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2007-A-033-FEL - Abstract

Grant Information

Aging - Fellowship
Genetic Dissection of Mitochondrial Calcium Signaling in Neurodegeneration
Hong Xu, PhD
Biochemistry & Biophysics
Funding Status
  • Withdrawn
  • 3 years, $60,000 per year
  • 7/1/2007 to 6/30/2010


2007-A-033-FEL - Abstract
Brief Summary
"Genetic Dissection of Mitochondrial Calcium Signaling in Neurodegeneration"

Life is the tale of two genomes. Besides nuclear genome, there are hundreds to thousands mitochondrial genomes in virtually every single cells of our body. Mitochondrial DNA (mtDNA) encodes essential subunits of mitochondrial respiration chain, the generator of cellular energy source, ATP. mtDNA variants have been linked to various age-onset human diseases. However, in many cases it remains to be determined whether the mtDNA mutations play a causative role and what are the underlying mechanisms. Drosophila has been applied to modeling wild range of conserved physiological or pathological processes. The fact that same set of genes are encoded in fly and human mitochondrial genome, make it very attractive to study mtDNA biology in Drosophila. But a lack of genetic tools hinders genetic studies of mtDNA biology in most model organisms.

I have developed a restriction enzyme based approach to select mtDNA mutants and isolated several lines that were homoplasmic for mtDNA mutants. More importantly, these flies showed various maternally inherited traits, including male sterility, neuronal and muscular degeneration, abnormal sensory organ development, and reduced life span. Furthermore, moderate expression of the enzyme in eye caused tumor like growth. The flies lacking a restriction site in their mtDNA were resistant to this dramatic effect, demonstrating that damage to mitochondrial DNA is indeed the direct cause of overgrowth. Now, I am on the way to characterize these mitochondrial DNA mutants and the tumor, and dissect the nuclear signals that interact with mtDNA defects cause the phenotypic consequences.

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