The role of cnd-1 in mitochondrial biogenesis during Caenorhabditis elegans nervous system development
Disciplines
Cell and Developmental Biology
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.
Academic department under which the project should be listed
CSM - Molecular and Cellular Biology
Primary Investigator (PI) Name
Dr. Martin L. Hudson
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.