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XB-ART-34992
Genesis 2007 Jan 01;451:1-10.
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tBid mediated activation of the mitochondrial death pathway leads to genetic ablation of the lens in Xenopus laevis.

Du Pasquier D , Chesneau A , Ymlahi-Ouazzani Q , Boistel R , Pollet N , Ballagny C , Sachs LM , Demeneix B , Mazabraud A .


Abstract
Xenopus is a well proven model for a wide variety of developmental studies, including cell lineage. Cell lineage in Xenopus has largely been addressed by injection of tracer molecules or by micro-dissection elimination of blastomeres. Here we describe a genetic method for cell ablation based on the use of tBid, a direct activator of the mitochondrial apoptotic pathway. In mammalian cells, cross-talk between the main apoptotic pathways (the mitochondrial and the death domain protein pathways) involve the pro-death protein BID, the active form of which, tBID, results from protease truncation and translocation to mitochondria. In transgenic Xenopus, restricting tBID expression to the lens-forming cells enables the specific ablation of the lens without affecting the development of other eye structures. Thus, overexpression of tBid can be used in vivo as a tool to eliminate a defined cell population by apoptosis in a developing organism and to evaluate the degree of autonomy or the inductive effects of a specific tissue during embryonic development.

PubMed ID: 17154276
Article link: Genesis


Species referenced: Xenopus laevis
Genes referenced: bax bcl2 bid rho rpe
Antibodies: Rho Ab6


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