Psychiatry related information on slgA

• In view of the neurological phenotype of the D. melanogaster sluggish-A mutant, it is of interest that schizophrenia and bipolar disorder susceptibility genes also map in this region [1].

High impact information on slgA

• The sluggish-A gene of Drosophila melanogaster is expressed in the nervous system and encodes proline oxidase, a mitochondrial enzyme involved in glutamate biosynthesis [2].
• We have localized the transcription unit of the sluggish-A gene to a 14.7-kb region at the base of the X chromosome and have cloned corresponding cDNAs [2].
• During embryonic development the sluggish-A transcript is predominantly expressed in the nervous system [2].
• Glutamate levels in nerve terminal varicosities of slgA mutants and controls were similar [3].
• Levels of glutamate and proline in different cell compartments, and functional properties of synaptic transmission were compared in slgA and control specimens [3].

Biological context of slgA

• In addition, we found that glutamatergic synaptic transmission at individual nerve endings and at the whole-cell level was similar in slgA mutants and controls [3].

Anatomical context of slgA

• Localization of the genes shaking-B, small optic lobes, sluggish-A, stoned and stress-sensitive-C to a well-defined region on the X-chromosome of Drosophila melanogaster [4].
• In vitro studies on rat liver mitochondria showed that only 4-methylene-L-proline was able to inactivate proline dehydrogenase [5].
• Thus, proline oxidase does not play a major role in generating neuronal glutamate pools at the Drosophila larval neuromuscular junction, and larval neuromuscular performance is not altered significantly in slgA mutants [3].
• We tested the hypothesis that glutamate, and synaptic transmission mediated by glutamate, are reduced at synapses of glutamatergic motor neurons in slgA mutants [3].
• Proline is elevated in muscle cells of slgA mutants, indicating that the slgA gene regulates tissue proline levels [3].

References