In normal mice the eyelids grow across the eye and fuse together during days 15 and 16 of gestation, and the mice are born with their eyes closed. In mutant lgM1/lgM1 (lidgap-Miller) foetuses this growth and fusion does not occur and the mice are born with their eyes open. A single prenatal treatment with cortisone on day 14 of gestation masks the genetic defect, and the mice are born with their eyes closed. In the present study, a scanning electron microscope was used to investigate: (1) whether eyelid closure in cortisone-treated lgM1/lgM1 foetuses differs from that in normal foetuses of the CBA/J and ICR/M1 strains and, if so, how; and (2) how developing eyelids of untreated lgM1/lgM1 foetuses differ from normal.

The induced closure differs from normal. During their growth, eyelids of treated mutant foetuses have a deficiency of rounded periderm cells at their margins; the margin cells agglomerate and flatten prematurely. In closed eyes of treated mutants there is a gap between periderm cells of the upper and lower eyelids along part of the fusion line. Fusion is completed late, during day 17. Maturation of the head periderm is advanced in treated lgM1/lgM1 foetuses on day 16, relative to normal CBA/J and untreated lgM1/lgM1 foetuses.

Untreated lgM1/lgM1 foetuses differ from normal in that the eyelids never cover the eye and lack rounded periderm cells at their perimeter. The periderm cells present form a flattened band along the eyelid margin rather than, as in normal eyelids, along the fusion line.

The results of the cortisone study suggest that the route to eyelid closure in mice may not be narrowly canalized either in cell morphology or number, or in timing, and that closed eyes may be achieved after cortisone treatment in lgM1/lgM1 foetuses as part of an induced maturation of the periderm.

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