title: Lens-forming competence in the epidermis of Xenopus laevis during development.
abstract: In larval X. laevis the capacity to regenerate a lens under the influence of inductive factors present in the vitreous chamber is restricted to the outer cornea and pericorneal epidermis (Lentogenic Area, LA). However, in early embryos, the whole ectoderm is capable of responding to inductive factors of the larval eye forming lens cells. In a previous paper, Cannata et al. (2003) demonstrated that the persistence of lens-forming competence in the LA is the result of early signals causing lens-forming bias in the presumptive LA and of late signals from the eye causing cornea development. This paper analyzes 1) the decrease of the lens-forming capacity in ectodermal regions both near LA (head epidermis) and far from LA (flank epidermis) during development, 2) the capacity of the head epidermis and flank epidermis to respond to lens-competence promoting factors released by an eye transplanted below these epidermal regions, and 3) the eye components responsible for the promoting effect of the transplanted eye. Results were obtained by implanting fragments of ectoderm or epidermis into the vitreous chamber of host tadpoles and by evaluating the percentage of implants positive to a monoclonal antibody anti-lens. These results demonstrated that the lens-forming competence in the flank region is lost at the embryonic stage 30/31 and is weakly restored by eye transplantation; however, lens-forming competence in the head region is lost at the larval stage 48 and is strongly restored by eye transplantation. The authors hypothesize that during development the head ectoderm outside the LA is attained by low levels of the same signals that attain the LA and that these signals are responsible for the maintenance of lens-forming competence in the cornea and pericorneal epidermis of the larva. In this hypothesis, low levels of these signals slacken the decrease of the lens-forming competence in the head ectoderm and make the head epidermis much more responsive than the flank epidermis to the effect of promoting factors released by a transplanted eye. Results obtained after transplantation of eyes deprived of some components indicate that the lens and the retina are the main source of these promoting factors. The immunohistochemical detection of the FGFR-2 (bek variant) protein in the epidermis of stage 53 larvae submitted to eye transplantation at stage 46 showed that the eye transplantation increased the level of FGFR-2 protein in the head epidermis but not in the flank epidermis, indicating that the lens-forming competence in X. laevis epidermis could be related to the presence of an activated FGF receptor system in the responding tissue.
authors.affiliation: Dipartimento di Biologia, Università di Roma Tor Vergata, via della Ricerca Scientifica, I - 00133 Rome, Italy.
authors.forename: Emiliano
authors.initials: E
authors.lastname: Arresta
authors.forename: Sergio
authors.initials: S
authors.lastname: Bernardini
authors.forename: Cesare
authors.initials: C
authors.lastname: Gargioli
authors.forename: Sergio
authors.initials: S
authors.lastname: Filoni
authors.forename: Stefano M
authors.initials: SM
authors.lastname: Cannata
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D004475:Ectoderm / Q000502:physiology; D004627:Embryonic Induction / Q000502:physiology*; D004817:Epidermis / Q000196:embryology* / Q000378:metabolism; D005123:Eye / Q000196:embryology / Q000637:transplantation; D007150:Immunohistochemistry; D007908:Lens, Crystalline / Q000196:embryology*; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism; D051497:Receptor, Fibroblast Growth Factor, Type 2; D017468:Receptors, Fibroblast Growth Factor / Q000378:metabolism; D029867:Xenopus Proteins; D014982:Xenopus laevis / Q000196:embryology*
chemical_list: D000911:Antibodies, Monoclonal; D017468:Receptors, Fibroblast Growth Factor; D029867:Xenopus Proteins; C496357:Fgfr2 protein, Xenopus; D020794:Receptor Protein-Tyrosine Kinases; D051497:Receptor, Fibroblast Growth Factor, Type 2