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Non-muscle myosin II and cytoplasmic dynein regulate cytoskeleton translocation during axonal elongation

Posted on:2015-09-12Degree:Ph.DType:Dissertation
University:Michigan State UniversityCandidate:Roossien, Douglas H., JrFull Text:PDF
GTID:1474390017998535Subject:Biology
Abstract/Summary:
Neurons are complex cellular machines that utilize a dynamic cytoskeleton to elaborate long axonal processes. During embryonic development, these long processes eventually terminate and form a synapse with a prescribed target. Elongation is driven in part by a unique structure called the growth cone at the tip of the axon. A recently developed biophysical model for axonal elongation has proposed that forces cause the growth cone to translocate in bulk, while stretching the axon. This is followed by intercalated mass addition along the length of the axon to prevent thinning. As a result of axonal stretching, the cytoskeleton undergoes en masse translocation. While this has been observed in cultured neurons from a variety of different species, whether this occurs in vivo is unknown. In addition, the molecular force generating mechanisms in the axon that regulate axonal stretching and cytoskeleton translocation have not been characterized.;Here, we use mitochondria docked to the cytoskeleton as fiduciary markers for bulk cytoskeletal movements. We use this technique in cultured Drosophila neurons to show that cytoskeleton translocation is conserved between vertebrates and invertebrates. Then we track the movement of docked mitochondria in the aCC motoneuron in stage 16 Drosophila embryos to show that the cytoskeleton translocates during axonal elongation. This suggests that axons grow by stretching in vivo.
Keywords/Search Tags:Cytoskeleton, Axonal, Elongation, Stretching
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