ArticleG3 (Bethesda, Md.)2014
An RNAi-based suppressor screen identifies interactors of the Myt1 ortholog of Caenorhabditis elegans.
Article in G3 (Bethesda, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
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
26 citing papers in PubMed, 30 citations in OpenAlex.
- Box C/D snoRNPs and MDT-15/MED15 regulate mitochondrial surveillance and mitophagy via fatty acid metabolism.GeroScience · 2026Article
- Muscular dystrophy-associated lamin variants disrupt cellular organization through a nucleolar-ribosomal axis.Science advances · 2026Article
- Nuclear envelope-dependent heterochromatin positioning gates the timing of nucleolar assembly in the early embryo.bioRxiv : the preprint server for biology · 2026Article
- Wee Kinases, Big Impact: Wee and Myt Kinases as Critical Regulators of Meiotic Progression.Journal of developmental biology · 2026Review
- The SPN-4 Rbfox RNA-binding protein selects maternal mRNAs for CCR4-NOT-dependent clearance in early Caenorhabditis elegans embryos.Development (Cambridge, England) · 2026Article
- The SPN-4 Rbfox RNA-binding protein selects maternal mRNAs for CCR4-NOT-dependent clearance in earlybioRxiv : the preprint server for biology · 2025Article
- Muscular dystrophy-associated lamin variants disrupt cellular organization through a nucleolar-ribosomal axis controlling cytoplasmic macromolecular crowding.bioRxiv : the preprint server for biology · 2025Article
- Biased regulation of protein synthesis and hypoxic death by a conditional raptor mutation.Current biology : CB · 2025Article
- A multiparametric anti-aging CRISPR screen uncovers a role for BAF in protein synthesis regulation.Nature communications · 2025Article
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- Box C/D small nucleolar ribonucleoproteins regulate mitochondrial surveillance and innate immunity.PLoS genetics · 2022Article
- Proteasomal subunit depletions differentially affect germline integrity inFrontiers in cell and developmental biology · 2022Article
- Comparison of N- and C-terminally endogenously GFP-tagged WEE-1.3 strains inmicroPublication biology · 2021Article
- The Rheb-TORC1 signaling axis functions as a developmental checkpoint.Development (Cambridge, England) · 2020Article
- TheDevelopment (Cambridge, England) · 2019Article
- Multiple Mechanisms Inactivate the LIN-41 RNA-Binding Protein To Ensure a Robust Oocyte-to-Embryo Transition inGenetics · 2018Article
- OrthoList 2: A New Comparative Genomic Analysis of Human andGenetics · 2018Article
- The C. elegans eggshell.WormBook : the online review of C. elegans biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Oocyte maturation in all species is controlled by a protein complex termed the maturation promoting factor (MPF). MPF comprises a cyclin-dependent kinase (CDK) and its partner cyclin, and it is regulated by dueling regulatory phosphorylation events on the CDK. In Caenorhabditis elegans, the Wee1/Myt1 ortholog WEE-1.3 provides the inhibitory phosphorylations on CDK-1 that keep MPF inactive and halt meiosis. Prior work has shown that depletion of WEE-1.3 in C. elegans results in precocious oocyte maturation in vivo and a highly penetrant infertility phenotype. This study sought to further define the precocious maturation phenotype and to identify novel interactors with WEE-1.3. We found that WEE-1.3 is expressed throughout the germline and in developing embryos in a perinuclear pattern, and demonstrated that oocytes in WEE-1.3-depleted germlines have begun to transcribe embryonic genes and exhibit inappropriate expression of proteins normally restricted to fertilized eggs. In addition, we performed an RNAi suppressor screen of the infertile phenotype to identify novel factors that, when co-depleted with WEE-1.3, restore fertility to these animals. We screened ∼1900 essential genes by RNAi feeding and identified 44 (∼2% of the tested genes) that are suppressors of the WEE-1.3 depletion phenotype. The suppressors include many previously unidentified players in the meiotic cell cycle and represent a pool of potential WEE-1.3 interacting proteins that function during C. elegans oocyte maturation and zygotic development.
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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.