Our previous studies showed that transgenic mice designed for overexpression of human aldose reductase developed lens defects reminiscent of PCO.
yata mutants also displayed various eye defects, including irregular arrangement of ommatidia, black discoloration, and lens defects (Figure 3D 3I).
A total of 59 potential mutants were found, with the great majority (n = 52) displaying lens defects.
The lenses of WT/R49Cneo and R49Cneo/R49Cneo mice displayed remarkable posterior lens defects and accumulation of swollen cells in the lens cortex, and developed nuclear cataracts.
Other minor phenotypes evident in HREM included enlarged lymph sacs, eye lens defects, abnormalities of the liver and an abnormal topology of the intestine.
Our previous study showed that lens defects in R49C/R49C knock-in mice are the result of a drastic alteration of lens fiber cell morphology, although early fiber cell elongation is normal [ 55].
In the present study, we did not observe as strong an effect on lens fiber morphology in young R49Cneo mice as in R49C/R49C mice, but did observe varied posterior lens defects beginning at an early postnatal age, as well as posterior migration of nuclei at older ages and posterior rupture.
Ltbp1 hypomorphs show facial dysmorphia [ 19] and Ltbp1L loss leads to embryonic lethality due to heart malformation [ 20], Ltbp2 loss-of-function mutations cause glaucoma in humans and lens defects in mice [ 21], Ltbp3 loss-of-function mutation results in severe bone malformation [ 3, 22, 23] and Ltbp4S-null mice show multiple organ defects [ 4, 9, 10].
After all, with an image of that size (they're 300MB each, compressed, lossless, proprietary), especially if you're going to be blowing up pieces of it for print media, defects in your lens (or defects with your wallet, leading to a cheap lens) are going to be amplified quite a bit.
