MORPHOGENESIS OF EYE LENS IN A MOUSE STRAIN WITH HEREDITARY CATARACTS

Mice carrying the gene “Shrivelled, ” also known as “Cataract‐Fraser” or “Cataracta hereditaria subcapsularis, ” invariably develop lens opacities which are visible when the animals open their eyes on the fourteenth postnatal day. Lens development in normal and mutant embryos is the same until day 14 of gestation. At this stage the nuclei of the lens fibers in the controls are large and vesicular with prominent nucleoli. In the mutants the centrally located nuclei are smaller and darker with indistinct nucleoli. The nuclei of normal fibers remain large and open even after birth; those in the mutants continue to undergo pyknosis after passing through the equatorial zone in the regular fashion. The nuclear degeneration is followed, with a delay of about 24–48 hours, by swelling and vacuolization of the fibers concerned. In the adult the lens core forms an amorphous eosinophilic mass or may partly be resorbed. The cortical fibers remain normal. Anterior polar cataracts develop: the epithelial cells proliferate to form multiple layers of atypical cells, surrounded by lens capsule‐like material. The fiber degeneration may be caused by precocious cessation of protein synthesis after the cell nucleus becomes defunct. The late epithelial aberrations may be secondary to the changes in the underlying fibers and are possibly related to the reactivation of cell replication in the central part of lens epithelium seen after traum. Copyright © 1968 Wiley‐Liss, Inc., A Wiley Company