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Gene Review

Syt4  -  synaptotagmin IV

Rattus norvegicus

Synonyms: Synaptotagmin IV, Synaptotagmin-4, SytIV
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Disease relevance of Syt4


High impact information on Syt4

  • Overexpression of synaptotagmin I prolonged the time from fusion pore opening to dilation, whereas synaptotagmin IV shortened this time [2].
  • The first C2 domains of synaptotagmins I-III exhibit similar Ca2+ affinities in phospholipid-binding assays, whereas that of synaptotagmin IV is unable to bind Ca2+ [3].
  • SytIV mRNA accumulation is transiently induced in PC12 cells by potassium depolarization, calcium ionophore, ATP, and forskolin [4].
  • Kainic acid-induced seizures in rats are followed by accumulation of SytIV message in the hippocampus and piriform cortex [4].
  • The SytIV gene may provide a direct link between depolarization-induced neuronal gene expression and subsequent modulation of synaptic structure and function [4].

Biological context of Syt4


Anatomical context of Syt4


Associations of Syt4 with chemical compounds

  • Sucrose density gradient fractionation and vesicle immunoisolation experiments suggest that Syt IV protein is present in both synaptic-like microvesicles and secretory granules [11].
  • However, conversion of the unique serine in SytIV to an aspartate eliminated this inhibitory activity [1].
  • Unlike other synaptotagmins, SytIV has an evolutionarily conserved substitution of an aspartate to a serine in the Ca(2+) coordination site of its C2A domain, preventing SytIV from binding anionic lipids in a Ca(2+)-dependent fashion [1].
  • We have examined the pattern of expression of Syt IV mRNA following the administration of cocaine and amphetamine [12].
  • Effect of acute and chronic treatment with methamphetamine on mRNA expression of synaptotagmin IV and 25 KDa-synaptic-associated protein in the rat brain [13].

Other interactions of Syt4

  • In the present study, we examined the time course of the seizure-induced changes in the expression of Syt4 and Syt1, both in adult animals and during the postnatal period [8].
  • Synaptotagmin III is about 10 times greater in the neural tissues versus the pituitary, and synaptotagmin IV was the least abundant isoform in all the tissues [14].
  • We further characterized the expression of two genes linked to neurogenesis (nestin and stathmin), and two genes likely involved in reconfiguring neuronal networks (semaphorin VIa and synaptotagmin IV) [15].
  • These included furin, prosaposin, synaptotagmin IV, heat shock protein 105, and the neutral and basic amino acid transporter (NBAT) [16].

Analytical, diagnostic and therapeutic context of Syt4


  1. Synaptotagmin IV overexpression inhibits depolarization-induced exocytosis in PC12 cells. Machado, H.B., Liu, W., Vician, L.J., Herschman, H.R. J. Neurosci. Res. (2004) [Pubmed]
  2. Synaptotagmin modulation of fusion pore kinetics in regulated exocytosis of dense-core vesicles. Wang, C.T., Grishanin, R., Earles, C.A., Chang, P.Y., Martin, T.F., Chapman, E.R., Jackson, M.B. Science (2001) [Pubmed]
  3. Functional properties of multiple synaptotagmins in brain. Ullrich, B., Li, C., Zhang, J.Z., McMahon, H., Anderson, R.G., Geppert, M., Südhof, T.C. Neuron (1994) [Pubmed]
  4. Synaptotagmin IV is an immediate early gene induced by depolarization in PC12 cells and in brain. Vician, L., Lim, I.K., Ferguson, G., Tocco, G., Baudry, M., Herschman, H.R. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  5. Nerve growth factor-dependent sorting of synaptotagmin IV protein to mature dense-core vesicles that undergo calcium-dependent exocytosis in PC12 cells. Fukuda, M., Kanno, E., Ogata, Y., Saegusa, C., Kim, T., Loh, Y.P., Yamamoto, A. J. Biol. Chem. (2003) [Pubmed]
  6. Effect of forskolin on synaptotagmin IV protein trafficking in PC12 cells. Fukuda, M., Yamamoto, A. J. Biochem. (2004) [Pubmed]
  7. Synaptotagmin IV does not alter excitatory fast synaptic transmission or fusion pore kinetics in mammalian CNS neurons. Ting, J.T., Kelley, B.G., Sullivan, J.M. J. Neurosci. (2006) [Pubmed]
  8. Two synaptotagmin genes, Syt1 and Syt4, are differentially regulated in adult brain and during postnatal development following kainic acid-induced seizures. Tocco, G., Bi, X., Vician, L., Lim, I.K., Herschman, H., Baudry, M. Brain Res. Mol. Brain Res. (1996) [Pubmed]
  9. Developmental regulation of synaptotagmin I, II, III, and IV mRNAs in the rat CNS. Berton, F., Iborra, C., Boudier, J.A., Seagar, M.J., Marquèze, B. J. Neurosci. (1997) [Pubmed]
  10. Synaptotagmin I and IV define distinct populations of neuronal transport vesicles. Berton, F., Cornet, V., Iborra, C., Garrido, J., Dargent, B., Fukuda, M., Seagar, M., Marquèze, B. Eur. J. Neurosci. (2000) [Pubmed]
  11. Synthesis degradation, and subcellular localization of synaptotagmin IV, a neuronal immediate early gene product. Ferguson, G.D., Thomas, D.M., Elferink, L.A., Herschman, H.R. J. Neurochem. (1999) [Pubmed]
  12. Acute administration of cocaine, but not amphetamine, increases the level of synaptotagmin IV mRNA in the dorsal striatum of rat. Denovan-Wright, E.M., Newton, R.A., Armstrong, J.N., Babity, J.M., Robertson, H.A. Brain Res. Mol. Brain Res. (1998) [Pubmed]
  13. Effect of acute and chronic treatment with methamphetamine on mRNA expression of synaptotagmin IV and 25 KDa-synaptic-associated protein in the rat brain. Isao, T., Akiyama, K. Psychiatry and clinical neurosciences. (2004) [Pubmed]
  14. Analysis of synaptotagmin I-IV messenger RNA expression and developmental regulation in the rat hypothalamus and pituitary. Xi, D., Chin, H., Gainer, H. Neuroscience (1999) [Pubmed]
  15. Long-term gene expression changes in the cortex following cortical ischemia revealed by transcriptional profiling. Krüger, C., Cira, D., Sommer, C., Fischer, A., Schäbitz, W.R., Schneider, A. Exp. Neurol. (2006) [Pubmed]
  16. Identification of differentially expressed genes in rat hippocampus after transient global cerebral ischemia using subtractive cDNA cloning based on polymerase chain reaction. Yokota, N., Uchijima, M., Nishizawa, S., Namba, H., Koide, Y. Stroke (2001) [Pubmed]
  17. Structural basis for the evolutionary inactivation of Ca2+ binding to synaptotagmin 4. Dai, H., Shin, O.H., Machius, M., Tomchick, D.R., Südhof, T.C., Rizo, J. Nat. Struct. Mol. Biol. (2004) [Pubmed]
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