ArticleDevelopment (Cambridge, England)2010
Mouse Emi2 as a distinctive regulatory hub in second meiotic metaphase.
Article in Development (Cambridge, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 88 citations in OpenAlex.
- MOS is a key regulator of meiotic midbody assembly and prevents abnormal divisions in mouse eggs and their polar bodies.Journal of cell science · 2026Article
- 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
- ZneLife · 2023Article
- ZnbioRxiv : the preprint server for biology · 2023Article
- Biallelic mutations in MOS cause female infertility characterized by human early embryonic arrest and fragmentation.EMBO molecular medicine · 2021Article
- Functional implications of CaMKII alternative splicing.The European journal of neuroscience · 2021Review
- Role of zinc in female reproduction.Biology of reproduction · 2021Review
- 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
- FRET-based sensor for CaMKII activity (FRESCA): A useful tool for assessing CaMKII activity in response to CaThe Journal of biological chemistry · 2019Article
- Calcineurin promotes APC/C activation at meiotic exit by acting on both XErp1 and Cdc20.EMBO reports · 2018Article
- Importance of ERK1/2 in Regulation of Protein Translation during Oocyte Meiosis.International journal of molecular sciences · 2018Review
- Postovulatory cell death: why eggs die via apoptosis in biological species with external fertilization.The Journal of reproduction and development · 2018Review
- Cyclin A2 modulates kinetochore-microtubule attachment in meiosis II.The Journal of cell biology · 2017Article
- Emi2 Is Essential for Mouse Spermatogenesis.Cell reports · 2017Article
- Article
- Zinc availability during germline development impacts embryo viability in Caenorhabditis elegans.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2017Article
- Mice produced by mitotic reprogramming of sperm injected into haploid parthenogenotes.Nature communications · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The oocytes of vertebrates are typically arrested at metaphase II (mII) by the cytostatic factor Emi2 until fertilization. Regulatory mechanisms in Xenopus Emi2 (xEmi2) are understood in detail but contrastingly little is known about the corresponding mechanisms in mammals. Here, we analyze Emi2 and its regulatory neighbours at the molecular level in intact mouse oocytes. Emi2, but not xEmi2, exhibited nuclear targeting. Unlike xEmi2, separable N- and C-terminal domains of mouse Emi2 modulated metaphase establishment and maintenance, respectively, through indirect and direct mechanisms. The C-terminal activity was mapped to the potential phosphorylation target Tx(5)SxS, a destruction box (D-box), a lattice of Zn(2+)-coordinating residues and an RL domain. The minimal region of Emi2 required for its cytostatic activity was mapped to a region containing these motifs, from residue 491 to the C terminus. The cytostatic factor Mos-MAPK promoted Emi2-dependent metaphase establishment, but Mos autonomously disappeared from meiotically competent mII oocytes. The N-terminal Plx1-interacting phosphodegron of xEmi2 was apparently shifted to within a minimal fragment (residues 51-300) of mouse Emi2 that also contained a calmodulin kinase II (CaMKII) phosphorylation motif and which was efficiently degraded during mII exit. Two equimolar CaMKII gamma isoform variants were present in mII oocytes, neither of which phosphorylated Emi2 in vitro, consistent with the involvement of additional factors. No evidence was found that calcineurin is required for mouse mII exit. These data support a model in which mammalian meiotic establishment, maintenance and exit converge upon a modular Emi2 hub via evolutionarily conserved and divergent mechanisms.
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.