ArticleMolecular biology of the cell2016
Nerve growth factor stimulates axon outgrowth through negative regulation of growth cone actomyosin restraint of microtubule advance.
Article in Molecular biology of the cell, 2016. 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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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
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- The Role of Nerve Growth Factor on the Ocular Surface: A Review of the Current Experimental Research and Clinical Practices.International journal of molecular sciences · 2025Review
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- Communicating pain: emerging axonal signaling in peripheral neuropathic pain.Frontiers in neuroanatomy · 2024Review
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- Advances in biotechnology and clinical therapy in the field of peripheral nerve regeneration based on magnetism.Frontiers in neurology · 2023Review
- Computational simulations reveal that Abl activity controls cohesiveness of actin networks in growth cones.Molecular biology of the cell · 2022Article
- Improved post-stroke spontaneous recovery by astrocytic extracellular vesicles.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Parallels between the Developing Vascular and Neural Systems: Signaling Pathways and Future Perspectives for Regenerative Medicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- With the Permission of Microtubules: An Updated Overview on Microtubule Function During Axon Pathfinding.Frontiers in molecular neuroscience · 2021Review
- Manipulation of Axonal Outgrowth via Exogenous Low Forces.International journal of molecular sciences · 2020Review
- Role of neurotrophic factors in enhancing linear axonal growth of ganglionic sensory neuronsNeural regeneration research · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Nerve growth factor (NGF) promotes growth, differentiation, and survival of sensory neurons in the mammalian nervous system. Little is known about how NGF elicits faster axon outgrowth or how growth cones integrate and transform signal input to motor output. Using cultured mouse dorsal root ganglion neurons, we found that myosin II (MII) is required for NGF to stimulate faster axon outgrowth. From experiments inducing loss or gain of function of MII, specific MII isoforms, and vinculin-dependent adhesion-cytoskeletal coupling, we determined that NGF causes decreased vinculin-dependent actomyosin restraint of microtubule advance. Inhibition of MII blocked NGF stimulation, indicating the central role of restraint in directed outgrowth. The restraint consists of myosin IIB- and IIA-dependent processes: retrograde actin network flow and transverse actin bundling, respectively. The processes differentially contribute on laminin-1 and fibronectin due to selective actin tethering to adhesions. On laminin-1, NGF induced greater vinculin-dependent adhesion-cytoskeletal coupling, which slowed retrograde actin network flow (i.e., it regulated the molecular clutch). On fibronectin, NGF caused inactivation of myosin IIA, which negatively regulated actin bundling. On both substrates, the result was the same: NGF-induced weakening of MII-dependent restraint led to dynamic microtubules entering the actin-rich periphery more frequently, giving rise to faster elongation.
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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.