High impact information on msx1

• Xenopus msx1 mediates epidermal induction and neural inhibition by BMP4 [1].
• Consistent with mediating a BMP type of signaling, overexpression of msx1 is sufficient to induce epidermis in dissociated ectoderm cells, which would otherwise form neural tissue [1].
• A balance between the anti-apoptotic activity of Slug and the apoptotic activity of msx1 is required for the proper development of the neural crest [2].
• The protective effect of expressing Slug can be reversed by expressing the apoptotic factor Bax, while the apoptosis promoted by msx1 can be abolished by expressing the Xenopus homologue of Bcl2 (XR11) [2].
• Through gain- and loss-of-function experiments with inducible forms of both Slug and msx1 genes, we showed that Slug acts as an anti-apoptotic factor whereas msx1 promotes cell death, either in the neural folds of the whole embryos, in isolated or induced neural crest and in animal cap assays [2].

Biological context of msx1

• Furthermore, we show that Slug and msx1 control the transcription of XR11 and several caspases required for programmed cell death [2].
• We show that the expression of Slug and msx1 controls cell death in certain areas of the neural folds, and we discuss how this equilibrium is necessary to generate sharp boundaries in the neural crest territory, and to precisely control cell number among neural crest derivatives [2].
• Exogenously applied FGF-10 successfully stimulated the regenerative capacity, resulting in the reinduction of all gene expressions (including shh, msx-1, and fgf-10) that we examined and the regeneration of well-patterned limb structures [3].

Other interactions of msx1

• On the other hand, shh expression was not detected in the froglet blastema, which expresses fgf8 and msx1 [4].

References