The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

dco  -  discs overgrown

Drosophila melanogaster

Synonyms: 0538/13, 0915/10, 1396/02, 1447/01, 1460/09, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Psychiatry related information on dco

  • We have isolated a new dbt allele, dbt(ar), which causes arrhythmic locomotor activity in homozygous viable adults, as well as molecular arrhythmicity, with constitutively high levels of PER proteins, and low levels of TIMELESS (TIM) proteins [1].

High impact information on dco

  • Molecular and genetic characterizations of circadian rhythms in Drosophila indicate that function of an intracellular pacemaker requires the activities of proteins encoded by three genes: period (per), timeless (tim), and doubletime (dbt) [2].
  • A third allele, dbtP, causes pupal lethality and eliminates circadian cycling of per and tim gene products in larvae [3].
  • DBT is capable of binding to PER in vitro and in Drosophila cells, suggesting that a physical association of PER and DBT regulates PER phosphorylation and accumulation in vivo [4].
  • This was first shown in Drosophila with the characterization of Doubletime (Dbt), a homologue of vertebrate casein kinase Iepsilon [5].
  • Per and Tim undergo rhythmic changes in phosphorylation, and evidence supports roles for two kinases in this process: Doubletime (Dbt) phosphorylates Per, whereas Shaggy (Sgg) phosphorylates Tim [6].

Biological context of dco


Anatomical context of dco

  • In the present study, the expression profiles of CKIepsilon and CKIdelta mRNAs were examined in the mice clock center, suprachiasmatic nucleus (SCN) [11].
  • In situ hybridization showed presumably identical distribution of dbt, CKI[.alpha], and per transcripts in the putative clock neurons of the head ganglia, as well as in the retina, where CKI-and PER-like immunoreactivities were colocalized, suggesting a possible involvement of both CKIs in the B. mori circadian system [12].
  • One allele of dco (dcole88) prevents egg development when homozygous in the germ line, whereas the dco18 allele has no effect on germ-line development [13].
  • Chimeras and mosaics were produced in which developing oocytes and nurse cells were mutant at one of five imaginal disc overgrowth loci (fat, lgd, lgl, c43 and dco) while the enveloping follicle cells were normal [13].

Associations of dco with chemical compounds

  • Yet Sgg and Dbt often require a phosphoserine in their target site, and analysis of Per phosphorylation in dbt mutants suggests a role for other kinases [6].
  • Genetic studies in Drosophila have identified double-time (dbt), a serine/threonine protein kinase that is highly homologous to human casein kinase I epsilon (CKIepsilon), as the first kinase linked to behavioral rhythms [10].
  • Based on staining with PY and DIg antibodies, the apico-lateral junctional complexes appeared normal in tissue from the hyperplastic overgrowth mutants fat, dco, gd and wts [14].
  • Sensitization to repeated cocaine exposures, a phenomenon also seen in humans and animal models and associated with enhanced drug craving, is eliminated in flies mutant for period, clock, cycle, and doubletime, but not in flies lacking the gene timeless [15].
  • Moreover, lithium also lengthens the period in GSK-3beta heterozygous mutants and doubletime long mutants [16].

Regulatory relationships of dco

  • We find that increased CKIepsilon stimulates whereas dominant-negative or a null CKIepsilon mutation inhibits Wg signaling [17].

Other interactions of dco


Analytical, diagnostic and therapeutic context of dco

  • Here we show, using a cell culture system, that Dbt promotes the progressive phosphorylation of Per, leading to the rapid degradation of hyperphosphorylated isoforms by the ubiquitin-proteasome pathway [5].


