RESUMEN
Myopia development in humans depends on a complex interplay between genetic and environmental factors. Many of those who become myopic when exposed to a myopigenic environment are likely to do so because of a genetic susceptibility, whereas others somehow remain immune. In the most intensively studied model of environmentally induced myopia, form-deprivation myopia in the chick, there is convincing evidence of differential genetic susceptibility to myopia development, both within-strains and between-strains. To date, however, these have involved relatively small differential responses. The aim of this investigation was to examine genetic susceptibility to a highly uniform regimen of form-deprivation in three strains of chick (white leghorn, brown leghorn and broiler) expected to differ greatly in genetic background and in normal eye size, and to gauge the potential for mapping the quantitative trait loci (QTL) underlying this differential susceptibility. Despite striking differences in normal eye size, all three strains studied developed a similar degree of induced myopia. Whilst the degree of induced vitreous chamber elongation differed significantly between-strains, it was concluded that the high within-strain variation in the response to form-deprivation would prevent the effective application of QTL mapping approaches to identify genes conferring this susceptibility. In contrast, the strains used here would be ideal for use in mapping QTL controlling normal ocular component dimensions.