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Gene Review

eas  -  easily shocked

Drosophila melanogaster

Synonyms: CG3525, Dmel\CG3525, EK, EP770, Ethanolamine kinase, ...
 
 
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Disease relevance of eas

  • A screen utilizing the Drosophila easily shocked (eas) "epilepsy" mutant identified dominant suppressors of seizure sensitivity [1].
  • In the present report, the eas gene product, expressed in Escherichia coli as fusion protein, is found to have highly specific ethanolamine kinase activity [2].
 

High impact information on eas

  • Assays of phospholipid composition reveal that total phosphatidylethanolamine is decreased in eas mutants [3].
  • We have characterized easily shocked (eas), a Drosophila "band-sensitive" paralytic mutant [3].
  • Here we show that the alpha-lobes-absent (ala) mutant lacks either the two vertical lobes of the mushroom body or two of the three median lobes which contain branches of vertical lobe neurons [4].
  • Furthermore, synaptic currents in ala transformants were characterized by greater variability, suggesting an important role of CaM kinase in the stability of transmission [5].
  • Finally, when a CaMKII inhibitory peptide (ala) was expressed in sensory neurons, the initial response was reduced, followed by facilitation [6].
 

Biological context of eas

 

Anatomical context of eas

 

Associations of eas with chemical compounds

  • Rat liver kinase activity specific for ethanolamine was separated chromatographically and by an immunological procedure using anti-choline kinase antibody, associated with the 86 kDa protein, and immunoprecipitated by anti-eas antibody [2].
  • Ethanolamine kinase catalyzes the initial step in the CDP-ethanolamine pathway for phosphatidylethanolamine synthesis [2].
  • In both vector control and Etn kinase overexpressor cells, phosphocholine (PCho) and insulin synergistically stimulated DNA synthesis; their effects were further enhanced by physiologically relevant (5-60 microM) concentrations of Etn by a mechanism independent of mitogen-activated protein (MAP) kinase [12].
  • For this purpose, NIH 3T3 sublines highly overexpressing Drosophila Etn kinase and an appropriate vector control line were utilized and the effects of Etn, MeEtn, Me2Etn, methylamine (MeNH2), and dimethylamine (Me2NH) were studied [10].
 

Other interactions of eas

  • Among several mutations identified, neuronal escargot (esg) reduced eas seizures almost 90% [1].
  • Seizures caused by easily shocked (eas) and technical knockout (tko) mutations are partially suppressed by shakB2 [13].
  • The BS phenotypic class includes at least eight genes, including three examined in this study, bss, eas, and sda [14].
 

Analytical, diagnostic and therapeutic context of eas

  • Electrophysiological recordings from flight muscles in the giant fiber pathway of adult eas flies reveal that induction of paralysis with electrical stimulation results in a brief seizure, followed by a failure of the muscles to respond to giant fiber stimulation [3].
  • Molecular cloning, germline transformation, and biochemical experiments show that eas mutants are defective in the gene for ethanolamine kinase, which is required for a pathway of phosphatidylethanolamine synthesis [3].

References

  1. Seizure suppression by gain-of-function escargot mutations. Hekmat-Scafe, D.S., Dang, K.N., Tanouye, M.A. Genetics (2005) [Pubmed]
  2. A novel high-molecular mass mammalian ethanolamine kinase. Uchida, T. Biochim. Biophys. Acta (1997) [Pubmed]
  3. The Drosophila easily shocked gene: a mutation in a phospholipid synthetic pathway causes seizure, neuronal failure, and paralysis. Pavlidis, P., Ramaswami, M., Tanouye, M.A. Cell (1994) [Pubmed]
  4. Localization of long-term memory within the Drosophila mushroom body. Pascual, A., Préat, T. Science (2001) [Pubmed]
  5. Concomitant alterations of physiological and developmental plasticity in Drosophila CaM kinase II-inhibited synapses. Wang, J., Renger, J.J., Griffith, L.C., Greenspan, R.J., Wu, C.F. Neuron (1994) [Pubmed]
  6. Presynaptic calcium/calmodulin-dependent protein kinase II regulates habituation of a simple reflex in adult Drosophila. Jin, P., Griffith, L.C., Murphey, R.K. J. Neurosci. (1998) [Pubmed]
  7. Altered mechanoreceptor response in Drosophila bang-sensitive mutants. Engel, J.E., Wu, C.F. J. Comp. Physiol. A (1994) [Pubmed]
  8. Ethanolamine kinase controls neuroblast divisions in Drosophila mushroom bodies. Pascual, A., Chaminade, M., Préat, T. Dev. Biol. (2005) [Pubmed]
  9. Tissue-specific and developmental effects of the easily shocked mutation on ethanolamine kinase activity and phospholipid composition in Drosophila melanogaster. Nyako, M., Marks, C., Sherma, J., Reynolds, E.R. Biochem. Genet. (2001) [Pubmed]
  10. Phosphorylation of ethanolamine, methylethanolamine, and dimethylethanolamine by overexpressed ethanolamine kinase in NIH 3T3 cells decreases the co-mitogenic effects of ethanolamines and promotes cell survival. Malewicz, B., Mukherjee, J.J., Crilly, K.S., Baumann, W.J., Kiss, Z. Eur. J. Biochem. (1998) [Pubmed]
  11. Seizures and failures in the giant fiber pathway of Drosophila bang-sensitive paralytic mutants. Pavlidis, P., Tanouye, M.A. J. Neurosci. (1995) [Pubmed]
  12. Ethanolamine, but not phosphoethanolamine, potentiates the effects of insulin, phosphocholine, and ATP on DNA synthesis in NIH 3T3 cells--role of mitogen-activated protein-kinase-dependent and protein-kinase-independent mechanisms. Kiss, Z., Mukherjee, J.J., Crilly, K.S., Chung, T. Eur. J. Biochem. (1997) [Pubmed]
  13. Seizure suppression by shakB2, a gap junction mutation in Drosophila. Song, J., Tanouye, M.A. J. Neurophysiol. (2006) [Pubmed]
  14. Genetic suppression of seizure susceptibility in Drosophila. Kuebler, D., Zhang, H., Ren, X., Tanouye, M.A. J. Neurophysiol. (2001) [Pubmed]
 
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