Report: Genetics Lab Experiment
Transport of vesicles facilitated by kinesin and the effects of mutations in nerve transmission in Caenorhabditis elegans
Introduction
A nerve cell is made up of three main structures: the soma, the axon and the synapse. When a nerve cell receives a signal, a protein called kinesin travels anterograde along the axon and guides the synaptic vesicles until it reaches the synapse. This triggers the release of the neurotransmitters stored within the vesicles. Once released, the neurotransmitters then bind to receptors of the receiving cell. It would be nearly impossible to have the transportation of vesicles without kinesin to guide it. And without the transportation of these synaptic vesicles to release their neurotransmitters, there would be no movement in the cell at all.
This experiment is so important because vesicle transport in neurons helps to identify many neurological disorders. One such example is a research on Drosophila. Since there is only one kinesin light gene in the subject, the mutants in that one chain gene exhibit severe motor neuronal disease (Hirokawa, 2008). The disruption of the anterograde and retrograde transport of membrane vesicles was found to interrupt the function of kinesin in the mutated organisms causing them to be paralyzed (Hirokawa, 2008). This research into the function of kinesin in neurological disorders helps doctors and researchers to better understand the effects of kinesin in mutated organisms.
The goal of the experiment was to better understand kinesin facilitated transport of vesicles and to observe the effects of mutations in nerve transmission in Caenorhabditis elegans. C. elegans is a species of nematode that has a simple nervous system and has synaptic vesicles that can be easily tagged with green fluorescent protein (GFP) and viewed under fluorescence microscopy. The experiment was to observe three strains of C. elegans and determine which of the phenotypes observed showed certain mutations and then do a comparison
Introduction
A nerve cell is made up of three main structures: the soma, the axon and the synapse. When a nerve cell receives a signal, a protein called kinesin travels anterograde along the axon and guides the synaptic vesicles until it reaches the synapse. This triggers the release of the neurotransmitters stored within the vesicles. Once released, the neurotransmitters then bind to receptors of the receiving cell. It would be nearly impossible to have the transportation of vesicles without kinesin to guide it. And without the transportation of these synaptic vesicles to release their neurotransmitters, there would be no movement in the cell at all.
This experiment is so important because vesicle transport in neurons helps to identify many neurological disorders. One such example is a research on Drosophila. Since there is only one kinesin light gene in the subject, the mutants in that one chain gene exhibit severe motor neuronal disease (Hirokawa, 2008). The disruption of the anterograde and retrograde transport of membrane vesicles was found to interrupt the function of kinesin in the mutated organisms causing them to be paralyzed (Hirokawa, 2008). This research into the function of kinesin in neurological disorders helps doctors and researchers to better understand the effects of kinesin in mutated organisms.
The goal of the experiment was to better understand kinesin facilitated transport of vesicles and to observe the effects of mutations in nerve transmission in Caenorhabditis elegans. C. elegans is a species of nematode that has a simple nervous system and has synaptic vesicles that can be easily tagged with green fluorescent protein (GFP) and viewed under fluorescence microscopy. The experiment was to observe three strains of C. elegans and determine which of the phenotypes observed showed certain mutations and then do a comparison