ArticleCurrent biology : CB2019
HLH-2/E2A Expression Links Stochastic and Deterministic Elements of a Cell Fate Decision during C. elegans Gonadogenesis.
Article in Current biology : CB, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed.
- Regulation of hlh-2 transcription during specification of the anchor cell of the C. elegans hermaphrodite gonad.G3 (Bethesda, Md.) · 2026Article
- Modes of Notch signalling in development and disease.Nature reviews. Molecular cell biology · 2025Review
- Beyond genes and environment: mapping biological stochasticity in aging.GeroScience · 2025Review
- RAP-2 and CNH-MAP4 Kinase MIG-15 confer resistance in bystander epithelium to cell-fate transformation by excess Ras or Notch activity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Rac pathway prevents cell fragmentation in a nonprotrusively migrating leader cell during C. elegans gonad organogenesis.Current biology : CB · 2024Article
- The C. elegans anchor cell: A model to elucidate mechanisms underlying invasion through basement membrane.Seminars in cell & developmental biology · 2024Review
- Article
- Getting there in one piece: The Rac pathway prevents cell fragmentation in a nonprotrusively migrating leader cell during organogenesis.bioRxiv : the preprint server for biology · 2023Article
- Article
- Transcription factor fluctuations underlie cell-to-cell variability in a signaling pathway response.Genetics · 2023Article
- Differential production rates of cytosolic and transmembrane GFP reporters inmicroPublication biology · 2023Article
- EGFR signal transduction is downregulated in C. elegans vulval precursor cells during dauer diapause.Development (Cambridge, England) · 2022Article
- SALSA, a genetically encoded biosensor for spatiotemporal quantification of Notch signal transduction in vivo.Developmental cell · 2022Article
- Influences of HLH-2 stability on anchor cell fate specification during Caenorhabditis elegans gonadogenesis.G3 (Bethesda, Md.) · 2022Article
- A DNA replication-independent function of pre-replication complex genes during cell invasion in C. elegans.PLoS biology · 2022Article
- AnmicroPublication biology · 2022Article
- A new toolkit to visualize and perturb endogenous LIN-12/Notch signaling inmicroPublication biology · 2022Article
- Article
- Deletion of a putative HDA-1 binding site in themicroPublication biology · 2021Article
- Positive autoregulation ofDevelopment (Cambridge, England) · 2020Article
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4 authors.
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Abstract
Stochastic mechanisms diversify cell fate in organisms ranging from bacteria to humans [1-4]. In the anchor cell/ventral uterine precursor cell (AC/VU) fate decision during C. elegans gonadogenesis, two "α cells," each with equal potential to be an AC or a VU, interact via LIN-12/Notch and its ligand LAG-2/DSL [5, 6]. This LIN-12/Notch-mediated interaction engages feedback mechanisms that amplify a stochastic initial difference between the two α cells, ensuring that the cell with higher lin-12 activity becomes the VU while the other becomes the AC [7-9]. The initial difference between the α cells was originally envisaged as a random imbalance from "noise" in lin-12 expression/activity [6]. However, subsequent evidence that the relative birth order of the α cells biases their fates suggested other factors may be operating [7]. Here, we investigate the nature of the initial difference using high-throughput lineage analysis [10]; GFP-tagged endogenous LIN-12, LAG-2, and HLH-2, a conserved transcription factor that orchestrates AC/VU development [7, 11]; and tissue-specific hlh-2 null alleles. We identify two stochastic elements: relative birth order, which largely originates at the beginning of the somatic gonad lineage three generations earlier, and onset of HLH-2 expression, such that the α cell whose parent expressed HLH-2 first is biased toward the VU fate. We find that these elements are interrelated, because initiation of HLH-2 expression is linked to the birth of the parent cell. Finally, we provide a potential deterministic mechanism for the HLH-2 expression bias by showing that hlh-2 is required for LIN-12 expression in the α cells.
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