ArticleNature2011
Control of Drosophila endocycles by E2F and CRL4(CDT2).
Article in Nature, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
111 citing papers in PubMed, 161 citations in OpenAlex.
- Whole genome duplication through mitotic slippage causes nuclear instability.The EMBO journal · 2026Article
- Spargel/dPGC-1 influences cell growth through the E2F1-mediated endocycle pathway.G3 (Bethesda, Md.) · 2026Article
- Integrative role of CTPS cytoophidia in polyploid tissue growth and nutrient adaptation.Insect science · 2026Article
- Metabolic and developmental rate divergence between serially homologous cells underlies an evolutionary innovation in Drosophila.PLoS biology · 2026Article
- Transcription factor Tono mediates histone H3K4 trimethylation to regulate endoreplication through transcriptional reprogramming.Science advances · 2026Article
- Bombyx mori Jun gene is involved in endoreplication of silk gland cells by regulating S-phase cell cycle genes.Journal of advanced research · 2026Article
- Morphological innovation without gene co-option: thebioRxiv : the preprint server for biology · 2026Article
- The Drosophila proventriculus lacks stem cells but compensates for age-related cell loss via endoreplication-mediated cell growth.Nature communications · 2026Article
- A novel role for the E2F transcription factor and the ER stress sensor IRE1 in cytoplasmic DNA accumulation.Genetics · 2025Article
- The dual role of whole-genome duplication: biological mechanisms, functional consequences, and detection advances.Acta biochimica et biophysica Sinica · 2025Review
- Oncogenic signaling in the Drosophila prostate-like accessory gland activates a pro-tumorigenic program in the absence of proliferation.Disease models & mechanisms · 2025Article
- USP8 and Hsp70 regulate endoreplication by synergistically promoting Fzr deubiquitination and stabilization.Science advances · 2025Article
- Post-eclosion growth in the Drosophila ejaculatory duct is driven by Juvenile hormone signaling and is essential for male fertility.Developmental biology · 2025Article
- Review
- Postsynaptic BMP signaling regulates myonuclear properties in Drosophila larval muscles.The Journal of cell biology · 2025Article
- Long noncoding RNAScience advances · 2024Article
- DCAF2 regulates the proliferation and differentiation of mouse progenitor spermatogonia by targeting p21 and thymine DNA glycosylase.Cell proliferation · 2024Article
- Cell cycle re-entry in the agingbioRxiv : the preprint server for biology · 2024Article
- Post-eclosion growth in thebioRxiv : the preprint server for biology · 2024Article
- Cell cycle variants during Drosophila male accessory gland development.G3 (Bethesda, Md.) · 2024Article
51 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 8 institutions in 4 countries.
Funding
Abstract
Endocycles are variant cell cycles comprised of DNA synthesis (S)- and gap (G)-phases but lacking mitosis. Such cycles facilitate post-mitotic growth in many invertebrate and plant cells, and are so ubiquitous that they may account for up to half the world's biomass. DNA replication in endocycling Drosophila cells is triggered by cyclin E/cyclin dependent kinase 2 (CYCE/CDK2), but this kinase must be inactivated during each G-phase to allow the assembly of pre-Replication Complexes (preRCs) for the next S-phase. How CYCE/CDK2 is periodically silenced to allow re-replication has not been established. Here, using genetic tests in parallel with computational modelling, we show that the endocycles of Drosophila are driven by a molecular oscillator in which the E2F1 transcription factor promotes CycE expression and S-phase initiation, S-phase then activates the CRL4(CDT2) ubiquitin ligase, and this in turn mediates the destruction of E2F1 (ref. 7). We propose that it is the transient loss of E2F1 during S phases that creates the window of low Cdk activity required for preRC formation. In support of this model overexpressed E2F1 accelerated endocycling, whereas a stabilized variant of E2F1 blocked endocycling by deregulating target genes, including CycE, as well as Cdk1 and mitotic cyclins. Moreover, we find that altering cell growth by changing nutrition or target of rapamycin (TOR) signalling impacts E2F1 translation, thereby making endocycle progression growth-dependent. Many of the regulatory interactions essential to this novel cell cycle oscillator are conserved in animals and plants, indicating that elements of this mechanism act in most growth-dependent cell cycles.
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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.