ArticleCell death and differentiation2015
The function of Drosophila p53 isoforms in apoptosis.
Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Transcription-dependent and -independent functions of Drosophila p53 isoforms in the induction of apoptosis and senescence-associated tumorigenesis.Cell death & disease · 2026Article
- Noc1 downregulation induces nucleolar stress and upregulates p53 isoforms, with a robust increase of the truncated p53E isoform in Drosophila wing discs.G3 (Bethesda, Md.) · 2026Article
- Replication stress promotes cellular transformation in Drosophila epithelium.Cell death discovery · 2025Article
- Dominant suppressor genes of p53-induced apoptosis in Drosophila melanogaster.G3 (Bethesda, Md.) · 2024Article
- Distinct p53 isoforms code for opposing transcriptional outcomes.Developmental cell · 2022Article
- Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022Review
- Coordination between cell proliferation and apoptosis after DNA damage in Drosophila.Cell death and differentiation · 2022Article
- Article
- VCP maintains nuclear size by regulating the DNA damage-associated MDC1-p53-autophagy axis in Drosophila.Nature communications · 2021Article
- Life as a Vector of Dengue Virus: The Antioxidant Strategy of Mosquito Cells to Survive Viral Infection.Antioxidants (Basel, Switzerland) · 2021Review
- The Evolutionary Conserved Transmembrane BAX Inhibitor Motif (TMBIM) Containing Protein Family Members 5 and 6 Are Essential for the Development and Survival ofFrontiers in cell and developmental biology · 2021Article
- DNA Damaged Induced Cell Death in Oocytes.Molecules (Basel, Switzerland) · 2020Review
- The Splicing Factor SF2 Is Critical for Hyperproliferation and Survival in a TORC1-Dependent Model of Early Tumorigenesis inInternational journal of molecular sciences · 2020Article
- Role of p53 isoforms in the DNA damage response during Drosophila oogenesis.Scientific reports · 2019Article
- Drosophila p53 integrates the antagonism between autophagy and apoptosis in response to stress.Autophagy · 2019Article
- The p53 mRNA: an integral part of the cellular stress response.Nucleic acids research · 2019Review
- P53 and Apoptosis in the Drosophila Model.Advances in experimental medicine and biology · 2019Review
- p53-dependent programmed necrosis controls germ cell homeostasis during spermatogenesis.PLoS genetics · 2017Article
- Differential regulated microRNA by wild type and mutant p53 in induced pluripotent stem cells.Cell death & disease · 2016Article
- miR-34a inhibits the apoptosis of MDSCs by suppressing the expression of N-myc.Immunology and cell biology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The p53 protein is a major mediator of the cellular response to genotoxic stress and is a crucial suppressor of tumor formation. In a variety of organisms, p53 and its paralogs, p63 and p73, each encode multiple protein isoforms through alternative splicing, promoters, and translation start sites. The function of these isoforms in development and disease are still being defined. Here, we evaluate the apoptotic potential of multiple isoforms of the single p53 gene in the genetic model Drosophila melanogaster. Most previous studies have focused on the p53A isoform, but it has been recently shown that a larger p53B isoform can induce apoptosis when overexpressed. It has remained unclear, however, whether one or both isoforms are required for the apoptotic response to genotoxic stress. We show that p53B is a much more potent inducer of apoptosis than p53A when overexpressed. Overexpression of two newly identified short isoforms perturbed development and inhibited the apoptotic response to ionizing radiation. Analysis of physiological protein expression indicated that p53A is the most abundant isoform, and that both p53A and p53B can form a complex and co-localize to sub-nuclear compartments. In contrast to the overexpression results, new isoform-specific loss-of-function mutants indicated that it is the shorter p53A isoform, not full-length p53B, that is the primary mediator of pro-apoptotic gene transcription and apoptosis after ionizing radiation. Together, our data show that it is the shorter p53A isoform that mediates the apoptotic response to DNA damage, and further suggest that p53B and shorter isoforms have specialized functions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.