ArticlePLoS genetics2014
Low levels of p53 protein and chromatin silencing of p53 target genes repress apoptosis in Drosophila endocycling cells.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 69 citations in OpenAlex.
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- Growth under pressure: The pros and cons of polyploidy induced by stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Review
- Epithelial cell fusion is required for tissue repair following UV-A irradiation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Ring canals in the larval adipose of Drosophila buffer stress response.The Journal of cell biology · 2026Article
- Transcription-dependent and -independent functions of Drosophila p53 isoforms in the induction of apoptosis and senescence-associated tumorigenesis.Cell death & disease · 2026Article
- Proteostasis failure and mitochondrial dysfunction contribute to chromosomal instability-induced microcephaly.Nature communications · 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
- Unusual modes of cell and nuclear divisions characterise Drosophila development.Biochemical Society transactions · 2024Review
- Integrating the Study of Polyploidy Across Organisms, Tissues, and Disease.Annual review of genetics · 2024Review
- Dominant suppressor genes of p53-induced apoptosis in Drosophila melanogaster.G3 (Bethesda, Md.) · 2024Article
- An unscheduled switch to endocycles induces a reversible senescent arrest that impairs growth of the Drosophila wing disc.PLoS genetics · 2024Article
- A feedback loop that drives cell death and proliferation and its defect in intestinal stem cells.Life science alliance · 2024Article
- The antagonistic relationship between apoptosis and polyploidy in development and cancer.Seminars in cell & developmental biology · 2024Review
- An unscheduled switch to endocycles induces a reversible senescent arrest that impairs growth of thebioRxiv : the preprint server for biology · 2024Article
- Article
- Functional consequences of somatic polyploidy in development.Development (Cambridge, England) · 2024Review
- Polyploid Cancer Cell Models in Drosophila.Genes · 2024Review
- Nacα protects the larval fat body from cell death by maintaining cellular proteostasis in Drosophila.Nature communications · 2023Article
- Lack of apoptosis leads to cellular senescence and tumorigenesis in Drosophila epithelial cells.Cell death discovery · 2023Article
- Chitinase-like proteins promoting tumorigenesis through disruption of cell polarityFrontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Apoptotic cell death is an important response to genotoxic stress that prevents oncogenesis. It is known that tissues can differ in their apoptotic response, but molecular mechanisms are little understood. Here, we show that Drosophila polyploid endocycling cells (G/S cycle) repress the apoptotic response to DNA damage through at least two mechanisms. First, the expression of all the Drosophila p53 protein isoforms is strongly repressed at a post-transcriptional step. Second, p53-regulated pro-apoptotic genes are epigenetically silenced in endocycling cells, preventing activation of a paused RNA Pol II by p53-dependent or p53-independent pathways. Over-expression of the p53A isoform did not activate this paused RNA Pol II complex in endocycling cells, but over-expression of the p53B isoform with a longer transactivation domain did, suggesting that dampened p53B protein levels are crucial for apoptotic repression. We also find that the p53A protein isoform is ubiquitinated and degraded by the proteasome in endocycling cells. In mitotic cycling cells, p53A was the only isoform expressed to detectable levels, and its mRNA and protein levels increased after irradiation, but there was no evidence for an increase in protein stability. However, our data suggest that p53A protein stability is regulated in unirradiated cells, which likely ensures that apoptosis does not occur in the absence of stress. Without irradiation, both p53A protein and a paused RNA pol II were pre-bound to the promoters of pro-apoptotic genes, preparing mitotic cycling cells for a rapid apoptotic response to genotoxic stress. Together, our results define molecular mechanisms by which different cells in development modulate their apoptotic response, with broader significance for the survival of normal and cancer polyploid cells in mammals.
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