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Corneal morphogenesis in the Mov13 mutant mouse is characterized by normal cellular organization but disordered and
1MRC Clinical & Population Cytogenetics Unit, Western General Hospital, Edinburgh, UK.
Abstract:
This paper compares corneal development in the normal and in the Mov13 mutant mouse homozygote which does not synthesize type I collagen. During the period 12-14 days of development, there is no obvious difference between cellular organization in the normal and the mutant corneas or, indeed, elsewhere in the eye. In particular, there is normal colonization of the mutant cornea by the mesenchymal cells which will form the endothelium and the fibroblasts. In the early stages of stromal deposition (less than 14 days), when relatively little collagen is normally laid down, mutant and wild-type corneas differ only in that mutant collagen fibrils are less uniform than normal ones. Later development in the Mov13 mutant cannot usually be studied because almost all mutant embryos are dead by 14 days, but we now have two homozygous embryos from a single, 16-day litter. Their stromas obviously differed from those of their normal littermates: there was markedly less collagen in the mutant cornea and the collagen that was deposited lacked orthogonal organization. Fibril morphology also differed: the diameters of fibrils in the normal corneas peaked sharply at about 20 nm, whereas the diameters of mutant fibrils were spread over the range 5-15 nm, with only a small percentage overlapping the normal distribution. These results suggest that type I collagen is of negligible importance in controlling the cellular organization of the cornea, but has a dominant role in the formation of normal 20 nm fibrils and of normal stromal organization. They also show that, as collagen production is markedly lower in the mutant than in the wild-type cornea, the production of other collagens cannot compensate in any way for the lack of type I collagen.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Type I collagen is not crucial for corneal cellular organization but is dominant in forming normal collagen fibrils and stromal organization in mice. Its absence leads to reduced collagen deposition and altered fibril morphology.
Area of Science:
- Developmental Biology
- Ophthalmology
- Biochemistry
Background:
- Corneal development relies on extracellular matrix components, including collagen.
- Type I collagen is a major structural protein, but its specific role in corneal development is not fully understood.
Purpose of the Study:
- To investigate the role of type I collagen in corneal development using the Mov13 mutant mouse.
- To compare corneal cellular organization and collagen structure in normal and type I collagen-deficient mice.
Main Methods:
- Comparative analysis of corneal development in wild-type and Mov13 mutant mouse embryos.
- Histological examination of cellular organization and collagen fibril morphology.
- Assessment of collagen deposition and organization in developing corneas.
Main Results:
- Mov13 mutant corneas showed normal cellular organization and mesenchymal cell colonization up to 14 days.
- Later development (16 days) in mutants revealed significantly less collagen and a lack of orthogonal organization.
- Mutant collagen fibrils were smaller and less uniform in diameter compared to normal fibrils.
Conclusions:
- Type I collagen is essential for the formation of normal 20 nm collagen fibrils and stromal organization in the cornea.
- It plays a negligible role in controlling corneal cellular organization.
- Other collagens cannot compensate for the absence of type I collagen in the developing mouse cornea.