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CaMKII  -  Calcium/calmodulin-dependent protein...

Drosophila melanogaster

 
 
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Disease relevance of CaMKII

  • To elucidate the mechanism of transcriptional regulation, rat hepatoma (H-411E) cells were transfected with DNA constructs containing the putative CaM promoters coupled to a luciferase reporter and challenged with insulin [1].
  • A novel selection strategy, exploiting the CaM tag, was then used to isolate four single chain Fv fragments (scFvs) specific for GP6 from a non-immune phage display library [2].
  • Preferential dCaMKII immunoreactivity in the embryonic nervous system, adult thoracic ganglion and gut, and larval neuro-muscular junction (NMJ) was consistent with previous observations by in situ hybridization and immunostaining with a polyclonal antibody at the NMJ, indicating that the antibody is applicable to immunohistochemistry [3].
 

Psychiatry related information on CaMKII

 

High impact information on CaMKII

  • Here we show that neural activity directs the mRNA of the Drosophila Ca(2+), Calcium/Calmodulin-dependent Kinase II (CaMKII), to postsynaptic sites, where it is rapidly translated [5].
  • In vitro, CaMKII phosphorylated a DLG fragment with a stoichiometry close to one [6].
  • Moreover, expression of site-directed dlg mutants that blocked or mimicked phosphorylation had effects similar to those observed upon inhibiting or constitutively activating CaMKII [6].
  • The ability of CaMKII to act as a molecular switch, becoming Ca(2+) independent after activation and autophosphorylation at T287, is critical for experience-dependent plasticity [7].
  • Consistently, we show that glutamate receptor mutants also have a higher number of T bars; this increase is suppressed by postsynaptic activation of CaMKII [8].
 

Biological context of CaMKII

 

Anatomical context of CaMKII

  • Inhibition of CaMKII and mutation of the eag gene both cause hyperexcitability at the larval neuromuscular junction (NMJ) and memory formation defects in the adult [9].
  • By using this system, we previously demonstrated that expression of activated calcium/calmodulin-dependent protein kinase II (CaMKII) in the muscle cell promotes coordinated maturation of pre- and postsynaptic sites of larvae just after hatching (JAH larvae) in a synapse-specific manner [12].
  • CaMKII increases the dynamic nature and formation of dendritic filopodia throughout larval development but only affects neurons that normally contain dendritic filopodia [13].
  • Targeted expression of a calcium-independent CaMKII construct (T287D) in the sensory neurons eliminated habituation [14].
  • Transcripts of CaM kinase II are expressed in great quantities in the central nervous system in the late embryonic stage of development and are more abundant in the head than in the body of the adult fly [15].
 

Associations of CaMKII with chemical compounds

  • Displacement results in autophosphorylation-independent activation of CaMKII which persists even when Ca(2+) levels have gone down [16].
  • Moreover, both CaMKII inhibition and the alanine mutation accelerated inactivation [9].
  • Injection of either a specific CaMKII inhibitor peptide or lavendustin C, another CaMKII inhibitor, reduced Eag current amplitude acutely [9].
  • In this study, we use a tripartite transgenic system combining GAL4/UAS with the tetracycline-off system to spatially and temporally manipulate levels of Ca2+-independent CaMKII activity in Drosophila [4].
  • Most transcript changes were transient except for the decrease of the CaMKIIalpha transcript which persisted even 40 h after the single dose of diazepam [17].
  • We show that phosphorylation of CaMKII is greatly enhanced by okadaic acid, and indeed, purified PP2A catalyzes the dephosphorylation of CaMKII [18].
 

Physical interactions of CaMKII

  • These results favor a model in which the CaMKII-binding domain of Eag displaces the CaMKII autoinhibitory region [16].
  • In the presence of Ca(2+)/CaM, CaMKII complexed to Cmg can autophosphorylate at T287 and become constitutively active [11].
 

Regulatory relationships of CaMKII

  • In Drosophila, CaMKII regulates the eag potassium channel, but if and how this regulation was spatially restricted was unknown [16].
  • Here we demonstrate that synaptic localization of DLG itself is regulated by CaMKII [6].
  • Cmg coexpression suppresses CaMKII activity in transfected cells, and the level of Cmg expression in Drosophila modulates postsynaptic T306 phosphorylation [11].
 

Other interactions of CaMKII

  • Integrins regulate DLG/FAS2 via a CaM kinase II-dependent pathway to mediate synapse elaboration and stabilization during postembryonic development [19].
  • Recent work has shown that DLG and FAS2 function together to modulate activity-dependent synaptic development and that this role is regulated by activation of CaMKII [19].
  • These studies demonstrate that betaPS integrins act through CaMKII activation to control the localization of synaptic proteins involved in the development of NMJ synaptic morphology [19].
  • We found that at least one isoform of Drosophila neuronal CaMKII is conjugated to DmSUMO-1 in vivo [20].
  • In contrast to CaMKII activity, Rac1 does not alter filopodia stability but instead causes de novo filopodia formation on all da neurons [13].
 

