Myosin 10 and Neurodevelopment
Location
Room 2911
Session Format
Paper Presentation
Research Area Topic:
MBI - Molecular Biology Initiative
Co-Presenters and Faculty Mentors or Advisors
Vinoth Sittaramane, PhD
Abstract
During neurodevelopment, nervous system cells (neurons) extend a long protrusion called an axon that migrates and innervates with postsynaptic targets via molecular cues received by a structure at the distal tip of the axon called the growth cone. However, molecular deficits can cause failure of axons to migrate appropriately. This can lead to a wide array of neurodevelopment disorders such as autism spectrum conditions, attention deficit hyperactivity disorder, motor dysfunctions, learning disabilities, and mental retardation. While there is a noteworthy amount of information known about external molecular cues in the extracellular matrix, the amount known about molecules within the axons that drive axon guidance is lacking. A potential contributor to axon guidance within the neuron is the protein Myosin 10 (myo10). We used the caudal primary (CaP) motor neurons in the trunk of the zebrafish (Danio rerio) as a model to investigate the molecular mechanisms of myo10 in the development of the nervous system. Normally, CaP motor neuron axons migrate from the spinal cord in a synchronous manner with trunk neural crest cells and ultimately innervate at neuromuscular junctions where they release signals in the form of ions and molecules such as acetylcholine. The postsynaptic muscle is lined with acetylcholine receptors that respond with muscular contraction upon the release of acetylcholine from the presynaptic axon terminus. Using gene knock-down and immunohistochemistry protocols, we have statistically significant data that shows that the CaP motor neurons of myo10 deficient zebrafish embryos have stunted growth and an unorganized distribution pattern of acetylcholine receptors. This corroborates that myo10 deficient embryos are not making appropriate synapses with the muscles. Additionally, we have illustrated that there is a statistically significant decrease in neural crest cell migration. This suggests that one potential mechanisms of myo10 is through neural crest cells migration.
Keywords
Neurodevelopment, Myosin 10, Axon guidance, Migration
Presentation Type and Release Option
Presentation (Open Access)
Start Date
4-24-2015 1:30 PM
End Date
4-24-2015 2:30 PM
Recommended Citation
Ivey, Crystal, "Myosin 10 and Neurodevelopment" (2015). GS4 Georgia Southern Student Scholars Symposium. 66.
https://digitalcommons.georgiasouthern.edu/research_symposium/2015/2015/66
Myosin 10 and Neurodevelopment
Room 2911
During neurodevelopment, nervous system cells (neurons) extend a long protrusion called an axon that migrates and innervates with postsynaptic targets via molecular cues received by a structure at the distal tip of the axon called the growth cone. However, molecular deficits can cause failure of axons to migrate appropriately. This can lead to a wide array of neurodevelopment disorders such as autism spectrum conditions, attention deficit hyperactivity disorder, motor dysfunctions, learning disabilities, and mental retardation. While there is a noteworthy amount of information known about external molecular cues in the extracellular matrix, the amount known about molecules within the axons that drive axon guidance is lacking. A potential contributor to axon guidance within the neuron is the protein Myosin 10 (myo10). We used the caudal primary (CaP) motor neurons in the trunk of the zebrafish (Danio rerio) as a model to investigate the molecular mechanisms of myo10 in the development of the nervous system. Normally, CaP motor neuron axons migrate from the spinal cord in a synchronous manner with trunk neural crest cells and ultimately innervate at neuromuscular junctions where they release signals in the form of ions and molecules such as acetylcholine. The postsynaptic muscle is lined with acetylcholine receptors that respond with muscular contraction upon the release of acetylcholine from the presynaptic axon terminus. Using gene knock-down and immunohistochemistry protocols, we have statistically significant data that shows that the CaP motor neurons of myo10 deficient zebrafish embryos have stunted growth and an unorganized distribution pattern of acetylcholine receptors. This corroborates that myo10 deficient embryos are not making appropriate synapses with the muscles. Additionally, we have illustrated that there is a statistically significant decrease in neural crest cell migration. This suggests that one potential mechanisms of myo10 is through neural crest cells migration.
