Project Title

The role of cnd-1 in mitochondrial biogenesis during Caenorhabditis elegans nervous system development

Academic department under which the project should be listed

CSM - Molecular and Cellular Biology

Faculty Sponsor Name

Dr. Martin L. Hudson

Abstract (300 words maximum)

Mitochondria are responsible for energy production in cells. Mitochondrial defects underpin a plethora of neurological conditions including Parkinson’s disease, creating an imperative for further study. When cells are oxidatively stressed, energy production decreases and stress responses increase. Transcriptome data from the Hudson lab showed that the transcription factor cnd-1 controls aspects of mitochondrial gene expression, although how this occurs at the molecular level is not known. Using a mitochondrial GFP reporter gene whose expression is specific to the touch neurons, we examined mitochondrial distribution and morphology in wild type and cnd-1 mutants. We found that mitochondrial morphology and distribution was normal in cnd-1 mutants. We are currently using a mitochondrial stress response reporter gene to investigate if touch neurons (or other cell types) show defects in mitochondrial function in cnd-1 mutants.

Project Type

Poster

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The role of cnd-1 in mitochondrial biogenesis during Caenorhabditis elegans nervous system development

Mitochondria are responsible for energy production in cells. Mitochondrial defects underpin a plethora of neurological conditions including Parkinson’s disease, creating an imperative for further study. When cells are oxidatively stressed, energy production decreases and stress responses increase. Transcriptome data from the Hudson lab showed that the transcription factor cnd-1 controls aspects of mitochondrial gene expression, although how this occurs at the molecular level is not known. Using a mitochondrial GFP reporter gene whose expression is specific to the touch neurons, we examined mitochondrial distribution and morphology in wild type and cnd-1 mutants. We found that mitochondrial morphology and distribution was normal in cnd-1 mutants. We are currently using a mitochondrial stress response reporter gene to investigate if touch neurons (or other cell types) show defects in mitochondrial function in cnd-1 mutants.