  1. Short-period mutations of per affect a double-time-dependent step in the Drosophila circadian clock. Rothenfluh, A., Abodeely, M., Young, M.W. Curr. Biol. (2000) [Pubmed]
  2. The molecular control of circadian behavioral rhythms and their entrainment in Drosophila. Young, M.W. Annu. Rev. Biochem. (1998) [Pubmed]
  3. double-time is a novel Drosophila clock gene that regulates PERIOD protein accumulation. Price, J.L., Blau, J., Rothenfluh, A., Abodeely, M., Kloss, B., Young, M.W. Cell (1998) [Pubmed]
  4. The Drosophila clock gene double-time encodes a protein closely related to human casein kinase Iepsilon. Kloss, B., Price, J.L., Saez, L., Blau, J., Rothenfluh, A., Wesley, C.S., Young, M.W. Cell (1998) [Pubmed]
  5. Role for Slimb in the degradation of Drosophila Period protein phosphorylated by Doubletime. Ko, H.W., Jiang, J., Edery, I. Nature (2002) [Pubmed]
  6. A role for casein kinase 2alpha in the Drosophila circadian clock. Lin, J.M., Kilman, V.L., Keegan, K., Paddock, B., Emery-Le, M., Rosbash, M., Allada, R. Nature (2002) [Pubmed]
  7. Drosophila doubletime mutations which either shorten or lengthen the period of circadian rhythms decrease the protein kinase activity of casein kinase I. Preuss, F., Fan, J.Y., Kalive, M., Bao, S., Schuenemann, E., Bjes, E.S., Price, J.L. Mol. Cell. Biol. (2004) [Pubmed]
  8. double-time is identical to discs overgrown, which is required for cell survival, proliferation and growth arrest in Drosophila imaginal discs. Zilian, O., Frei, E., Burke, R., Brentrup, D., Gutjahr, T., Bryant, P.J., Noll, M. Development (1999) [Pubmed]
  9. Planar polarity is positively regulated by casein kinase Iepsilon in Drosophila. Strutt, H., Price, M.A., Strutt, D. Curr. Biol. (2006) [Pubmed]
  10. Casein kinase I: another cog in the circadian clockworks. Eide, E.J., Virshup, D.M. Chronobiol. Int. (2001) [Pubmed]
  11. Constitutive expression and delayed light response of casein kinase Iepsilon and Idelta mRNAs in the mouse suprachiasmatic nucleus. Ishida, Y., Yagita, K., Fukuyama, T., Nishimura, M., Nagano, M., Shigeyoshi, Y., Yamaguchi, S., Komori, T., Okamura, H. J. Neurosci. Res. (2001) [Pubmed]
  12. Casein Kinases I of the Silkworm, Bombyx mori: Their Possible Roles in Circadian Timing and Developmental Determination. Trang, l.e. .T.D., Sehadova, H., Ichihara, N., Iwai, S., Mita, K., Takeda, M. J. Biol. Rhythms (2006) [Pubmed]
  13. Requirement for cell-proliferation control genes in Drosophila oogenesis. Szabad, J., Jursnich, V.A., Bryant, P.J. Genetics (1991) [Pubmed]
  14. Localization of proteins to the apico-lateral junctions of Drosophila epithelia. Woods, D.F., Wu, J.W., Bryant, P.J. Dev. Genet. (1997) [Pubmed]
  15. Requirement of circadian genes for cocaine sensitization in Drosophila. Andretic, R., Chaney, S., Hirsh, J. Science (1999) [Pubmed]
  16. Lithium- and valproate-induced alterations in circadian locomotor behavior in Drosophila. Dokucu, M.E., Yu, L., Taghert, P.H. Neuropsychopharmacology (2005) [Pubmed]
  17. Regulation of wingless signaling by the CKI family in Drosophila limb development. Zhang, L., Jia, J., Wang, B., Amanai, K., Wharton, K.A., Jiang, J. Dev. Biol. (2006) [Pubmed]
  18. Casein kinase I in the Mammalian circadian clock. Eide, E.J., Kang, H., Crapo, S., Gallego, M., Virshup, D.M. Meth. Enzymol. (2005) [Pubmed]
  19. Isolation and characterization of casein kinase I from Dictyostelium discoideum. Moreno-Bueno, G., Calés, C., Behrens, M.M., Fernández-Renart, M. Biochem. J. (2000) [Pubmed]
  20. Neurons producing specific neuropeptides in the central nervous system of normal and pupariation-delayed Drosophila. Zitnan, D., Sehnal, F., Bryant, P.J. Dev. Biol. (1993) [Pubmed]
WikiGenes - Universities