein coupled receptor (GPCR) protein with embedded 11-cis retinal.[11] It is a transmembrane protein that has seven membrane domains, with the N-terminal being extracellular and the C-terminal being cytoplasmic.[5] The LWS pigment has a maximum absorption of about 564nm, with an absorption range of around 500-570 nm.[6] This opsin is known as the red opsin because it is the most sensitive to red light out of the three cone opsin types, not because its peak sensitivity is for red light.[7] The peak absorption of 564nm actually falls in the yellow-green section of the visible light spectrum.[7] When the protein comes in contact with light at a wavelength within its spectral range, the 11-cis-retinal chromophore becomes excited.[10] The amount of energy in the light breaks the pi bond that holds the chromophore in its cis configuration, which causes photoisomerization and a shift to the trans configuration.[10] This shift is what begins the chemical reaction sequence responsible for getting the LWS cone signal to the brain.[10]

LWS opsin resides in disks of the outer segment of LWS cone cells, which mediate photopic vision along with MWS and SWS cones.[10][12] Cone representation in the retina is substantially smaller than rod representation, with the majority of cones localizing in the fovea.[12] When light within the LWS opsin spectral range reaches the retina, the 11-cis-retinal chromophore within the opsin protein becomes excited.[10] This excitation causes a conformational change in the protein and triggers a series of chemical reactions.[10] This reaction series passes from the LWS cone cells into horizontal cells, bipolar cells, amacrine cells, and finally ganglion cells before continuing to the brain via the optic nerve.[10] Ganglion cells compile the signal from the LWS cones with all other cone signals that occurred in response to the light that was seen, and pass the overall signal into the optic nerve.[6] The cones themselves do not process colour, it is the brain that decides what colour is being seen by the signal combination it receives from the ganglion cells.[10]

Before humans evolved to be a trichromatic species, our vision was dichromatic and consisted of only the OPN1LW and OPN1SW genes.[8] OPN1LW is thought to have undergone a duplication event that lead to an extra copy of the gene, which then evolved independently to become OPN1MW.[8] OPN1LW and OPN1MW share almost all of their DNA sequences, whereas OPN1LW and OPN1SW share less than half, suggesting that the long wave and medium wave genes diverged from each other much more recently than with OPN1SW.[11] The emergence of OPN1MW is directly associated with dichromacy evolving to trichromacy.[6] The presence of both LSW and MSW opsins improves colour recognition time, memorization for coloured objects, and distance-dependent discrimination, giving trichromatic organisms an evolutionary advantage over dichromatic organisms when searching for nutrient-rich food sources.[6] Cone pigments are the product of ancestral visual pigments, which consisted of only cone cells and no rod cells.[10] These ancestral cones evolved to become the cone cells we know today (LWS, MWS, SWS), as well as rod cells.[10]