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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Gene Review

gsb  -  gooseberry

Drosophila melanogaster

Synonyms: BSH-9, BSH9, BSH9c2, CG3388, Dmel\CG3388, ...
 
 
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Disease relevance of gsb

 

High impact information on gsb

  • Specification of neuroblast identity in the Drosophila embryonic central nervous system by gooseberry-distal [2].
  • Here we show that the Pax-type gooseberry-distal gene specifies row 5 neuroblast identity [2].
  • Thus, in addition to their functions in epidermal pattern formation, at least four of the segment polarity genes (gooseberry, patched, Cell, and wingless) appear to have specific roles in the control of cell fates during neurogenesis [3].
  • Sequence analysis of genomic DNA and cDNA shows that BSH9 and BSH4 can encode proteins of 427 and 452 amino acids, respectively [4].
  • During germ-band extension, BSH9 is induced in the mesoderm in register with the ectoderm and neurectoderm and in the tail segments A9-A11 [4].
 

Biological context of gsb

  • Here we show that different non-overlapping enhancer or upstream control elements drive the specific expression of gsb and gsbn [5].
  • During Drosophila embryogenesis, paired acts as one of several pair-rule genes that define the boundaries of future parasegments and segments, via the regulation of segment polarity genes such as gooseberry, which in turn regulates gooseberry-neuro, a gene expressed later in the developing nervous system [6].
  • NBs 6-4 and 7-3, arising from the engrailed domain, were also found to be specified by the differential expression of two homeobox genes, gooseberry-distal and engrailed [7].
 

Anatomical context of gsb

 

Other interactions of gsb

  • Our results suggest that the gooseberry-distal protein is required for the specification of naked cuticle in the epidermis and specific neuroblasts in the central nervous system [8].
  • Mutations in either domain abolished the normal regulation of the target genes engrailed, hedgehog, gooseberry and even-skipped, suggesting that these in vivo functions of Paired require DNA binding through both domains rather than either domain alone [10].
 

Analytical, diagnostic and therapeutic context of gsb

References

  1. Pax 1, a member of a paired box homologous murine gene family, is expressed in segmented structures during development. Deutsch, U., Dressler, G.R., Gruss, P. Cell (1988) [Pubmed]
  2. Specification of neuroblast identity in the Drosophila embryonic central nervous system by gooseberry-distal. Skeath, J.B., Zhang, Y., Holmgren, R., Carroll, S.B., Doe, C.Q. Nature (1995) [Pubmed]
  3. The role of segment polarity genes during Drosophila neurogenesis. Patel, N.H., Schafer, B., Goodman, C.S., Holmgren, R. Genes Dev. (1989) [Pubmed]
  4. Structure of two genes at the gooseberry locus related to the paired gene and their spatial expression during Drosophila embryogenesis. Baumgartner, S., Bopp, D., Burri, M., Noll, M. Genes Dev. (1987) [Pubmed]
  5. Compatibility between enhancers and promoters determines the transcriptional specificity of gooseberry and gooseberry neuro in the Drosophila embryo. Li, X., Noll, M. EMBO J. (1994) [Pubmed]
  6. Pax group III genes and the evolution of insect pair-rule patterning. Davis, G.K., Jaramillo, C.A., Patel, N.H. Development (2001) [Pubmed]
  7. hedgehog signaling independent of engrailed and wingless required for post-S1 neuroblast formation in Drosophila CNS. Matsuzaki, M., Saigo, K. Development (1996) [Pubmed]
  8. Ectopic expression of either the Drosophila gooseberry-distal or proximal gene causes alterations of cell fate in the epidermis and central nervous system. Zhang, Y., Ungar, A., Fresquez, C., Holmgren, R. Development (1994) [Pubmed]
  9. patched overexpression causes loss of wingless expression in Drosophila embryos. Schuske, K., Hooper, J.E., Scott, M.P. Dev. Biol. (1994) [Pubmed]
  10. Both the paired domain and homeodomain are required for in vivo function of Drosophila Paired. Miskiewicz, P., Morrissey, D., Lan, Y., Raj, L., Kessler, S., Fujioka, M., Goto, T., Weir, M. Development (1996) [Pubmed]
 
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