Cataracts are the leading cause of blindness worldwide. They can be caused by congenital mutations of lens proteins or by various diseases including diabetes. We have recently studied mice carrying connexin mutations (Cx46fs380 and Cx50D47A) that mimic human cataract-linked mutations. The lenses of these mice accumulate calcium which forms precipitates that correspond to the cataracts. We hypothesize that bio- mineralization is a general mechanism of cataract formation. We will characterize the composition of calcium precipitates in connexin mutant mice and the relation between their formation and cataract development. We will test whether mice with mutations of a different lens protein (γB-crystallin) or mice with experimentally- induced cataracts also contain calcium precipitates. This proposal may give insights into fundamental pathogenic mechanisms of cataracts and lead to new preventative/therapeutic approaches.