Rescue of neural tube defects in Pax-3-deficient embryos by p53 loss of function: implications for Pax-3- dependent development and tumorigenesis
Copyright policy )Rescue of neural tube defects in Pax-3-deficient embryos by p53 loss of function: implications for Pax-3- dependent development and tumorigenesis
Pax-3 is a transcription factor that is expressed in the neural tube, neural crest, and dermomyotome. We previously showed that apoptosis is associated with neural tube defects (NTDs) in Pax-3-deficient Splotch ( Sp/Sp ) embryos. Here we show that p53 deficiency, caused by germ-line mutation or by pifithrin-α, an inhibitor of p53-dependent apoptosis, rescues not only apoptosis, but also NTDs, in Sp/Sp embryos. Pax-3 deficiency had no effect on p53 mRNA, but increased p53 protein levels. These results suggest that Pax-3 regulates neural tube closure by inhibiting p53-dependent apoptosis, rather than by inducing neural tube-specific gene expression.
- Harvard University United States
- JOSLIN DIABETES CENTER INC United States
Heterozygote, Time Factors, Genotype, Reverse Transcriptase Polymerase Chain Reaction, Blotting, Western, Down-Regulation, Apoptosis, Genes, p53, DNA-Binding Proteins, Mice, Inbred C57BL, Mice, Thiazoles, Neural Crest, In Situ Nick-End Labeling, Animals, Paired Box Transcription Factors, Benzothiazoles, Neural Tube Defects, RNA, Messenger, PAX3 Transcription Factor
Heterozygote, Time Factors, Genotype, Reverse Transcriptase Polymerase Chain Reaction, Blotting, Western, Down-Regulation, Apoptosis, Genes, p53, DNA-Binding Proteins, Mice, Inbred C57BL, Mice, Thiazoles, Neural Crest, In Situ Nick-End Labeling, Animals, Paired Box Transcription Factors, Benzothiazoles, Neural Tube Defects, RNA, Messenger, PAX3 Transcription Factor
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