ArticleMolecular systems biology2012
Cell-cycle regulation of NOTCH signaling during C. elegans vulval development.
Article in Molecular systems biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
- Notch activity is modulated by the aGPCR Latrophilin binding the DSL ligand in C. elegans.Nature communications · 2025Article
- Reevaluating the relationship between EGL-43 (EVI1) and LIN-12 (Notch) during C. elegans anchor cell invasion.Biology open · 2022Article
- Tissue-specific inhibition of protein sumoylation uncovers diverse SUMO functions during C. elegans vulval development.PLoS genetics · 2022Article
- Notch controls the cell cycle to define leader versus follower identities during collective cell migration.eLife · 2022Article
- Genetic analysis of Caenorhabditis elegans pry-1/Axin suppressors identifies genes involved in reproductive structure development, stress responses, and aging.G3 (Bethesda, Md.) · 2022Article
- A DNA replication-independent function of pre-replication complex genes during cell invasion in C. elegans.PLoS biology · 2022Article
- Microfluidic-based imaging of complete Caenorhabditis elegans larval development.Development (Cambridge, England) · 2021Article
- Negative feedback by conserved kinases patterns the degradation ofDevelopment (Cambridge, England) · 2020Article
- Executable cancer models: successes and challenges.Nature reviews. Cancer · 2020Review
- The Caenorhabditis elegans homolog of the Evi1 proto-oncogene, egl-43, coordinates G1 cell cycle arrest with pro-invasive gene expression during anchor cell invasion.PLoS genetics · 2020Article
- The hypoxia-response pathway modulates RAS/MAPK-mediated cell fate decisions inLife science alliance · 2019Article
- Subunits of the DNA polymerase alpha-primase complex promote Notch-mediated proliferation with discrete and shared functions in C. elegans germline.The FEBS journal · 2018Article
- Long-Term High-Resolution Imaging of Developing C. elegans Larvae with Microfluidics.Developmental cell · 2017Article
- Computational Modeling, Formal Analysis, and Tools for Systems Biology.PLoS computational biology · 2016Review
- Cell cycle features of C. elegans germline stem/progenitor cells vary temporally and spatially.Developmental biology · 2016Article
- Inferring Infection Patterns Based on a Connectivity Map of Host Transcriptional Responses.Scientific reports · 2015Article
- Invasive Cell Fate Requires G1 Cell-Cycle Arrest and Histone Deacetylase-Mediated Changes in Gene Expression.Developmental cell · 2015Article
- A model of the regulatory network involved in the control of the cell cycle and cell differentiation in the Caenorhabditis elegans vulva.BMC bioinformatics · 2015Article
- Logic programming to predict cell fate patterns and retrodict genotypes in organogenesis.Journal of the Royal Society, Interface · 2014Article
- Divide and differentiate: CDK/Cyclins and the art of development.Cell cycle (Georgetown, Tex.) · 2014Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C. elegans vulval development is one of the best-characterized systems to study cell fate specification during organogenesis. The detailed knowledge of the signaling pathways determining vulval precursor cell (VPC) fates permitted us to create a computational model based on the antagonistic interactions between the epidermal growth factor receptor (EGFR)/RAS/MAPK and the NOTCH pathways that specify the primary and secondary fates, respectively. A key notion of our model is called bounded asynchrony, which predicts that a limited degree of asynchrony in the progression of the VPCs is necessary to break their equivalence. While searching for a molecular mechanism underlying bounded asynchrony, we discovered that the termination of NOTCH signaling is tightly linked to cell-cycle progression. When single VPCs were arrested in the G1 phase, intracellular NOTCH failed to be degraded, resulting in a mixed primary/secondary cell fate. Moreover, the G1 cyclins CYD-1 and CYE-1 stabilize NOTCH, while the G2 cyclin CYB-3 promotes NOTCH degradation. Our findings reveal a synchronization mechanism that coordinates NOTCH signaling with cell-cycle progression and thus permits the formation of a stable cell fate pattern.
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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.