ArticlePloS one2018
Segmentally homologous neurons acquire two different terminal neuropeptidergic fates in the Drosophila nervous system.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- A Tale of Two States: Similarities and Differences in Neuropeptide Signaling in Larval and Adult Drosophila.The Journal of comparative neurology · 2026Review
- PBX-dependent and independent Hox programs establish and maintain motor neuron terminal Identity.bioRxiv : the preprint server for biology · 2025Article
- Article
- Maintenance of neurotransmitter identity by Hox proteins through a homeostatic mechanism.Nature communications · 2022Article
- Dachshund acts with Abdominal-B to trigger programmed cell death in the Drosophila central nervous system at the frontiers of Abd-B expression.Developmental neurobiology · 2022Article
- Emerging Roles for Hox Proteins in the Last Steps of Neuronal Development in Worms, Flies, and Mice.Frontiers in neuroscience · 2021Review
- CAPA neuropeptides and their receptor form an anti-diuretic hormone signaling system in the human disease vector, Aedes aegypti.Scientific reports · 2020Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
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Abstract
In this study, we identify the means by which segmentally homologous neurons acquire different neuropeptide fates in Drosophila. Ventral abdominal (Va)-neurons in the A1 segment of the ventral nerve cord express DH31 and AstA neuropeptides (neuropeptidergic fate I) by virtue of Ubx activity, whereas the A2-A4 Va-neurons express the Capa neuropeptide (neuropeptidergic fate II) under the influence of abdA. These different fates are attained through segment-specific programs of neural subtype specification undergone by segmentally homologous neurons. This is an attractive alternative by which Hox genes can shape Drosophila segmental neural architecture (more sophisticated than the previously identified binary "to live" or "not to live" mechanism). These data refine our knowledge of the mechanisms involved in diversifying neuronal identity within the central nervous system.
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