ArticlePloS one2007
Mechanisms of TSC-mediated control of synapse assembly and axon guidance.
Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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
37 citing papers in PubMed, 57 citations in OpenAlex.
- The role of TSC1 and TSC2 proteins in neuronal axons.Molecular psychiatry · 2024Review
- Unraveling the Role of Ras Homolog Enriched in Brain (Rheb1 and Rheb2): Bridging Neuronal Dynamics and Cancer Pathogenesis through Mechanistic Target of Rapamycin Signaling.International journal of molecular sciences · 2024Review
- Article
- Two new cases of interstitial 7q35q36.1 deletion including CNTNAP2 and KMT2C.Molecular genetics & genomic medicine · 2021Article
- The TOR Pathway at the Neuromuscular Junction: More Than a Metabolic Player?Frontiers in molecular neuroscience · 2020Review
- Early patterns of functional brain development associated with autism spectrum disorder in tuberous sclerosis complex.Autism research : official journal of the International Society for Autism Research · 2019Article
- Exosomes mediate the acquisition of the disease phenotypes by cells with normal genome in tuberous sclerosis complex.Oncogene · 2016Article
- The PHR proteins: intracellular signaling hubs in neuronal development and axon degeneration.Neural development · 2016Review
- Visual Evoked Potentials as a Readout of Cortical Function in Infants With Tuberous Sclerosis Complex.Journal of child neurology · 2016Article
- Visual Processing in Infants with Tuberous Sclerosis Complex.Pediatric neurology briefs · 2016Article
- S6 Kinase Reflects and Regulates Ethanol-Induced Sedation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Diminished MTORC1-Dependent JNK Activation Underlies the Neurodevelopmental Defects Associated with Lysosomal Dysfunction.Cell reports · 2015Article
- Reduction in retinal nerve fiber layer thickness in tuberous sclerosis complex.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2015Article
- Early life nutrition and neural plasticity.Development and psychopathology · 2015Review
- In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1, and Costello syndrome.Frontiers in cellular neuroscience · 2015Article
- RhoGAP18B Isoforms Act on Distinct Rho-Family GTPases and Regulate Behavioral Responses to Alcohol via Cofilin.PloS one · 2015Article
- unfulfilled interacting genes display branch-specific roles in the development of mushroom body axons in Drosophila melanogaster.G3 (Bethesda, Md.) · 2014Article
- Mechanism-based treatment in tuberous sclerosis complex.Pediatric neurology · 2014Review
- Insulin signaling regulates neurite growth during metamorphic neuronal remodeling.Biology open · 2014Article
- Longevity pathways and memory aging.Frontiers in genetics · 2014Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Tuberous sclerosis complex is a dominant genetic disorder produced by mutations in either of two tumor suppressor genes, TSC1 and TSC2; it is characterized by hamartomatous tumors, and is associated with severe neurological and behavioral disturbances. Mutations in TSC1 or TSC2 deregulate a conserved growth control pathway that includes Ras homolog enriched in brain (Rheb) and Target of Rapamycin (TOR). To understand the function of this pathway in neural development, we have examined the contributions of multiple components of this pathway in both neuromuscular junction assembly and photoreceptor axon guidance in Drosophila. Expression of Rheb in the motoneuron, but not the muscle of the larval neuromuscular junction produced synaptic overgrowth and enhanced synaptic function, while reductions in Rheb function compromised synapse development. Synapse growth produced by Rheb is insensitive to rapamycin, an inhibitor of Tor complex 1, and requires wishful thinking, a bone morphogenetic protein receptor critical for functional synapse expansion. In the visual system, loss of Tsc1 in the developing retina disrupted axon guidance independently of cellular growth. Inhibiting Tor complex 1 with rapamycin or eliminating the Tor complex 1 effector, S6 kinase (S6k), did not rescue axon guidance abnormalities of Tsc1 mosaics, while reductions in Tor function suppressed those phenotypes. These findings show that Tsc-mediated control of axon guidance and synapse assembly occurs via growth-independent signaling mechanisms, and suggest that Tor complex 2, a regulator of actin organization, is critical in these aspects of neuronal development.
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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 OpenQuestion graph.