ArticleCell reports2022
A developmental pathway for epithelial-to-motoneuron transformation in C. elegans.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- The SynMuvA lin-15A licenses natural transdifferentiation by antagonizing identity safeguarding mechanisms.PLoS genetics · 2026Article
- Developmental Exposures to Three Mammalian Teratogens Produce Dysmorphic Phenotypes in AdultToxics · 2025Article
- Divergence in neuronal signaling pathways despite conserved neuronal identity among Caenorhabditis species.Current biology : CB · 2025Article
- Essential and dual effects of Notch activity on a natural transdifferentiation event.Nature communications · 2025Article
- Glia Development and Function in the NematodeCold Spring Harbor perspectives in biology · 2024Review
- Neurogenesis in Caenorhabditis elegans.Genetics · 2024Review
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Motoneurons and motoneuron-like pancreatic β cells arise from radial glia and ductal cells, respectively, both tube-lining progenitors that share molecular regulators. To uncover programs underlying motoneuron formation, we studied a similar, cell-division-independent transformation of the C. elegans tube-lining Y cell into the PDA motoneuron. We find that lin-12/Notch acts through ngn-1/Ngn and its regulator hlh-16/Olig to control transformation timing. lin-12 loss blocks transformation, while lin-12(gf) promotes precocious PDA formation. Early basal expression of ngn-1/Ngn and hlh-16/Olig depends on sem-4/Sall and egl-5/Hox. Later, coincident with Y cell morphological changes, ngn-1/Ngn expression is upregulated in a sem-4/Sall and egl-5/Hox-dependent but hlh-16/Olig-independent manner. Subsequently, Y cell retrograde extension forms an anchored process priming PDA axon extension. Extension requires ngn-1-dependent expression of the cytoskeleton organizers UNC-119, UNC-44/ANK, and UNC-33/CRMP, which also activate PDA terminal-gene expression. Our findings uncover cell-division-independent regulatory events leading to motoneuron generation, suggesting a conserved pathway for epithelial-to-motoneuron/motoneuron-like cell differentiation.
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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 Socratic graph.