Search Criteria |
Gene/Clone | Species | Stage | Anatomy Item | Experimenter |
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tp53 | xenopus | somite [+] |
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Experiment details for tp53
Wallingford JB et al. (1997) Assayp53 activity is essential for normal development in Xenopus.
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Figure 3. Mutant p53 blocks differentiation. (a) Dorsal view of an embryo injected with p53Tthr280 mRNA plus beta-galactosidase mRNA into blastomere B1 of a 32-cell embryo, reared to tailbud stage, and stained with the anti-neural antibody XAN3/6F11 (dark blue/purple [48]). Anterior is to the left. Note that the beta- galactosidase-positive tumor (light blue) does not stain with the neural marker, and that the large tumor distorts the brain into which it is embedded. (b)Transverse section through a sample similar to that shown in (a). Neural staining (dark purple) with antibody 2G9 (XenopusMolecular Marker Resource, URL http://vize222.zo.utexas.edu) and beta- galactosidase (light blue). beta-galactosidase- positive cells do not stain with the neural marker, and vice versa. (c) Control side of a tailbud stage embryo stained (dark blue/purple) with the somite differentiation marker 12/101[49]. Note that the differentiated somites extend anteriorly to the head of the embryo. (d)The opposite side of the embryo shown in (c), illustrating a tumor derived from blastomere C2 injected with p53thr280mRNA plus beta-galactosidase mRNA. Note that the region in which anterior somites should have formed does not stain with 12/101, but is beta- galactosidase positive (light blue). (e)The control side of a tailbud stage embryo stained with antibody 3G8 [50] to detect pronephric tubules (dark purple substrate, arrow).(f)The opposite side of the embryo shown in (e), illustrating a tumor derived from the blastomere C3 injected with p53thr280mRNA plus beta- galactosidase mRNA. The region in which the embryonic kidney, the pronephros, should have formed does not stain with antibody 3G8. The beta-galactosidase-positive tumor (light blue) is displaced dorsally from the region in which the pronephros normally develops, but such displacement is common for mutant p53- induced tumors (see Figures 1 and 5). |