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Gene Review

mbc  -  myoblast city

Drosophila melanogaster

Synonyms: CG10379, DOCK180, Dm MBC, Dmel\CG10379, Dock180, ...
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High impact information on mbc

  • Myoblast city, the Drosophila homolog of DOCK180/CED-5, is required in a Rac signaling pathway utilized for multiple developmental processes [1].
  • These results suggest that Mbc is a specific upstream regulator of Rac activity that mediates several morphogenetic processes in Drosophila embryogenesis [1].
  • In myoblast city mutant embryos, myoblasts do not fuse but form fully differentiated mononucleate muscles, which make functional neuromuscular synapses with correctly localized presynaptic active zones [2].
  • We show that DOCK2, which is a mammalian homologue of Caenorhabditis elegans CED-5 and Drosophila melanogaster Myoblast City, regulates motility and polarity during neutrophil chemotaxis [3].
  • It was earlier shown that Mbc, a CDM family protein, and its effector, Rac, transduced the guidance signal from PVR during border cell migration [4].

Biological context of mbc


Anatomical context of mbc

  • The mbc transcript and its encoded protein are expressed in a broad range of tissues, including somatic myoblasts, cardial cells, and visceral mesoderm [8].

Regulatory relationships of mbc

  • Both the mesodermal and ectodermal defects are reminiscent of those induced by altered forms of Drac1 and suggest that mbc may function in the same pathway [8].

Other interactions of mbc

  • Because of the predicted structural similarities of the Rols7 and Rols6 proteins, we argue that genetic interaction of rols6, mbc and rac might lead to proper MpT morphology [5].
  • ANTS, which is expressed specifically in founder cells, interacts with the cytoplasmic domain of Dumbfounded, a founder cell transmembrane receptor, and with Myoblast city, a cytoskeletal protein, both of which are also required for myoblast fusion [9].
  • We have identified a Drosophila protein with homology to vertebrate Crk, termed dCRK, by interaction with the protein encoded by the Drosophila myoblast city (mbc) gene [10].


  1. Myoblast city, the Drosophila homolog of DOCK180/CED-5, is required in a Rac signaling pathway utilized for multiple developmental processes. Nolan, K.M., Barrett, K., Lu, Y., Hu, K.Q., Vincent, S., Settleman, J. Genes Dev. (1998) [Pubmed]
  2. Presynaptic development at the Drosophila neuromuscular junction: assembly and localization of presynaptic active zones. Prokop, A., Landgraf, M., Rushton, E., Broadie, K., Bate, M. Neuron (1996) [Pubmed]
  3. DOCK2 is a Rac activator that regulates motility and polarity during neutrophil chemotaxis. Kunisaki, Y., Nishikimi, A., Tanaka, Y., Takii, R., Noda, M., Inayoshi, A., Watanabe, K., Sanematsu, F., Sasazuki, T., Sasaki, T., Fukui, Y. J. Cell Biol. (2006) [Pubmed]
  4. PVR plays a critical role via JNK activation in thorax closure during Drosophila metamorphosis. Ishimaru, S., Ueda, R., Hinohara, Y., Ohtani, M., Hanafusa, H. EMBO J. (2004) [Pubmed]
  5. In Drosophila melanogaster, the Rolling pebbles isoform 6 (Rols6) is essential for proper Malpighian tubule morphology. Pütz, M., Kesper, D.A., Buttgereit, D., Renkawitz-Pohl, R. Mech. Dev. (2005) [Pubmed]
  6. Mutations in a novel gene, myoblast city, provide evidence in support of the founder cell hypothesis for Drosophila muscle development. Rushton, E., Drysdale, R., Abmayr, S.M., Michelson, A.M., Bate, M. Development (1995) [Pubmed]
  7. Essential genes for myoblast fusion in Drosophila embryogenesis. Paululat, A., Holz, A., Renkawitz-Pohl, R. Mech. Dev. (1999) [Pubmed]
  8. Drosophila myoblast city encodes a conserved protein that is essential for myoblast fusion, dorsal closure, and cytoskeletal organization. Erickson, M.R., Galletta, B.J., Abmayr, S.M. J. Cell Biol. (1997) [Pubmed]
  9. Antisocial, an intracellular adaptor protein, is required for myoblast fusion in Drosophila. Chen, E.H., Olson, E.N. Dev. Cell (2001) [Pubmed]
  10. Identification of a Drosophila homologue to vertebrate Crk by interaction with MBC. Galletta, B.J., Niu, X.P., Erickson, M.R., Abmayr, S.M. Gene (1999) [Pubmed]
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