Extended Data Figure 1: Model for examining p53-associated developmental phenotypes. | Nature

Extended Data Figure 1: Model for examining p53-associated developmental phenotypes.

From: Inappropriate p53 activation during development induces features of CHARGE syndrome

Extended Data Figure 1

a, Schematic of p5325,26, p5353,54 and p5325,26,53,54 mutant p53 proteins. Basic, basic-residue-rich domain; PRD, proline-rich domain; TAD, transcriptional activation domain 1 or 2; Tet, tetramerization domain. b, p53LSL-mut/+ mice (where mut can denote any of the p53 TAD mutants) were crossed to p53+/+; CMV-Cre mice, which express Cre in the germline, to assess the viability and developmental phenotypes of the p53-mutant-expressing progeny. c, Table summarizing the actual genotypes and ultimate functional genotypes of progeny from crosses of p53LSL-25,26,53,54/+ and p53+/−; CMV-Cre mice, as used throughout the manuscript. While p53LSL-25,26,53,54/+CMV-Cre is the actual initial genotype, when Cre acts to delete the lox–Stop–lox (LSL) cassette, the genotype is written as p5325,26,53,54/+ to reflect this recombination. In the text and figure labels, the Cre nomenclature for both control and p5325,26,53,54/+ embryos is excluded for simplicity. Controls for analyses comprised embryos both with and without the CMV-Cre transgene, as summarized in Extended Data Fig. 3.

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