Following are the answers to questions raised in the update page to Chapter 1.
In their reinvestigation of the role of the optic vesicle in embryonic lens development, Grainger et al. (1988) worked with Xenopus laevis, the amphibian species preferred by modern embryologists, and with Rana palustris, the species used by Lewis (1904).
In their experiments with Xenopus, Grainger and coworkers labeled either the donor or the host embryo by injecting it at the 1-cell stage with horseradish peroxidase (HRP), an enzyme that generates a blue reaction-product after histological fixation and sectioning. This host-versus-donor labeling scheme allowed them to clearly distinguish transplant-derived tissues from host-derived tissues. In all cases where lenses developed next to heterotopically transplanted optic vesicles, the lenses were derived from contaminating donor tissue, presumably from ectoderm adhering to the optic vesicle.
In their experiments with Rana palustris, Grainger and coworkers found that the HRP marker was toxic to the embryos and could not be used. Instead, the investigators used modified surgical techniques to minimize the chances that ectopic lenses could develop from contaminating tissue adhering to the transplanted optic vesicles. No ectopic lenses were formed under these conditions.
These results are important because they do not support the widely held notion that optic vesicles are by themselves sufficient to induce lens formation in any overlying ectoderm. Rather, the results of Granger et al. (1988), Jacobson (1966), and others indicate that lens induction is a multistep process, and that the optic vesicle induces, or just allows, lens formation only in ectoderm that has been appropriately primed by earlier interactions with head endoderm and mesoderm.
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