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Dissecting neuronal specification in the Drosophila taste system

  • Author(s): Dennison, Lisa Marie
  • Advisor(s): Scott, Kristin
  • et al.
Abstract

Establishing a complex brain and nervous system requires a wide array of neurons with diverse forms, functions, and characteristics. Developing nervous systems employ many strategies to create this neuronal diversity, and these strategies remain the subject of ongoing investigations in developmental neuroscience.

Neuronal diversity in the taste system of Drosophila melanogaster is important for the appropriate detection of chemosensory signals in the fly's environment. Drosophila can distinguish sweet substances, bitter compounds, pheromones, and pure water using distinct populations of taste neurons. The correct detection of such substances is critical for correct ingestion of nutritive foods, avoidance of toxins, recognition of appropriate mates, and hydration, all of which are essential for the survival and propagation of the fly. The first part of this thesis focuses on the developmental relationship between these classes of neurons and the signaling pathways used to diversify them. Mosaic analysis revealed at least two stereotyped lineages for taste neurons innervating bristles on the proboscis of the fly. Furthermore, mutant mosaic studies showed that Numb inheritance or lack thereof is necessary for correct cell fate decisions. The involvement of Numb strongly indicates that Notch signaling is the key player in establishing taste neuron diversity.

The second part of this thesis describes an expression screen for transcription factors with specific expression patterns in subsets of taste neurons. The transcription factors activated in each cell type ultimately establish that cell's unique identity by activating expression of appropriate receptors, axon guidance cues, neurotransmitters, and more. The screen identified two transcription factors, knot and Lim3, with specific expression in bitter-sensing neurons. Results of loss-of-function and gain-of-function studies with each gene indicate that neither one alone is necessary or sufficient to specify the full bitter neuron fate, but it remains possible that each could play a role in subsets of the bitter neuron's identity not observed by these analyses.

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