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GNAT1 and GNAT2 amorphs are known to cause forms of blindness. The molecular basis for one form of this disease is a knockout of the gene GNAT2.
1. In the retina, all the photo-opsins (LMS) are still present, why are they unable to signal to the brain correctly?
2. In a knockout of GNAT1 all the photo-opsins are still present. In contrast to GNAT2, they are able to signal to the brain correctly. Why are these mutants distinct in this regard?
Please answer the questions. Thanks in advance!
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