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Mouse vision has a rhythm all its own
Date:8/24/2007

at completely lack a critical component of the clocka gene known as Bmal1showed abnormal gene activity in hundreds of retinal genes and defective electrical responses in inner retinal cells critical for image processing. The animals' photoreceptors still sensed light normally and, upon close examination, their eyes appeared normal.

Mice deficient for the Bmal1clock gene only in their retinas had defects of vision essentially identical to those of mice lacking the gene in all tissues, evidence that the clock's function in the eye itself is the key. By contrast, the retinas of mice with brain lesions that disabled the SCN maintained normal visual responses and the regular ebb and flow of retinal gene activity.

"Circadian clocks in mammals are widely distributed, but except for the SCN clock known to regulate behavior, their physiological functions in vivo have largely been mysterious," Weitz concluded. "The studies described here indicate that an intrinsic retinal circadian clock regulates visual processing in vivo and that it does so autonomously, with no detectable contribution from the SCN or other clocks."

Whether the retina's ability to keep time on its own is the exception, "we don't know," Weitz said. Unlike other tissues, the eye's role as a light sensor does provide its component structures a unique ability to track the environment on their own authority, he noted.

Nonetheless, he said, "our work provides evidence that circadian clocks outside the SCN contribute important physiological functions in mammals. Over evolutionary time, different cell types have likely recruited the circadian clock mechanism inherited from a single-celled ancestor for control of specialized tissue-specific processes," he suggested.


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Contact: Nancy Wampler
nwampler@cell.com
617-386-2121
Cell Press
Source:Eurekalert

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