ArticleDevelopment (Cambridge, England)2003
Developmental defects observed in hypomorphic anaphase-promoting complex mutants are linked to cell cycle abnormalities.
Article in Development (Cambridge, England), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 65 citations in OpenAlex.
- The Small but Versatile Cyclin-Dependent Kinase Subunit CKS: C. elegans CKS-1 Regulates Anaphase Onset and Is Required for Anaphase B During Oocyte Meiosis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Anaphase onset requires CKS-1-mediated destruction of securin in meiosis I and cyclin B1 in meiosis II.The Journal of cell biology · 2026Article
- C. elegans spermatocyte divisions show a weak spindle checkpoint response.Journal of cell science · 2024Article
- Securin Regulates the Spatiotemporal Dynamics of Separase.bioRxiv : the preprint server for biology · 2023Article
- Article
- The APC/CFrontiers in cell and developmental biology · 2021Article
- Article
- Maternal MEMI Promotes Female Meiosis II in Response to Fertilization in Caenorhabditis elegans.Genetics · 2016Article
- CDK-1 and two B-type cyclins promote PAR-6 stabilization during polarization of the early C. elegans embryo.PloS one · 2015Article
- High-throughput capturing and characterization of mutations in essential genes of Caenorhabditis elegans.BMC genomics · 2014Article
- The Anaphase-Promoting Complex (APC) ubiquitin ligase regulates GABA transmission at the C. elegans neuromuscular junction.Molecular and cellular neurosciences · 2014Article
- The ubiquitin proteasome system in Caenorhabditis elegans and its regulation.Redox biology · 2014Review
- Article
- Control of oocyte growth and meiotic maturation in Caenorhabditis elegans.Advances in experimental medicine and biology · 2013Review
- Developmental genetics of secretory vesicle acidification during Caenorhabditis elegans spermatogenesis.Genetics · 2012Article
- emb-1 encodes the APC16 subunit of the Caenorhabditis elegans anaphase-promoting complex.Genetics · 2011Article
- Protein phosphatase 5 is a negative regulator of separase function during cortical granule exocytosis in C. elegans.Journal of cell science · 2011Article
- Article
- Functional redundancy of paralogs of an anaphase promoting complex/cyclosome subunit in Caenorhabditis elegans meiosis.Genetics · 2010Article
- Caenorhabditis elegans cyclin B3 is required for multiple mitotic processes including alleviation of a spindle checkpoint-dependent block in anaphase chromosome segregation.PLoS genetics · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
In C. elegans, mutants in the anaphase-promoting complex or cyclosome (APC/C) exhibit defects in germline proliferation, the formation of the vulva and male tail, and the metaphase to anaphase transition of meiosis I. Oocytes lacking APC/C activity can be fertilized but arrest in metaphase of meiosis I and are blocked from further development. To examine the cell cycle and developmental consequences of reducing but not fully depleting APC/C activity, we analyzed defects in embryos and larvae of mat-1/cdc-27 mutants grown at semi-permissive temperatures. Hypomorphic embryos developed to the multicellular stage but were slow to complete meiosis I and displayed aberrant meiotic chromosome separation. More severely affected embryos skipped meiosis II altogether and exhibited striking defects in meiotic exit. These latter embryos failed to produce normal eggshells or establish normal asymmetries prior to the first mitotic division. In developing larvae, extended M-phase delays in late-dividing cell lineages were associated with defects in the morphogenesis of the male tail. This study reveals the importance of dosage-specific mutants in analyzing molecular functions of a ubiquitously functioning protein within different cell types and tissues, and striking correlations between specific abnormalities in cell cycle progression and particular developmental defects.
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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.