ArticleThe EMBO journal2002
Chk1 is activated transiently and targets Cdc25A for degradation at the Xenopus midblastula transition.
Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 127 citations in OpenAlex.
- Randomized phase II trial of cytosine arabinoside with and without the CHK1 inhibitor MK-8776 in relapsed and refractory acute myeloid leukemia.Leukemia research · 2017Trial
- The timing of maternal protein degradation during mammalian preimplantation development is species-specific.Reproduction (Cambridge, England) · 2025Article
- Coordinated action of multiple active histone modifications shapes the zygotic genome activation in teleost embryos.Nature communications · 2025Article
- The maternal-to-zygotic transition: reprogramming of the cytoplasm and nucleus.Nature reviews. Genetics · 2025Review
- Inactivation of checkpoint kinase 1 (Chk1) during parvovirus minute virus of mice (MVM) infection inhibits cellular homologous recombination repair and facilitates viral genome replication.Journal of virology · 2024Article
- Muskelin acts as a substrate receptor of the highly regulatedbioRxiv : the preprint server for biology · 2024Article
- CHK1-CDC25A-CDK1 regulate cell cycle progression and protect genome integrity in early mouse embryos.EMBO reports · 2023Article
- The Nuclear-to-Cytoplasmic Ratio: Coupling DNA Content to Cell Size, Cell Cycle, and Biosynthetic Capacity.Annual review of genetics · 2022Review
- Cullin-5 mutants reveal collective sensing of the nucleocytoplasmic ratio in Drosophila embryogenesis.Current biology : CB · 2022Article
- Review
- The DNA-to-cytoplasm ratio broadly activates zygotic gene expression in Xenopus.Current biology : CB · 2021Article
- Cell cycle control during early embryogenesis.Development (Cambridge, England) · 2021Article
- Interphase-arrested Drosophila embryos activate zygotic gene expression and initiate mid-blastula transition events at a low nuclear-cytoplasmic ratio.PLoS biology · 2020Article
- The neglected part of early embryonic development: maternal protein degradation.Cellular and molecular life sciences : CMLS · 2020Review
- Fluorescence fluctuation analysis reveals PpV dependent Cdc25 protein dynamics in living embryos.PLoS genetics · 2020Article
- SSRP1-mediated histone H1 eviction promotes replication origin assembly and accelerated development.Nature communications · 2020Article
- Histone concentration regulates the cell cycle and transcription in early development.Development (Cambridge, England) · 2019Article
- Genome wide decrease of DNA replication eye density at the midblastula transition ofCell cycle (Georgetown, Tex.) · 2019Article
- On the Interplay of the DNA Replication Program and the Intra-S Phase Checkpoint Pathway.Genes · 2019Review
- Ciclopirox activates ATR-Chk1 signaling pathway leading to Cdc25A protein degradation.Genes & cancer · 2018Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In Xenopus embryos, cell cycle elongation and degradation of Cdc25A (a Cdk2 Tyr15 phosphatase) occur naturally at the midblastula transition (MBT), at which time a physiological DNA replication checkpoint is thought to be activated by the exponentially increased nucleo-cytoplasmic ratio. Here we show that the checkpoint kinase Chk1, but not Cds1 (Chk2), is activated transiently at the MBT in a maternal/zygotic gene product-regulated manner and is essential for cell cycle elongation and Cdc25A degradation at this transition. A constitutively active form of Chk1 can phosphorylate Cdc25A in vitro and can target it rapidly for degradation in pre-MBT embryos. Intriguingly, for this degradation, however, Cdc25A also requires a prior Chk1-independent phosphorylation at Ser73. Ectopically expressed human Cdc25A can be degraded in the same way as Xenopus Cdc25A. Finally, Cdc25A degradation at the MBT is a prerequisite for cell viability at later stages. Thus, the physiological replication checkpoint is activated transiently at the MBT by developmental cues, and activated Chk1, only together with an unknown kinase, targets Cdc25A for degradation to ensure later development.
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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.