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L.H. Pinto, M.H. Vitaterna, K. Shimomura, B. Young, S.M. Siepka, V.C. Sheffield, E.M. Stone, R.F. Mullins, M.T. Pletcher, J.S. Takahashi; ENU–Induced nob4 Mutant Mouse Available to the Vision Research Community . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5769.
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© ARVO (1962-2015); The Authors (2016-present)
The recessive nob4 mutation was generated by chemical mutagenesis. We wished to map the gene mutation responsible for the loss of post–receptor components of the electroretinogram and quantify the mutant’s vision.
At 8–12 weeks of age the dark– adapted electroretinogram of 28 G5 mice was measured and quantified and the fundus was photographed and analyzed for abnormalities. Six affected and two unaffected offspring of mapping crosses with the 129S1/SvImJ strain were analyzed with informative SNP markers to obtain a preliminary map position of the gene. Optomotor responses were used to compare the contrast sensitivity and acuity of the affected mice with those of unaffected control mice.
The electroretinograms of the affected mice showed no evidence for post–receptor components: the b–wave of the dark–adapted and light–adapted electroretinogram, and the scotopic threshold response (STR) were undetectable. The mutation mapped to Chromosome 11 between 29–57 Mb. No abnormalities were observed in the appearance of the fundus. However, the visual acuity of affected mice was reduced to about half that of unaffected mice when measured in the range of luminances between 0.0001 and 50 cd/m2. Peak contrast sensitivity (measured at 0.08 c/d) of affected mice was less than 30% that of unaffected mice in this range of luminances.
A mutant has been generated by random chemical mutagenesis that affects both rod and cone pathways and severely affects visual behavior at both low and high light levels. This mutant, and a previously–characterized mutant, Noerg–1, are available for the use of the vision research community at www.neuromice.org.
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