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. 2001 Feb 13;98(4):1859–1864. doi: 10.1073/pnas.98.4.1859

Figure 5.

Figure 5

Deregulated p53 signaling is responsible for the gastrulation defect in tsg101−/− embryos. (a) Immunohistochemical analysis of p53 protein levels. A few weakly p53-positive cells can be detected in a wild-type E6.5 embryo (WT), whereas strongly p53-positive nuclei occur throughout the tsg101−/− embryo (−/−). (Bar = 50 μm.) (b) Levels of p53, mdm2, and p21 mRNA expression. Quantitative reverse transcription–PCR on mRNA from individual E6.5 wild type (WT) and mutant (−/−) embryos (see Materials and Methods). Expression levels are calculated relative to β-actin. p21 expression is increased 5- to 10-fold in tsg101−/− embryos. (c) Partial rescue of tsg101−/− embryos by null mutation of p53. Whole mount preparations of embryos from tsg101+/−/p53+/− intercrosses at E8.5. Although less advanced than their tsg101+/−/p53−/− littermates (Left), tsg101−/−/p53−/− embryos at E8.5 are developing an anterior–posterior pattern with a head, trunk, and tail region (Middle). A remnant of a tsg101−/−/p53+/+ single mutant embryo at E8.5 is shown on the Right. (Bar = 100 μm.)