Expression data from acd, p53 and double mutant mouse embryos

In mouse, the adrenocortical dysplasia (acd) phenotype shows limb and body axis anomalies, as a result of p53-dependent apoptosis, and perinatal lethality. The p53 deficiency partially rescues anomalies, but not perinatal lethality, implicating the involvement of p53-independent mechanisms in the acd phenotype. Differentially expressed genes in acd mutant and double mutant embryos were identified. p53-dependent and –independent pathways contributing to acd phenotype were characterized. We used microarrays to analyze gene expression profiles of acd and double mutant embryos and to identify p53 dependent and –independent mechanisms underlying acd phenotype. Microarray analysis was performed with wild type (wt), acd mutant (Acdacd/acd), p53-/-, and double mutant (Acdacd/acd, p53-/-) embryos at E10.5. CEL files were normalized using justRMA algorithm and differentially expressed genes were selected using BRB-Array tools version 4.4.0. p53-dependent and –independent pathways contributing to the acd phenotype were identified.