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The Washington Research Foundation Fellowship
Marvin Nayan, Neurology & Biochemistry, 2012-13 WRFF
Marvin Nayan is a senior studying Neurobiology and Biochemistry. He began his research career as a freshman by joining the laboratory of Dr. Jay Parrish at the Department of Biology. Marvin's project investigates the genetic factors of dendrite patterning and maintenance morphology in fruit fly sensory neurons. He aims to characterize mutations in genes that affect dendrite morphology and gain insight on how the normal version of the gene contributes to normal dendrite patterning. Given that defects in dendrite patterning have been observed in diseases of cognition and in normal aging, he his hopeful this research will contribute to our understanding of genetic mechanisms underlying the maintenance of neuronal function.
Mentor: Jay Parrish, Biology
Project Title: Analyzing Genetic Regulators of Dendrite Maintenance in Drosophila
Abstract: The neuron is a highly branched and morphologically diverse cell type that constitutes the basic unit of the nervous system. Neurons form complex neural networks with each other through protrusions called axons and dendrites. Different types of neurons often have unique, type-specific dendrite morphologies and the patterning of dendrites influences neuronal function. Although many genes play a role in mediating dendrite patterning, the precise molecular mechanisms in which neurons accomplish their exquisite morphology is poorly understood. Underscoring the importance of dendrite morphology to neuronal function, defects in dendrite patterning likely contribute to numerous neurological disease states and the cognitive decline that accompanies normal aging. To determine which genes are involved in dendrite patterning, we previously identified several gene mutations that affect class IV dendritic arborization (da) neurons in Drosophila larvae. Here, we propose the comprehensive analysis of a novel mutant, mn29. Using live cell imaging and quantitative analysis, we found that mn29 leads to exuberant dendrite branching and intermingling of dendrites in sensory neurons. This latter defect is of particular interest since "self-avoidance" may represent a general mechanism for organizing sensory dendrites and little is known about the genetic basis for this phenomenon. Using time-lapse microscopy, we found that mn29 causes progressive dendrite defects: the dendrite patterning of mn29 mutants is indistinguishable from wild type early in development, but becomes abnormal later in development. Likewise, dendrite defects in many neurological disorders are progressive; therefore further analysis of mn29 may contribute to our understanding of how dendrite maintenance is deregulated in diseased states. Currently, we are working towards identifying the gene affected in mn29 mutants and determining whether mn29 affects dendrite patterning in other functional classes of sensory neurons.