Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Christner, P.J. et al.

Christner, Gentiletti, Peters, Ball, Yamauchi, Atsawasuwan, Beason, Soslowsky, Birk,

Collagen dysregulation in the dermis of the Sagg/+ mouse: a loose skin model.

The Sagg/+ mouse is an ethylnitrosourea-derived mutant with a dermal phenotype similar to some of the subtypes of Ehlers-Danlos syndrome (EDS) and cutis laxa. The dermis of the Sagg/+ mouse has less dense and more disorganized collagen fibers compared to controls. The size of extracted Type I dermal collagen was the same as that observed in normal skin; however, more collagen could be extracted from Sagg/+ skin, which also showed decreased collagen content and decreased steady-state levels of alpha1(I), alpha2(I), alpha1(V), and alpha2(V) procollagen mRNAs. The biomechanical properties of Sagg/+ skin were significantly decreased relative to normal skin. However, there were no significant differences in the quantities of the major collagen cross-links, that is, dehydrohydroxylysinonorleucine and dehydrohistidinohydroxymerodesmosine between Sagg/+ and normal skin. Electron microscopic evaluation of Sagg/+ skin indicated that the mutation interferes with the proper formation of collagen fibrils and the data are consistent with a mutation in Type V collagen leading to haploinsufficiency with the formation of two sub-populations of collagen fibrils, one normal and one with irregular shape and a larger diameter. Further study of this novel mutation will allow the identification of new mechanisms involved in the regulation of normal and pathologic collagen gene expression.[1]

References

Collagen dysregulation in the dermis of the Sagg/+ mouse: a loose skin model. Christner, P.J., Gentiletti, J., Peters, J., Ball, S.T., Yamauchi, M., Atsawasuwan, P., Beason, D.P., Soslowsky, L.J., Birk, D.E. J. Invest. Dermatol. (2006) [Pubmed]

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