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approach to resolving some of the in vivo functions of alpha-crystallin is to generate animal models where one or both of the alpha-crystallin gene products have been eliminated. Brady et al. [22] demonstrated, by targeted disruption of the mouse alphaA gene, that this protein was essential for the maintenance of lens transparency, possibly by maintaining the solubility of alphaB, or associated proteins, in the lens. These lenses were also reported to be smaller in equatorial and light axial dimensions than age matched wild type lens. It was not possible using the techniques employed in the study to determine if the smaller lenses were due to reduced volume or number of fiber cells. Targeted disruption of the mouse alphaB gene resulted in lenses similar in size to aged-matched wild type lens. Moreover, no cataract formation was observed in the alphaB knockout lenses. These animals have muscle cell abnormalities, severe postural anomalies, selective muscle degeneration, and shorter life spans compared to normal controls [23]."}

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