Related Experiment Video
Updated: Aug 18, 2026
A Simple Mechanical Procedure to Create Limbal Stem Cell Deficiency in Mouse
Published on: November 17, 2016
Eyelid development and fusion induced by cortisone treatment in mutant, lidgap-Miller, foetal mice. A scanning
Abstract:
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 lgMl)/lgMl) (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: whether eyelid closure in cortisone-treated lgMl/lgMl foetuses differs from that in normal foetuses of the CBA/J and ICR/Ml strains and, if so, how; and off developing eyelids of untreated lgMl/lgMl 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 lgMl/lgMl foetuses on day 16, relative to normal CBA/J and untreated lgMl/lgMl foetuses. Untreated lgMl/lgMl 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 lgMl/lgMl foetuses as part of an induced maturation of the periderm.
Insights
Cortisone treatment can induce eyelid closure in mutant mice (lgMl/lgMl) by promoting periderm maturation, though the process differs from normal eyelid fusion. This suggests eyelid closure timing and cell development are not strictly fixed.
Area of Science:
- Developmental Biology
- Genetics
- Teratology
Background:
- Normal mouse eyelid closure involves fusion during gestation (days 15-16).
- Mutant lgMl/lgMl mice exhibit open eyes at birth due to failed eyelid growth and fusion.
- Prenatal cortisone treatment on day 14 can rescue the eyelid closure defect in lgMl/lgMl mutants.
Purpose of the Study:
- To compare eyelid closure in cortisone-treated lgMl/lgMl fetuses with normal mice.
- To investigate differences in developing eyelids of untreated lgMl/lgMl fetuses compared to normal.
- To understand the role of periderm cell maturation in cortisone-induced eyelid closure.
Main Methods:
- Scanning electron microscopy (SEM) was used to examine fetal mouse eyelids.
- Comparison of eyelid morphology in normal (CBA/J, ICR/Ml) and mutant (lgMl/lgMl) fetuses.
- Analysis of eyelid development at different gestational stages, with and without cortisone treatment.
Main Results:
- Cortisone-treated mutant eyelids show premature agglomeration and flattening of periderm cells, with a gap at the fusion line and delayed fusion (day 17).
- Periderm maturation is advanced in treated mutants by day 16.
- Untreated mutant eyelids fail to cover the eye, lack rounded periderm cells at the margin, and have flattened periderm bands.
Conclusions:
- Cortisone treatment induces eyelid closure in lgMl/lgMl mutants through accelerated periderm maturation.
- Eyelid closure is not rigidly canalized, allowing for alternative developmental pathways.
- The study highlights the plasticity of periderm cell development and timing in achieving eyelid closure.
