GAINESVILLE, Fla. Retinas in newborn mice appear perfectly fine without any help from tiny bits of genetic material called microRNAs except for one thing the retinas do not work.
In the first-ever study of the effects of the absence of microRNAs in the mammalian eye, an international team of researchers directed by the University of Florida and the Italian National Research Council describes a gradual structural decline in retinas that lack microRNAs a sharp contrast to the immediate devastation that occurs in limbs, lungs and other tissues that develop without microRNAs.
The discovery, reported in todays (May 7) issue of the Journal of Neuroscience, may lead to new understanding of some blinding diseases and further penetrates the cryptic nature of microRNAs important gene regulators that a decade ago were considered to be little more than scraps floating around the cells working genetic machinery.
MicroRNAs are behaving differently in the nervous system than they are in other bodily tissues, said Brian Harfe, Ph.D., an assistant professor of molecular genetics and microbiology at the University of Florida College of Medicine. Judging by our previous studies in limb development, I was expecting to see lots of immediate cell death in the retina. I was not expecting a normal-looking retina in terms of its form. It would be something like finding a perfectly formed arm at birth that just did not work.
Production of microRNAs is dependent on Dicer, an enzyme widely used by living things to kick-start the process of silencing unwanted genetic messages. By breeding mice that lack one or both of the forms or alleles of the gene that produces Dicer in the retina, scientists were able to observe retinal development when Dicer levels were half of normal or completely eliminated.
Electrical activity in retinas devoid of Dicer was abnormally low at the time of eye opening and became progressively worse at 1-, 3- and 5-mon
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University of Florida