ArticleGenetics2014
Dual phosphorylation of cdk1 coordinates cell proliferation with key developmental processes in Drosophila.
Article in Genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 32 citations in OpenAlex.
- Wee Kinases, Big Impact: Wee and Myt Kinases as Critical Regulators of Meiotic Progression.Journal of developmental biology · 2026Review
- MPF Regulates Oocyte and Embryo Development During Parthenogenesis Induction in Silkworm,Insects · 2025Article
- Article
- Combination Therapy as a Promising Way to Fight Oral Cancer.Pharmaceutics · 2023Review
- Phosphorylation of VP1 Mediated by CDK1-Cyclin B1 Facilitates Infectious Bursal Disease Virus Replication.Journal of virology · 2023Article
- Proximity Labeling Reveals Spatial Regulation of the Anaphase-Promoting Complex/Cyclosome by a Microtubule Adaptor.ACS chemical biology · 2022Article
- Coordination between cell proliferation and apoptosis after DNA damage in Drosophila.Cell death and differentiation · 2022Article
- Regulation and coordination of the different DNA damage responses inFrontiers in cell and developmental biology · 2022Review
- Targeting the DNA Damage Response for Cancer Therapy by Inhibiting the Kinase Wee1.Frontiers in oncology · 2022Review
- The Atr-Chek1 pathway inhibits axon regeneration in response to Piezo-dependent mechanosensation.Nature communications · 2021Article
- Histone lysine methyltransferase Pr-set7/SETD8 promotes neural stem cell reactivation.EMBO reports · 2021Article
- Nuclear Export of Cyclin B Mediated by the Nup62 Complex Is Required for Meiotic Initiation inCells · 2020Article
- Kinesin 6 Regulation inG3 (Bethesda, Md.) · 2018Article
- Small proline-rich protein 2B drives stress-dependent p53 degradation and fibroblast proliferation in heart failure.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Kinase Inhibition Leads to Hormesis in a Dual Phosphorylation-Dephosphorylation Cycle.PLoS computational biology · 2016Article
- Inhibitory phosphorylation of Cdk1 mediates prolonged prophase I arrest in female germ cells and is essential for female reproductive lifespan.Cell research · 2016Article
- Myt1 inhibition of Cyclin A/Cdk1 is essential for fusome integrity and premeiotic centriole engagement in Drosophila spermatocytes.Molecular biology of the cell · 2016Article
- ISL1, a novel regulator of CCNB1, CCNB2 and c-MYC genes, promotes gastric cancer cell proliferation and tumor growth.Oncotarget · 2016Article
- TARANIS Functions with Cyclin A and Cdk1 in a Novel Arousal Center to Control Sleep in Drosophila.Current biology : CB · 2015Article
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Eukaryotic organisms use conserved checkpoint mechanisms that regulate Cdk1 by inhibitory phosphorylation to prevent mitosis from interfering with DNA replication or repair. In metazoans, this checkpoint mechanism is also used for coordinating mitosis with dynamic developmental processes. Inhibitory phosphorylation of Cdk1 is catalyzed by Wee1 kinases that phosphorylate tyrosine 15 (Y15) and dual-specificity Myt1 kinases found only in metazoans that phosphorylate Y15 and the adjacent threonine (T14) residue. Despite partially redundant roles in Cdk1 inhibitory phosphorylation, Wee1 and Myt1 serve specialized developmental functions that are not well understood. Here, we expressed wild-type and phospho-acceptor mutant Cdk1 proteins to investigate how biochemical differences in Cdk1 inhibitory phosphorylation influence Drosophila imaginal development. Phosphorylation of Cdk1 on Y15 appeared to be crucial for developmental and DNA damage-induced G2-phase checkpoint arrest, consistent with other evidence that Myt1 is the major Y15-directed Cdk1 inhibitory kinase at this stage of development. Expression of non-inhibitable Cdk1 also caused chromosome defects in larval neuroblasts that were not observed with Cdk1(Y15F) mutant proteins that were phosphorylated on T14, implicating Myt1 in a novel mechanism promoting genome stability. Collectively, these results suggest that dual inhibitory phosphorylation of Cdk1 by Myt1 serves at least two functions during development. Phosphorylation of Y15 is essential for the premitotic checkpoint mechanism, whereas T14 phosphorylation facilitates accumulation of dually inhibited Cdk1-Cyclin B complexes that can be rapidly activated once checkpoint-arrested G2-phase cells are ready for mitosis.
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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.