ArticlePLoS genetics2019
A Cyclin A-Myb-MuvB-Aurora B network regulates the choice between mitotic cycles and polyploid endoreplication cycles.
Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Transcription factor Tono mediates histone H3K4 trimethylation to regulate endoreplication through transcriptional reprogramming.Science advances · 2026Article
- Unscheduled polyploidy synergizes with oncogenic mutations to enhance genome instability and tumorigenesis.Cancer letters · 2025Article
- Activation of a Src-JNK pathway in unscheduled endocycling cells of the Drosophila wing disc induces a chronic wounding response.Genetics · 2025Article
- Characterization of transcriptomics during aging and genes required for lifespan in Drosophila intestine.Scientific reports · 2025Article
- Article
- E2F1-mediatedCytoJournal · 2025Article
- Cyclin A/Cdk1 promotes chromosome alignment and timely mitotic progression.Molecular biology of the cell · 2024Article
- An unscheduled switch to endocycles induces a reversible senescent arrest that impairs growth of the Drosophila wing disc.PLoS genetics · 2024Article
- A-MYB substitutes for B-MYB in activating cell cycle genes and in stimulating proliferation.Nucleic acids research · 2024Article
- YY2/BUB3 Axis promotes SAC Hyperactivation and Inhibits Colorectal Cancer Progression via Regulating Chromosomal Instability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Premature endocycling of Drosophila follicle cells causes pleiotropic defects in oogenesis.Genetics · 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
- High endoreduplication after drought-related conditions in haploid but not diploid mosses.Annals of botany · 2023Article
- Genetic and karyotype divergence between parents affect clonality and sterility in hybrids.eLife · 2023Article
- A genome-wide RNAi screen for genes important for proliferation of cultured Drosophila cells at low temperature identifies the Ball/VRK protein kinase.Chromosoma · 2023Article
- Polyploidy in development and tumor models in Drosophila.Seminars in cancer biology · 2022Review
- Challenges and Costs of Asexuality: Variation in Premeiotic Genome Duplication in Gynogenetic Hybrids fromInternational journal of molecular sciences · 2021Article
- Polyploidy in Tissue Repair and Regeneration.Cold Spring Harbor perspectives in biology · 2021Review
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Endoreplication is a cell cycle variant that entails cell growth and periodic genome duplication without cell division, and results in large, polyploid cells. Cells switch from mitotic cycles to endoreplication cycles during development, and also in response to conditional stimuli during wound healing, regeneration, aging, and cancer. In this study, we use integrated approaches in Drosophila to determine how mitotic cycles are remodeled into endoreplication cycles, and how similar this remodeling is between induced and developmental endoreplicating cells (iECs and devECs). Our evidence suggests that Cyclin A / CDK directly activates the Myb-MuvB (MMB) complex to induce transcription of a battery of genes required for mitosis, and that repression of CDK activity dampens this MMB mitotic transcriptome to promote endoreplication in both iECs and devECs. iECs and devECs differed, however, in that devECs had reduced expression of E2F1-dependent genes that function in S phase, whereas repression of the MMB transcriptome in iECs was sufficient to induce endoreplication without a reduction in S phase gene expression. Among the MMB regulated genes, knockdown of AurB protein and other subunits of the chromosomal passenger complex (CPC) induced endoreplication, as did knockdown of CPC-regulated cytokinetic, but not kinetochore, proteins. Together, our results indicate that the status of a CycA-Myb-MuvB-AurB network determines the decision to commit to mitosis or switch to endoreplication in both iECs and devECs, and suggest that regulation of different steps of this network may explain the known diversity of polyploid cycle types in development and disease.
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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.