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Gene Review

Sema-1a  -  CG18405 gene product from transcript...

Drosophila melanogaster

Synonyms: BcDNA:RE36155, CG18405, CT26404, D-Sema 1a, D-Sema I, ...
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Psychiatry related information on Sema-1a

  • Targeted expression of shibire ts and semaphorin 1a reveals critical periods for synapse formation in the giant fiber of Drosophila [1].

High impact information on Sema-1a

  • We also found that pre- but not postsynaptic gain-of-function Sema-1a was able to disrupt the GF-motor neuron synapse and that the phenotype depended on a proline-rich intracellular domain that contains a putative Enabled binding site [2].
  • Removal of sema-1a in ORNs does not affect the pathfinding toward their target area but disrupts local axonal convergence into a single glomerulus, resulting in two distinct targeting phenotypes: axons either intermingle with adjacent ORN classes or segregate according to their odorant receptor identity into ectopic sites [3].
  • In this issue of Neuron, two beautiful studies in Drosophila by Lattemann et al. and Sweeney et al. show that Semaphorin repulsion regulates interactions between olfactory receptor neurons to help axons find their correct targets [4].
  • In vivo, mutations in the otk gene lead to phenotypes resembling those of loss-of-function mutations of either Sema1a or PlexA [5].
  • In Drosophila, Plexin A (PlexA) is a receptor for the transmembrane semaphorin semaphorin-1a (Sema-1a) and is required for motor and central nervous system (CNS) axon guidance in the developing embryonic nervous system [6].

Biological context of Sema-1a

  • By co-expressing shibire(ts) and semaphorin 1a we provided evidence that Semaphorin 1a was one of the proteins being regulated by endocytosis and its removal was a necessary part of the program for synaptogenesis [1].

Anatomical context of Sema-1a

  • Loss of sema1a disrupts the association of neighboring R-cell growth cones leading to defects in local termination pattern, whereas overexpression of sema1a induces the hyper-fasciculation of R-cell axons [7].

Regulatory relationships of Sema-1a

  • Thus, Nervy couples cAMP-PKA signaling to PlexA to regulate Sema-1a-mediated axonal repulsion, revealing a simple molecular mechanism that allows growing axons to integrate inputs from multiple guidance cues [8].

Other interactions of Sema-1a

  • Additionally, we find that the integrity of the Gyc76C catalytic cyclase domain is critical for Gyc76C function in Sema-1a axon repulsion [9].


  1. Targeted expression of shibire ts and semaphorin 1a reveals critical periods for synapse formation in the giant fiber of Drosophila. Murphey, R.K., Froggett, S.J., Caruccio, P., Shan-Crofts, X., Kitamoto, T., Godenschwege, T.A. Development (2003) [Pubmed]
  2. Bi-directional signaling by Semaphorin 1a during central synapse formation in Drosophila. Godenschwege, T.A., Hu, H., Shan-Crofts, X., Goodman, C.S., Murphey, R.K. Nat. Neurosci. (2002) [Pubmed]
  3. Semaphorin-1a controls receptor neuron-specific axonal convergence in the primary olfactory center of Drosophila. Lattemann, M., Zierau, A., Schulte, C., Seidl, S., Kuhlmann, B., Hummel, T. Neuron (2007) [Pubmed]
  4. Semaphorin directs axon traffic in the fly olfactory system. Bashaw, G.J. Neuron (2007) [Pubmed]
  5. The transmembrane protein Off-track associates with Plexins and functions downstream of Semaphorin signaling during axon guidance. Winberg, M.L., Tamagnone, L., Bai, J., Comoglio, P.M., Montell, D., Goodman, C.S. Neuron (2001) [Pubmed]
  6. Drosophila Plexin B is a Sema-2a receptor required for axon guidance. Ayoob, J.C., Terman, J.R., Kolodkin, A.L. Development (2006) [Pubmed]
  7. Semaphorin-1a functions as a guidance receptor in the Drosophila visual system. Cafferty, P., Yu, L., Long, H., Rao, Y. J. Neurosci. (2006) [Pubmed]
  8. Nervy links protein kinase a to plexin-mediated semaphorin repulsion. Terman, J.R., Kolodkin, A.L. Science (2004) [Pubmed]
  9. The Drosophila receptor guanylyl cyclase Gyc76C is required for semaphorin-1a-plexin A-mediated axonal repulsion. Ayoob, J.C., Yu, H.H., Terman, J.R., Kolodkin, A.L. J. Neurosci. (2004) [Pubmed]
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