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Effect of GPA-16 on bilateral asymmetry, neuronal connectivity and learning behavior in C. elegans

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dc.contributor.author Han, Ping
dc.date.accessioned 2018-10-09T05:00:52Z
dc.date.available 2018-10-09T05:00:52Z
dc.identifier.uri http://hdl.handle.net/20.500.12090/339
dc.description.abstract ABSTRACT Visceral organs structures and brain functions show asymmetric patterns in vertebrates including humans. Generally, the asymmetric pattern has a stereotypic laterality. Under some conditions, the laterality may be broken which can lead to abnormal structures and functions. Left-handedness is a type of brain functional laterality breaking condition. Research has shown that left-handers have increased performance in associative memory tasks compared to right-handed population. Also, left-handers tend to occupy the opposite ends of the performance spectrum, being more frequently observed in gifted individuals and in persons with psychosis. C. elegans is an excellent research model to evaluate to answer basic biological questions, including the influence of laterality variations. Even though C. elegans shows predominantly bilaterally symmetric external anatomy, however bilateral asymmetry is observed in its visceral organs and some of the neuron pairs. The stereotypic placement of anterior gut locates towards the left. Certain neuron pairs such as ASE-L and ASE-R display functional asymmetry. They express different kinds of genes and detect different kinds of water-soluble chemical cues. gcy-5 can only express on ASE-R, and gcy-5::GFP was used as ASE-R fluorescence marker in research. GPA-16 protein plays an important role in establishing and regulating asymmetric cell division during early stage of embryogenesis. Previous results demonstrated that gpa-16 mutants showing anatomical reversal in both embryos and adult worms. gpa-16 mutants show defects in both non-associative learning and associative learning. We examined the placement of ASE-R sensory neuron in gpa-16 mutants, and found out 22% ASE-R neurons were mis-localized. The mis-localized ASE-R has the potential to generate atypical neuronal circuitry and abnormal synaptic connectivity to downstream neurons, which could lead to the observed learning defects.
dc.title Effect of GPA-16 on bilateral asymmetry, neuronal connectivity and learning behavior in C. elegans
dc.date.updated 2018-09-25T19:03:04Z
dc.language.rfc3066 en


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