Next Article in Journal
Mapping the Diverse and Inclusive Future of Parkinson’s Disease Genetics and Its Widespread Impact
Next Article in Special Issue
Impact of G-Quadruplexes and Chronic Inflammation on Genome Instability: Additive Effects during Carcinogenesis
Previous Article in Journal
Associations of Polymorphisms Localized in the 3′UTR Regions of the KRAS, NRAS, MAPK1 Genes with Laryngeal Squamous Cell Carcinoma
Previous Article in Special Issue
Gene Amplification and the Extrachromosomal Circular DNA
Review

Developmental Acquisition of p53 Functions

1
National Institute of Child Health and Human Development, Bethesda, MD 20892, USA
2
National Human Genome Research Institute, Bethesda, MD 20892, USA
3
National Cancer Institute, Bethesda, MD 20892, USA
*
Author to whom correspondence should be addressed.
These authors contributed equally to this review.
Academic Editor: Eishi Noguchi
Genes 2021, 12(11), 1675; https://doi.org/10.3390/genes12111675
Received: 27 August 2021 / Revised: 14 October 2021 / Accepted: 21 October 2021 / Published: 23 October 2021
(This article belongs to the Special Issue Genome Maintenance and Cancer Predisposition)
Remarkably, the p53 transcription factor, referred to as “the guardian of the genome”, is not essential for mammalian development. Moreover, efforts to identify p53-dependent developmental events have produced contradictory conclusions. Given the importance of pluripotent stem cells as models of mammalian development, and their applications in regenerative medicine and disease, resolving these conflicts is essential. Here we attempt to reconcile disparate data into justifiable conclusions predicated on reports that p53-dependent transcription is first detected in late mouse blastocysts, that p53 activity first becomes potentially lethal during gastrulation, and that apoptosis does not depend on p53. Furthermore, p53 does not regulate expression of genes required for pluripotency in embryonic stem cells (ESCs); it contributes to ESC genomic stability and differentiation. Depending on conditions, p53 accelerates initiation of apoptosis in ESCs in response to DNA damage, but cell cycle arrest as well as the rate and extent of apoptosis in ESCs are p53-independent. In embryonic fibroblasts, p53 induces cell cycle arrest to allow repair of DNA damage, and cell senescence to prevent proliferation of cells with extensive damage. View Full-Text
Keywords: pluripotent; embryo; stem cells; genomic stability; cell cycle; apoptosis; differentiation; cancer pluripotent; embryo; stem cells; genomic stability; cell cycle; apoptosis; differentiation; cancer
Show Figures

Graphical abstract

MDPI and ACS Style

Jaiswal, S.K.; Raj, S.; DePamphilis, M.L. Developmental Acquisition of p53 Functions. Genes 2021, 12, 1675. https://doi.org/10.3390/genes12111675

AMA Style

Jaiswal SK, Raj S, DePamphilis ML. Developmental Acquisition of p53 Functions. Genes. 2021; 12(11):1675. https://doi.org/10.3390/genes12111675

Chicago/Turabian Style

Jaiswal, Sushil K., Sonam Raj, and Melvin L. DePamphilis 2021. "Developmental Acquisition of p53 Functions" Genes 12, no. 11: 1675. https://doi.org/10.3390/genes12111675

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop