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A. Alizadeh, J. Hess, T. Blankenship, P. FitzGerald; Targeted Genomic Deletion of the Lens-Specific Intermediate Filament Protein Filensin . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1253.
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Purpose. To deduce the role of the beaded filament in the lens by creation of a "loss-of-function" mutant. Methods. Filensin expression was blocked by replacing exon 1 and additional upstream sequence, including the transcription initiation site, with the neomycin gene. PCR was utilized to successfully identify mouse embryonic stem cells bearing the mutant allele. Because the 129 strain of mice bear a mutation in CP49, mice bearing the mutant filensin allele were outbred to achieve a background of wild type CP49. Protein expression was assessed by western blotting, and lenses were analyzed by light microscopy. Results. Filensin expression was successfully negated. The absence of filensin resulted in reduced levels of filenisn's assembly partner CP49. Histologic examination showed that the absence of filensin, did not alter the histologic structure of the lens, when compared to wild type litter mate controls. Conclusions. We conclude that filensin, and by inference the beaded filament, is not required for fiber cell elongation, the assumption of the overall architecture of fiber cells, long range order of fiber cells, or the positioning of the fiber cell nucleus during differentiation.
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