Literature summary extracted from
Pareek, G.; Thomas, R.; Pallanck, L.
Loss of the Drosophila m-AAA mitochondrial protease paraplegin results in mitochondrial dysfunction, shortened lifespan, and neuronal and muscular degeneration article (2018), Cell Death Dis., 9, 304 .
Localization
EC Number |
Localization |
Comment |
Organism |
GeneOntology No. |
Textmining |
---|
Organism
EC Number |
Organism |
UniProt |
Comment |
Textmining |
---|
3.4.24.B18 |
Drosophila melanogaster |
Q9W4W8 |
- |
- |
Source Tissue
EC Number |
Source Tissue |
Comment |
Organism |
Textmining |
---|
Synonyms
EC Number |
Synonyms |
Comment |
Organism |
---|
3.4.24.B18 |
paraplegin |
- |
Drosophila melanogaster |
3.4.24.B18 |
SPG7 |
- |
Drosophila melanogaster |
General Information
EC Number |
General Information |
Comment |
Organism |
---|
3.4.24.B18 |
physiological function |
SPG7 mutants exhibit shortened lifespan, progressive locomotor defects, sensitivity to chemical and environmental stress, and muscular and neuronal degeneration. The neurodegenerative phenotype of SPG7 mutants initiates at the synaptic terminal. A variety of mitochondrial defects are observed in the mutants, including altered axonal transport of mitochondria, accumulation of electron-dense material in the matrix of flight muscle mitochondria, reduced activities of respiratory chain complexes I and II, and severely swollen and dysmorphic mitochondria in the synaptic terminals of photoreceptors |
Drosophila melanogaster |