[HTML][HTML] Severe ocular abnormalities in C57BL/6 but not in 129/Sv p53-deficient mice
S Ikeda, NL Hawes, B Chang, CS Avery… - … & visual science, 1999 - iovs.arvojournals.org
S Ikeda, NL Hawes, B Chang, CS Avery, RS Smith, PM Nishina
Investigative ophthalmology & visual science, 1999•iovs.arvojournals.orgpurpose. To demonstrate the importance of genetic background interaction on the
development of ocular phenotypes in p53-deficient mice. methods. Eyes of adult mice,
homozygous and heterozygous for the p53 gene disruption in the 129/SvJ and C57BL/6J
(B6) genetic backgrounds, and their F1 progeny were examined by indirect ophthalmoscopy
and by light microscopy. results. Indirect ophthalmoscopy revealed unilateral or bilateral
vitreal opacities, fibrous retrolental tissue, and retinal folds in adult B6 mice but not in 129/Sv …
development of ocular phenotypes in p53-deficient mice. methods. Eyes of adult mice,
homozygous and heterozygous for the p53 gene disruption in the 129/SvJ and C57BL/6J
(B6) genetic backgrounds, and their F1 progeny were examined by indirect ophthalmoscopy
and by light microscopy. results. Indirect ophthalmoscopy revealed unilateral or bilateral
vitreal opacities, fibrous retrolental tissue, and retinal folds in adult B6 mice but not in 129/Sv …
Abstract
purpose. To demonstrate the importance of genetic background interaction on the development of ocular phenotypes in p53-deficient mice.
methods. Eyes of adult mice, homozygous and heterozygous for the p53 gene disruption in the 129/SvJ and C57BL/6J (B6) genetic backgrounds, and their F1 progeny were examined by indirect ophthalmoscopy and by light microscopy.
results. Indirect ophthalmoscopy revealed unilateral or bilateral vitreal opacities, fibrous retrolental tissue, and retinal folds in adult B6 mice but not in 129/Sv mice homozygous for a p53 null mutation. In B6 p53−/− mice, blood vessels extended from the peripapillary inner retina through the posterior vitreous and into the retrolental membrane. Optic nerves were hypoplastic.
conclusions. These findings indicate that alleles from the B6 background contribute to the aberrant ocular phenotypes observed in p53 deficiency. They also suggest that p53 or the pathway in which it functions may be important for normal eye development.
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