ArticleThe EMBO journal2006
Mammalian Emi2 mediates cytostatic arrest and transduces the signal for meiotic exit via Cdc20.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
78 citing papers in PubMed, 185 citations in OpenAlex.
- The degradation of maternal RNA-binding protein 4E-T regulates translational activation to ensure maternal-to-zygotic transition in mouse embryos.Cellular and molecular life sciences : CMLS · 2026Article
- Mutation Severity ofHuman mutation · 2026Article
- TheBiomolecules · 2025Review
- Disrupted MOS signaling alters meiotic cell cycle regulation and the egg transcriptome.Reproduction (Cambridge, England) · 2025Article
- Egg Overactivation-An Overlooked Phenomenon of Gamete Physiology.International journal of molecular sciences · 2025Review
- The TRPV3 channel is a mediator of zinc influx and homeostasis in murine oocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The C-terminal domain of Emi2 conjugated to cell-penetrating peptide activates mouse oocyte.Frontiers in cell and developmental biology · 2025Article
- Advances in the genetic etiology of female infertility.Journal of assisted reproduction and genetics · 2024Review
- High-sensitivity whole-mount in situ Hybridization of Mouse Oocytes and Embryos Visualizes the Super-resolution Structures and Distributions of mRNA Molecules.Biological procedures online · 2024Article
- ZneLife · 2023Article
- ZnbioRxiv : the preprint server for biology · 2023Article
- The CCR4-NOT complex suppresses untimely translational activation of maternal mRNAs.Development (Cambridge, England) · 2023Article
- Review
- Egg Development AfterThe journal of poultry science · 2023Article
- Mitochondrial aggregation caused by cytochalasin B compromises the efficiency and safety of three-parent embryo.Molecular human reproduction · 2022Article
- A proteomics-MM/PBSA dual approach for the analysis of SARS-CoV-2 main protease substrate peptide specificity.Peptides · 2022Article
- Biallelic mutations in MOS cause female infertility characterized by human early embryonic arrest and fragmentation.EMBO molecular medicine · 2021Article
- Deprotection of centromeric cohesin at meiosis II requires APC/C activity but not kinetochore tension.The EMBO journal · 2021Article
- Tracking intracellular forces and mechanical property changes in mouse one-cell embryo development.Nature materials · 2020Article
- Recent advances in mammalian reproductive biology.Science China. Life sciences · 2020Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fertilizable mammalian oocytes are arrested at the second meiotic metaphase (mII) by the cyclinB-Cdc2 heterodimer, maturation promoting factor (MPF). MPF is stabilized via the activity of an unidentified cytostatic factor (CSF), thereby suspending meiotic progression until fertilization. We here present evidence that a conserved 71 kDa mammalian orthologue of Xenopus XErp1/Emi2, which we term endogenous meiotic inhibitor 2 (Emi2) is an essential CSF component. Depletion in situ of Emi2 by RNA interference elicited precocious meiotic exit in maturing mouse oocytes. Reduction of Emi2 released mature mII oocytes from cytostatic arrest, frequently inducing cytodegeneration. Mos levels autonomously declined to undetectable levels in mII oocytes. Recombinant Emi2 reduced the propensity of mII oocytes to exit meiosis in response to activating stimuli. Emi2 and Cdc20 proteins mutually interact and Cdc20 ablation negated the ability of Emi2 removal to induce metaphase release. Consistent with this, Cdc20 removal prevented parthenogenetic or sperm-induced meiotic exit. These studies show in intact oocytes that the interaction of Emi2 with Cdc20 links activating stimuli to meiotic resumption at fertilization and during parthenogenesis in mammals.
Indexed as
Identifiers
What OpenQuestion holds
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.