ArticleGenes & development2006
Reduced growth of Drosophila neurofibromatosis 1 mutants reflects a non-cell-autonomous requirement for GTPase-Activating Protein activity in larval neurons.
Article in Genes & development, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 59 citations in OpenAlex.
- Excessive activation of the RAS/MAPK pathway triggers adult-onset motor axonal degeneration.iScience · 2026Article
- Metabolic and behavioral effects of neurofibromin result from differential recruitment of MAPK and mTOR signaling.PLoS genetics · 2026Article
- Inhibition of Cxcr4 chemokine receptor signaling improves habituation learning in a zebrafish model of neurofibromatosis.Disease models & mechanisms · 2026Article
- Cognition and behavior in neurofibromatosis type 1: report and perspective from the Cognition and Behavior in NF1 (CABIN) Task Force.Genes & development · 2025Article
- Neurofibromin Deficiency Alters the Patterning and Prioritization of Motor Behaviors in a State-Dependent Manner.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Inhibition of autophagy as a novel treatment for neurofibromatosis type 1 tumors.Molecular oncology · 2025Article
- Unraveling neuronal and metabolic alterations in neurofibromatosis type 1.Journal of neurodevelopmental disorders · 2024Review
- Neurofibromin deficiency alters the patterning and prioritization of motor behaviors in a state-dependent manner.bioRxiv : the preprint server for biology · 2024Article
- Modeling neurodegenerative and neurodevelopmental disorders in theLearning & memory (Cold Spring Harbor, N.Y.) · 2024Review
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- Neurofibromin 1 mediates sleep depth in Drosophila.PLoS genetics · 2023Article
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- A Targeted, Low-Throughput Compound Screen in aeNeuro · 2023Article
- SREBP modulates the NADPNature communications · 2023Article
- Loss ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Mechanistic insights from animal models of neurofibromatosis type 1 cognitive impairment.Disease models & mechanisms · 2022Review
- RAS and beyond: the many faces of the neurofibromatosis type 1 protein.Disease models & mechanisms · 2022Article
- Neurofibromin 1 in mushroom body neurons mediates circadian wake drive through activating cAMP-PKA signaling.Nature communications · 2021Article
- Neurofibromin regulates metabolic rate via neuronal mechanisms in Drosophila.Nature communications · 2021Article
- Associative Learning Requires Neurofibromin to Modulate GABAergic Inputs to Drosophila Mushroom Bodies.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
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8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurofibromatosis type 1 (NF1) is among the most common genetic disorders of humans and is caused by loss of neurofibromin, a large and highly conserved protein whose only known function is to serve as a GTPase-Activating Protein (GAP) for Ras. However, most Drosophila NF1 mutant phenotypes, including an overall growth deficiency, are not readily modified by manipulating Ras signaling strength, but are rescued by increasing signaling through the cAMP-dependent protein kinase A pathway. This has led to suggestions that NF1 has distinct Ras- and cAMP-related functions. Here we report that the Drosophila NF1 growth defect reflects a non-cell-autonomous requirement for NF1 in larval neurons that express the R-Ras ortholog Ras2, that NF1 is a GAP for Ras1 and Ras2, and that a functional NF1-GAP catalytic domain is both necessary and sufficient for rescue. Moreover, a Drosophila p120RasGAP ortholog, when expressed in the appropriate cells, can substitute for NF1 in growth regulation. Our results show that loss of NF1 can give rise to non-cell-autonomous developmental defects, implicate aberrant Ras-mediated signaling in larval neurons as the primary cause of the NF1 growth deficiency, and argue against the notion that neurofibromin has separable Ras- and cAMP-related functions.
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