Does ngn-1/Neurogenin Control Sensory Neuron Cell Fate?
Disciplines
Developmental Biology | Developmental Neuroscience | Genetics
Abstract (300 words maximum)
Defects in nervous system development have been linked to multiple neurological conditions including autism spectrum disorder. Neurogenins are one of the earliest acting classes of pro-neural transcription factors. Mutations in human neurogenin1 have been associated with autism, strongly implicating this gene in the etiology of this complex polygenic disorder. Defects in neurogenin transcription/translation have the potential to contribute to autism phenotypes, creating an imperative for further study.
Our long-term goal is to understand the gene regulatory environment surrounding neurogenin during nervous system development. The nematode Caenorhabditis elegans is a powerful model to study gene regulatory processes. The C. elegans genome contains paralogs of most major vertebrate transcription factors required for nervous system development including ngn-1/neurogenin. We recently showed that ngn-1 is required, in part, for AIY interneuron fate specification and axon guidance. However, we have not established if this role extends to sensory and other neuron cell types. We used a sensory neuron-specific fluorescent reporter gene to examine the role of ngn-1 in sensory neuron axon guidance. gcy-33::GFP is exclusively expressed in the BAG sensory neurons. Preliminary data reveals that GFP-positive cells are still present in ngn-1 mutants, suggesting that ngn-1 is not required for BAG neuron cell fate. Work is on-going to determine the role of ngn-1 in BAG neuron axon and dendrite morphology.
Academic department under which the project should be listed
CSM - Molecular and Cellular Biology
Primary Investigator (PI) Name
Martin L. Hudson
Does ngn-1/Neurogenin Control Sensory Neuron Cell Fate?
Defects in nervous system development have been linked to multiple neurological conditions including autism spectrum disorder. Neurogenins are one of the earliest acting classes of pro-neural transcription factors. Mutations in human neurogenin1 have been associated with autism, strongly implicating this gene in the etiology of this complex polygenic disorder. Defects in neurogenin transcription/translation have the potential to contribute to autism phenotypes, creating an imperative for further study.
Our long-term goal is to understand the gene regulatory environment surrounding neurogenin during nervous system development. The nematode Caenorhabditis elegans is a powerful model to study gene regulatory processes. The C. elegans genome contains paralogs of most major vertebrate transcription factors required for nervous system development including ngn-1/neurogenin. We recently showed that ngn-1 is required, in part, for AIY interneuron fate specification and axon guidance. However, we have not established if this role extends to sensory and other neuron cell types. We used a sensory neuron-specific fluorescent reporter gene to examine the role of ngn-1 in sensory neuron axon guidance. gcy-33::GFP is exclusively expressed in the BAG sensory neurons. Preliminary data reveals that GFP-positive cells are still present in ngn-1 mutants, suggesting that ngn-1 is not required for BAG neuron cell fate. Work is on-going to determine the role of ngn-1 in BAG neuron axon and dendrite morphology.