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Gene Review

futsch  -  futsch

Drosophila melanogaster

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Psychiatry related information on futsch


High impact information on futsch

  • These phenotypes mimic those observed in mutants of microtubule-associated Futsch [2].
  • Loss of pnt function leads to poorly differentiated glial cells and a marked decrease in the expression of the neuronal antigen 22C10 in the MP2 neurons, which are known to interact intimately with the pntP1-expressing longitudinal glial cells [3].
  • At the presynapse, aPKC regulates the stability of MTs by promoting the association of the MAP1Brelated protein Futsch to MTs [4].
  • An apparent rearrangement of microtubule loop architecture occurs during bouton division, and a genetic analysis indicates that Futsch is necessary for this process. futsch mutations disrupt synaptic microtubule organization, reduce bouton number, and increase bouton size [5].
  • We present evidence that Futsch, a novel protein with MAP1B homology, controls synaptic growth at the Drosophila neuromuscularjunction through the regulation of the synaptic microtubule cytoskeleton [5].

Biological context of futsch

  • Consistent with the predicted function of Futsch, we find abnormalities in the microtubule network and defects in axonal transport [1].
  • Loss-of-function analyses demonstrate that during embryogenesis Futsch is necessary for dendritic and axonal growth [6].
  • We have used tissue-specific beta-galactosidase expression in the enhancer trap strain A101.IF3 and the monoclonal antibody 22C10 as sensory cell markers, as well as the lineage tracer 5-bromo-2'-deoxyuridine (BrdU), to describe this process [7].

Anatomical context of futsch


Other interactions of futsch

  • We previously established a FraX model in Drosophila, showing that the fly FMRP homologue, dFXR, acts as a negative translational regulator of microtubule-associated Futsch to control stability of the microtubule cytoskeleton during nervous system development [9].
  • We also show that the recently described DVM founder cells can be labeled with 22C10 and beta-3 tubulin, and that they are present under conditions of dominant negative Rac1(N17) expression [10].
  • In the absence of Wingless the neuronal microtubule cytoskeleton regulator Futsch is down-regulated and synaptic growth impaired [11].
  • Finally, we show that Sgg controlled the microtubule cytoskeleton dynamics in the motoneuron and that Futsch, a microtubule-associated protein, was required for Shaggy function on synaptic growth [12].
  • The most striking result concerns the widespread distribution of DSC1 channels in the PNS, as confirmed by experiments done with the monoclonal antibody 22C10 [13].


  1. Disruption of the MAP1B-related protein FUTSCH leads to changes in the neuronal cytoskeleton, axonal transport defects, and progressive neurodegeneration in Drosophila. Bettencourt da Cruz, A., Schwärzel, M., Schulze, S., Niyyati, M., Heisenberg, M., Kretzschmar, D. Mol. Biol. Cell (2005) [Pubmed]
  2. Drosophila fragile X-related gene regulates the MAP1B homolog Futsch to control synaptic structure and function. Zhang, Y.Q., Bailey, A.M., Matthies, H.J., Renden, R.B., Smith, M.A., Speese, S.D., Rubin, G.M., Broadie, K. Cell (2001) [Pubmed]
  3. The Ets transcription factors encoded by the Drosophila gene pointed direct glial cell differentiation in the embryonic CNS. Klaes, A., Menne, T., Stollewerk, A., Scholz, H., Klämbt, C. Cell (1994) [Pubmed]
  4. New synaptic bouton formation is disrupted by misregulation of microtubule stability in aPKC mutants. Ruiz-Canada, C., Ashley, J., Moeckel-Cole, S., Drier, E., Yin, J., Budnik, V. Neuron (2004) [Pubmed]
  5. Drosophila Futsch regulates synaptic microtubule organization and is necessary for synaptic growth. Roos, J., Hummel, T., Ng, N., Klämbt, C., Davis, G.W. Neuron (2000) [Pubmed]
  6. Drosophila Futsch/22C10 is a MAP1B-like protein required for dendritic and axonal development. Hummel, T., Krukkert, K., Roos, J., Davis, G., Klämbt, C. Neuron (2000) [Pubmed]
  7. Cellular events during development of the olfactory sense organs in Drosophila melanogaster. Ray, K., Rodrigues, V. Dev. Biol. (1995) [Pubmed]
  8. The effects of 20-hydroxyecdysone on the differentiation in vitro of cells from the eye imaginal disc from Drosophila melanogaster. Li, C., Meinertzhagen, I.A. Invert. Neurosci. (1997) [Pubmed]
  9. The Drosophila fragile X-related gene regulates axoneme differentiation during spermatogenesis. Zhang, Y.Q., Matthies, H.J., Mancuso, J., Andrews, H.K., Woodruff, E., Friedman, D., Broadie, K. Dev. Biol. (2004) [Pubmed]
  10. A dominant negative form of Rac1 affects myogenesis of adult thoracic muscles in Drosophila. Fernandes, J.J., Atreya, K.B., Desai, K.M., Hall, R.E., Patel, M.D., Desai, A.A., Benham, A.E., Mable, J.L., Straessle, J.L. Dev. Biol. (2005) [Pubmed]
  11. Morphogens and synaptogenesis in Drosophila. Marqués, G. J. Neurobiol. (2005) [Pubmed]
  12. Shaggy, the homolog of glycogen synthase kinase 3, controls neuromuscular junction growth in Drosophila. Franco, B., Bogdanik, L., Bobinnec, Y., Debec, A., Bockaert, J., Parmentier, M.L., Grau, Y. J. Neurosci. (2004) [Pubmed]
  13. DSC1 channels are expressed in both the central and the peripheral nervous system of adult Drosophila melanogaster. Castella, C., Amichot, M., Bergé, J.B., Pauron, D. Invert. Neurosci. (2001) [Pubmed]
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