Term of Award

Summer 2015

Degree Name

Master of Science in Biology (M.S.)

Document Type and Release Option

Thesis (open access)

Copyright Statement / License for Reuse

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.


Department of Biology

Committee Chair

Vinoth Sittaramane

Committee Member 1

John Harrison

Committee Member 2

Oscar Pung


Neurodevelopmental disorders are disabilities caused by malfunctioning mechanisms within the developing nervous tissue. These abnormalities often result in conditions such as autism spectrum disorders, Attention Deficient Hyperactivity Disorder (ADHD), motor dysfunctions, learning disabilities and mental retardation. Recent surveys indicate that there will be a 12% increase of children in the United States alone who are affected by neurodevelopmental disorders. Thus, it is important to understand both the normal and abnormal mechanisms of neural development. Neural development involves specification of new neurons and formation of neural circuits that connect the nervous system to every organ of the developing embryo. Neural circuits are formed by extensions of neuronal cell bodies called axons. Axons grow towards their specific target organs at growth cones, by sensing the environment for molecular cues which reorganizes their cytoskeleton to allow for their growth. Growth cones are actin rich suggesting that actin binding molecules play a vital role in axon guidance. Myosins are a class of actin binding proteins. Myosin 10 (myo10) is a myosin that is highly localized in growth cones indicating their potential role in axon guidance and growth. While myo10 has been shown to be involved in axon guidance in neural cell cultures, this has not been demonstrated in vivo. This aim of this project was to identify the roles of myo10 in axon growth cone guidance in vivo utilizing a zebrafish (Danio rerio) model. I established that myo10 is required for spinal motor and hindbrain axon development in the zebrafish. In the absence of myo10, 100% of caudal primary motor neurons were defective and 88% of middle primary motor axons were defective. Additionally, I characterized the phenotype of myo10 deficient embryos further by examining the points of innervation of the motor axons. Spinal motor axons innervate the muscle. The post-synaptic muscle is lined with acetylcholine receptors. Myo10 deficient embryos have a defective patterning of acetylcholine receptors and the muscles show indications of atrophy. Lastly, I provide some evidence for possible mechanisms in which myo10 may be functioning.