ArticleDevelopmental cell2019
The Spatiotemporal Pattern and Intensity of p53 Activation Dictates Phenotypic Diversity in p53-Driven Developmental Syndromes.
Article in Developmental cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41 citing papers in PubMed, 64 citations in OpenAlex.
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- Vascular architecture regulates mesenchymal stromal cell heterogeneity via P53-PDGF signaling in the mouse incisor.Cell stem cell · 2024Article
- A common cellular response to broad splicing perturbations is characterized by metabolic transcript downregulation driven by the Mdm2-p53 axis.Disease models & mechanisms · 2024Article
- Nucleolus activity-dependent recruitment and biomolecular condensation by pH sensing.Molecular cell · 2023Article
- DNA damage and repair: underlying mechanisms leading to microcephaly.Frontiers in cell and developmental biology · 2023Review
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- The emerging significance of splicing in vertebrate development.Development (Cambridge, England) · 2022Review
- Craniofacial Defects in Embryos with Homozygous Deletion ofInternational journal of molecular sciences · 2022Article
- Dynamic regulation and requirement for ribosomal RNA transcription during mammalian development.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The p53 Transactivation Domain 1-Dependent Response to Acute DNA Damage in Endothelial Cells Protects against Radiation-Induced Cardiac Injury.Radiation research · 2022Article
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- Endoderm development requires centrioles to restrain p53-mediated apoptosis in the absence of ERK activity.Developmental cell · 2021Article
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7 authors at 2 institutions in 1 country.
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Abstract
Inappropriate activation of the p53 transcription factor contributes to numerous developmental syndromes characterized by distinct constellations of phenotypes. How p53 drives exquisitely specific sets of symptoms in diverse syndromes, however, remains enigmatic. Here, we deconvolute the basis of p53-driven developmental syndromes by leveraging an array of mouse strains to modulate the spatial expression pattern, temporal profile, and magnitude of p53 activation during embryogenesis. We demonstrate that inappropriate p53 activation in the neural crest, facial ectoderm, anterior heart field, and endothelium induces distinct spectra of phenotypes. Moreover, altering the timing and degree of p53 hyperactivation substantially affects the phenotypic outcomes. Phenotypes are associated with p53-driven cell-cycle arrest or apoptosis, depending on the cell type, with gene expression programs, rather than extent of mitochondrial priming, largely governing the specific response. Together, our findings provide a critical framework for decoding the role of p53 as a mediator of diverse developmental syndromes.
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