= T. M. Redmond
{c}
<T. M. Redmond> is the first author of a 1998 study establishing an essential role for <RPE65> in the mouse <visual cycle>. The team compared mice lacking <RPE65> with control animals using <electroretinography> and biochemical measurements of <vitamin A> derivatives. The mutant mice lacked normal <rod cell> responses and <rhodopsin>, despite retaining the <opsin> component of the light-sensitive <protein>.<Rpe65 is necessary for production of 11-cis-vitamin A in the retinal visual cycle by T. M. Redmond and others>[Abstract; Nature Genetics 20, 344–351, 1998]{ref}
This separates two possible explanations of failed light detection. A <rod cell> may contain <opsin> yet fail to assemble working <rhodopsin> if the required light-absorbing <retinal> is unavailable. The mutant mice accumulated one group of <vitamin A> derivatives while lacking the normal 11-cis products, linking the physiological defect to disrupted <visual cycle> chemistry. The experiment demonstrated a requirement for <RPE65> in this pathway; deleting a <gene> alone does not identify every reaction performed by its <protein>.<Rpe65 is necessary for production of 11-cis-vitamin A in the retinal visual cycle by T. M. Redmond and others>[Abstract: retained opsin, accumulated all-trans-retinyl esters and absent 11-cis-retinyl esters]{ref}
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