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Gene Review

chico  -  CG5686 gene product from transcript CG5686-RB

Drosophila melanogaster

Synonyms: BcDNA.GH11263, BcDNA:GH11263, CG5686, CHICO, Chico, ...
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Disease relevance of chico

  • However, female sterility of an insulin/IGF-like signaling mutant (chico(1)) of D. melanogaster is not mediated by downstream systemic signaling in terms of major alterations in JH or ecdysteroid levels. chico(1) is a null mutation in the insulin substrate protein (CHICO) gene of D. melanogaster [1].

High impact information on chico

  • These age-related changes are minimized or absent in long-lived flies when systemic levels of insulin-like peptides are reduced and by mutations of the only receptor, InR, or its substrate, chico [2].
  • In mosaic animals, chico homozygous cells grow slower than their heterozygous siblings, show an autonomous reduction in cell size, and form organs of reduced size [3].
  • The similarities of the growth defects caused by mutations in chico and the insulin receptor gene in Drosophila and by perturbations of the insulin/IGF1 signaling pathway in vertebrates suggest that this pathway plays a conserved role in the regulation of overall growth by controling cell size, cell number, and metabolism [3].
  • We found that mutation of chico extends fruit fly median life-span by up to 48% in homozygotes and 36% in heterozygotes [4].
  • Extension of life-span was not a result of impaired oogenesis in chico females, nor was it consistently correlated with increased stress resistance [4].

Biological context of chico

  • Our analyses also show that while chico(1) and Indy mutants both exhibit attenuated locomotor declines, the impact of chico loss of function on locomotor senescence is substantially greater [5].
  • As observed previously (Clancy et al. 2001), overall SOD activity was elevated in chico (1) homozygotes compared to the heterozygote or wild type [6].
  • Superoxide dismutase activities in long-lived Drosophila melanogaster females: chico (1) genotypes and dietary dilution [6].
  • Mortality deceleration is a phenotype of chico [7].
  • To understand this sex-difference, we conducted a large-scale demographic study with three new isogenic strains of alleles at chico, the insulin-receptor substrate homologue [7].

Anatomical context of chico

  • However, we obtained a cDNA encoding Drosophila IRS (dIRS), and we demonstrated expression of dIRS in a Drosophila cell line [8].
  • When coexpressed with dIRS in COS-7 cells, a chimeric receptor (the extracellular domain of human IR fused to the cytoplasmic domain of dIR) mediated insulin-stimulated tyrosine phosphorylation of dIRS [8].
  • Here, we describe the 10-day adult age course of JH synthesis from isolated corpus allatum (CA) of InR and of chico, the insulin receptor substrate homolog [9].

Associations of chico with chemical compounds

  • Insulin receptor substrate (IRS) proteins are phosphorylated by multiple tyrosine kinases, including the insulin receptor [8].
  • Like mammalian IRS proteins, the N-terminal portion of dIRS contains a pleckstrin homology domain and a phosphotyrosine binding domain that binds to phosphotyrosine residues in both human and Drosophila insulin receptors [8].

Regulatory relationships of chico

  • Drosophila tumor suppressor PTEN controls cell size and number by antagonizing the Chico/PI3-kinase signaling pathway [10].

Other interactions of chico

  • Results from the present study indicate that elevated CuZn SOD activity, not Mn SOD, is the basis for the relatively high level of SOD activity in the chico (1) homozygotes [6].
  • If the same form of SOD activity (CuZn SOD or Mn SOD) was elevated on the dilute diet that extends life span and in the long lived chico (1) homozygotes, then it would suggest that life span extension by dietary restriction and by insulin signaling mutations has a similar underlying mechanism [6].
  • We demonstrate that DPTEN modulates tissue mass by acting antagonistically to the Drosophila Class I phosphatidylinositol 3-kinase, Dp110, and its upstream activator Chico, an insulin receptor substrate homolog [10].
  • We also show that Drosophila AKT (DAKT) activation depends on the insulin receptor substrate, CHICO (IRS1-4) [11].
  • A search for mutations in the ME31B gene has established that the P element which causes the female-sterile mutation flipper lies in the 3' flank of the ME31B gene [12].

Analytical, diagnostic and therapeutic context of chico


  1. Insulin signaling is necessary for vitellogenesis in Drosophila melanogaster independent of the roles of juvenile hormone and ecdysteroids: female sterility of the chico1 insulin signaling mutation is autonomous to the ovary. Richard, D.S., Rybczynski, R., Wilson, T.G., Wang, Y., Wayne, M.L., Zhou, Y., Partridge, L., Harshman, L.G. J. Insect Physiol. (2005) [Pubmed]
  2. Insulin regulation of heart function in aging fruit flies. Wessells, R.J., Fitzgerald, E., Cypser, J.R., Tatar, M., Bodmer, R. Nat. Genet. (2004) [Pubmed]
  3. Autonomous control of cell and organ size by CHICO, a Drosophila homolog of vertebrate IRS1-4. Böhni, R., Riesgo-Escovar, J., Oldham, S., Brogiolo, W., Stocker, H., Andruss, B.F., Beckingham, K., Hafen, E. Cell (1999) [Pubmed]
  4. Extension of life-span by loss of CHICO, a Drosophila insulin receptor substrate protein. Clancy, D.J., Gems, D., Harshman, L.G., Oldham, S., Stocker, H., Hafen, E., Leevers, S.J., Partridge, L. Science (2001) [Pubmed]
  5. Distinct genetic influences on locomotor senescence in Drosophila revealed by a series of metrical analyses. Martin, I., Grotewiel, M.S. Exp. Gerontol. (2006) [Pubmed]
  6. Superoxide dismutase activities in long-lived Drosophila melanogaster females: chico (1) genotypes and dietary dilution. Kabil, H., Partridge, L., Harshman, L.G. Biogerontology (2007) [Pubmed]
  7. The demography of slow aging in male and female Drosophila mutant for the insulin-receptor substrate homologue chico. Tu, M.P., Epstein, D., Tatar, M. Aging Cell (2002) [Pubmed]
  8. Characterization of Drosophila insulin receptor substrate. Poltilove, R.M., Jacobs, A.R., Haft, C.R., Xu, P., Taylor, S.I. J. Biol. Chem. (2000) [Pubmed]
  9. Mutations in insulin signaling pathway alter juvenile hormone synthesis in Drosophila melanogaster. Tu, M.P., Yin, C.M., Tatar, M. Gen. Comp. Endocrinol. (2005) [Pubmed]
  10. Drosophila tumor suppressor PTEN controls cell size and number by antagonizing the Chico/PI3-kinase signaling pathway. Goberdhan, D.C., Paricio, N., Goodman, E.C., Mlodzik, M., Wilson, C. Genes Dev. (1999) [Pubmed]
  11. Use of double-stranded RNA interference in Drosophila cell lines to dissect signal transduction pathways. Clemens, J.C., Worby, C.A., Simonson-Leff, N., Muda, M., Maehama, T., Hemmings, B.A., Dixon, J.E. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  12. A second maternally expressed Drosophila gene encodes a putative RNA helicase of the "DEAD box" family. de Valoir, T., Tucker, M.A., Belikoff, E.J., Camp, L.A., Bolduc, C., Beckingham, K. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
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