Analytical, diagnostic and therapeutic context of CaMKII

References

  1. Transcription factor Sp1 is necessary for basal calmodulin gene transcription and for its selective stimulation by insulin. Solomon, S.S., Palazzolo, M.R., Takahashi, T., Raghow, R. Endocrinology (1997) [Pubmed]
  2. Production of calmodulin-tagged proteins in Drosophila Schneider S2 cells: A novel system for antigen production and phage antibody isolation. Jennings, N.S., Smethurst, P.A., Knight, C.G., O'connor, M.N., Joutsi-Korhonen, L., Stafford, P., Stephens, J., Garner, S.F., Harmer, I.J., Farndale, R.W., Watkins, N.A., Ouwehand, W.H. J. Immunol. Methods (2006) [Pubmed]
  3. Immunohistochemical study of Ca2+/calmodulin-dependent protein kinase II in the Drosophila brain using a specific monoclonal antibody. Takamatsu, Y., Kishimoto, Y., Ohsako, S. Brain Res. (2003) [Pubmed]
  4. Calcium-independent calcium/calmodulin-dependent protein kinase II in the adult Drosophila CNS enhances the training of pheromonal cues. Mehren, J.E., Griffith, L.C. J. Neurosci. (2004) [Pubmed]
  5. Synaptic protein synthesis associated with memory is regulated by the RISC pathway in Drosophila. Ashraf, S.I., McLoon, A.L., Sclarsic, S.M., Kunes, S. Cell (2006) [Pubmed]
  6. Regulation of DLG localization at synapses by CaMKII-dependent phosphorylation. Koh, Y.H., Popova, E., Thomas, U., Griffith, L.C., Budnik, V. Cell (1999) [Pubmed]
  7. Activity-dependent gating of CaMKII autonomous activity by Drosophila CASK. Hodge, J.J., Mullasseril, P., Griffith, L.C. Neuron (2006) [Pubmed]
  8. Retrograde control of synaptic transmission by postsynaptic CaMKII at the Drosophila neuromuscular junction. Haghighi, A.P., McCabe, B.D., Fetter, R.D., Palmer, J.E., Hom, S., Goodman, C.S. Neuron (2003) [Pubmed]
  9. Calcium/calmodulin-dependent protein kinase II phosphorylates and regulates the Drosophila eag potassium channel. Wang, Z., Wilson, G.F., Griffith, L.C. J. Biol. Chem. (2002) [Pubmed]
  10. Regulation of neuronal excitability in Drosophila by constitutively active CaMKII. Park, D., Coleman, M.J., Hodge, J.J., Budnik, V., Griffith, L.C. J. Neurobiol. (2002) [Pubmed]
  11. Regulation of the Ca2+/CaM-responsive pool of CaMKII by scaffold-dependent autophosphorylation. Lu, C.S., Hodge, J.J., Mehren, J., Sun, X.X., Griffith, L.C. Neuron (2003) [Pubmed]
  12. Developmental stage-dependent modulation of synapses by postsynaptic expression of activated calcium/calmodulin-dependent protein kinase II. Morimoto-Tanifuji, T., Kazama, H., Nose, A. Neuroscience (2004) [Pubmed]
  13. Calcium/calmodulin-dependent protein kinase II alters structural plasticity and cytoskeletal dynamics in Drosophila. Andersen, R., Li, Y., Resseguie, M., Brenman, J.E. J. Neurosci. (2005) [Pubmed]
  14. 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]
  15. Molecular characterization and expression of the Drosophila Ca2+/calmodulin-dependent protein kinase II gene. Identification of four forms of the enzyme generated from a single gene by alternative splicing. Ohsako, S., Nishida, Y., Ryo, H., Yamauchi, T. J. Biol. Chem. (1993) [Pubmed]
  16. The eag potassium channel binds and locally activates calcium/calmodulin-dependent protein kinase II. Sun, X.X., Hodge, J.J., Zhou, Y., Nguyen, M., Griffith, L.C. J. Biol. Chem. (2004) [Pubmed]
  17. Diazepam-induced adaptive plasticity revealed by alpha1 GABAA receptor-specific expression profiling. Huopaniemi, L., Keist, R., Randolph, A., Certa, U., Rudolph, U. J. Neurochem. (2004) [Pubmed]
  18. Role of Ca2+/calmodulin-dependent protein kinase II in Drosophila photoreceptors. Lu, H., Leung, H.T., Wang, N., Pak, W.L., Shieh, B.H. J. Biol. Chem. (2009) [Pubmed]
  19. Integrins regulate DLG/FAS2 via a CaM kinase II-dependent pathway to mediate synapse elaboration and stabilization during postembryonic development. Beumer, K., Matthies, H.J., Bradshaw, A., Broadie, K. Development (2002) [Pubmed]
  20. Identification and characterization of a SUMO-1 conjugation system that modifies neuronal calcium/calmodulin-dependent protein kinase II in Drosophila melanogaster. Long, X., Griffith, L.C. J. Biol. Chem. (2000) [Pubmed]
  21. The diversity of calcium/calmodulin-dependent protein kinase II isoforms in Drosophila is generated by alternative splicing of a single gene. Griffith, L.C., Greenspan, R.J. J. Neurochem. (1993) [Pubmed]
  22. Regulation of Drosophila Ca2+/calmodulin-dependent protein kinase II by autophosphorylation analyzed by site-directed mutagenesis. Wang, Z., Palmer, G., Griffith, L.C. J. Neurochem. (1998) [Pubmed]
  23. Mapping of the anatomical circuit of CaM kinase-dependent courtship conditioning in Drosophila. Joiner, M.A., Griffith, L.C. Learn. Mem. (1999) [Pubmed]
  24. The single calmodulin gene of the cephalochordate Branchiostoma. Karabinos, A., Riemer, D. Gene (1997) [Pubmed]
 
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