ArticlePLoS genetics2017
SYGL-1 and LST-1 link niche signaling to PUF RNA repression for stem cell maintenance in Caenorhabditis elegans.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed.
- Comprehensive comparative analysis of the effects of temperature on the Notch signaling response in vivo.Biology open · 2025Article
- Three lncRNAs promote PUM protein condensation and germline differentiation.Nature communications · 2025Article
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- Notch activity is modulated by the aGPCR Latrophilin binding the DSL ligand in C. elegans.Nature communications · 2025Article
- Mediator-29 limits Caenorhabditis elegans fecundity.Genetics · 2025Article
- LST1 expression correlates with immune infiltration and predicts poor prognosis in acute myeloid leukemia.Discover oncology · 2025Article
- A higher order PUF complex is central to regulation of C. elegans germline stem cells.Nature communications · 2025Article
- A nucleic acid binding protein map of germline regulation in Caenorhabditis elegans.Nature communications · 2024Article
- Notch signaling without the APH-2/nicastrin subunit of gamma secretase in Caenorhabditis elegans germline stem cells.Genetics · 2024Article
- A higher order PUF complex is central to regulation ofbioRxiv : the preprint server for biology · 2024Article
- DOS-3 mediates cell-non-autonomous DAF-16/FOXO activity in antagonizing age-related loss of C. elegans germline stem/progenitor cells.Nature communications · 2024Article
- Review
- The roles of TGFβ and serotonin signaling in regulating proliferation of oocyte precursors and germline aging.bioRxiv : the preprint server for biology · 2024Article
- COP9 signalosome component CSN-5 stabilizes PUF proteins FBF-1 and FBF-2 in Caenorhabditis elegans germline stem and progenitor cells.Genetics · 2024Article
- PUF partner interactions at a conserved interface shape the RNA-binding landscape and cell fate in Caenorhabditis elegans.Developmental cell · 2024Article
- Aging disrupts spatiotemporal regulation of germline stem cells and niche integrity.Biology open · 2024Article
- Intra- and inter-molecular regulation by intrinsically-disordered regions governs PUF protein RNA binding.Nature communications · 2023Article
- PUF-8, a C. elegans ortholog of the RNA-binding proteins PUM1 and PUM2, is required for robustness of the cell death fate.Development (Cambridge, England) · 2023Article
- LST-1 is a bifunctional regulator that feeds back on Notch-dependent transcription to regulateProceedings of the National Academy of Sciences of the United States of America · 2023Article
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6 authors.
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Abstract
Central questions in regenerative biology include how stem cells are maintained and how they transition from self-renewal to differentiation. Germline stem cells (GSCs) in Caeno-rhabditis elegans provide a tractable in vivo model to address these questions. In this system, Notch signaling and PUF RNA binding proteins, FBF-1 and FBF-2 (collectively FBF), maintain a pool of GSCs in a naïve state. An open question has been how Notch signaling modulates FBF activity to promote stem cell self-renewal. Here we report that two Notch targets, SYGL-1 and LST-1, link niche signaling to FBF. We find that SYGL-1 and LST-1 proteins are cytoplasmic and normally restricted to the GSC pool region. Increasing the distribution of SYGL-1 expands the pool correspondingly, and vast overexpression of either SYGL-1 or LST-1 generates a germline tumor. Thus, SYGL-1 and LST-1 are each sufficient to drive "stemness" and their spatial restriction prevents tumor formation. Importantly, SYGL-1 and LST-1 can only drive tumor formation when FBF is present. Moreover, both proteins interact physically with FBF, and both are required to repress a signature FBF mRNA target. Together, our results support a model in which SYGL-1 and LST-1 form a repressive complex with FBF that is crucial for stem cell maintenance. We further propose that progression from a naïve stem cell state to a state primed for differentiation relies on loss of SYGL-1 and LST-1, which in turn relieves FBF target RNAs from repression. Broadly, our results provide new insights into the link between niche signaling and a downstream RNA regulatory network and how this circuitry governs the balance between self-renewal and differentiation.
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