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Gene Review

hop  -  hopscotch

Drosophila melanogaster

Synonyms: CG1594, Dm JAK, DmHD-160, Dmel\CG1594, HD-160, ...
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Disease relevance of hop

  • Although the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway is part of the antiviral response in arthropods such as Drosophila, here we show that white spot syndrome virus (WSSV) uses a shrimp STAT as a transcription factor to enhance viral gene expression in host cells [1].
  • The Drosophila Tumorous-lethal (Tum-l) mutation acts as an activated oncogene, causing hematopoietic neoplasms, overproliferation, and premature differentiation [2].
  • Suppression of sterility by Wolbachia discriminates markedly among similar germline-specific Sxl alleles, and is not observed for mutations in other genes that produce similar 'tumorous ovary' phenotypes, including one that blocks Sxl germline expression [3].
  • A dominant gain-of-function allele, Tumorous-lethal (hopTum-l), leads to formation of melanotic tumors and hypertrophy of the larval lymph glands, the hematopoietic organs [4].
  • The structure, expression and possible function of the following four tumor suppressor genes are discussed: tumorous imaginal disc, lethal (3) malignant brain tumor, lethal (3) malignant blood neoplasm-1 and benign (2) gonial cell neoplasm [5].

High impact information on hop


Biological context of hop


Anatomical context of hop

  • Localized JAK/STAT signaling is required for oriented cell rearrangement in a tubular epithelium [14].
  • STAT92E-GFP fluorescence is increased in response to ectopic upd in the larval eye disc and mis-expression of the JAK kinase hopscotch in the adult fat body [15].
  • Upd is a secreted protein, associated with the extracellular matrix, that activates the JAK pathway [16].
  • By contrast, constitutively active hopscotch and hemipterous give massive activation of lamellocyte formation with little or no increase in total hemocyte numbers [17].
  • In Drosophila, a conserved JAK/STAT signaling pathway controls segmentation in embryos, as well as blood cell development and other processes in larvae and adults [18].

Associations of hop with chemical compounds

  • We present a model in which the Hop tyrosine kinase is involved in the control of pair-rule gene transcription in a stripe-specific manner [19].

Physical interactions of hop


Other interactions of hop

  • Our results demonstrate the existence of an invertebrate JAK/STAT system [7].
  • These data show that mom functions as a receptor of the Drosophila JAK/STAT signal transduction pathway [10].
  • The difference in effect between localized expression of ligand (Unpaired) and dominant active JAK (Hopscotch) demonstrates that the ligand plays a cell non-autonomous role in hindgut cell rearrangement [14].
  • In addition, an activated form of Hop results in increased levels of Cactus and Dorsal proteins, modifying the Dorsal/Cactus ratio and consequently DV patterning [22].
  • Here, we demonstrate that Hop requires the activity of the Raf pathway to promote the activation response of larval plasmatocytes, and provide evidence to suggest that the Hop and D-Raf proteins physically interact [23].

Analytical, diagnostic and therapeutic context of hop

  • Mosaic analysis of both JAK pathway transducers, hopscotch and Stat92E, reveals that JAK signaling is specifically required in the somatic follicle cells [24].
  • Genetic experiments showed that the Jak kinase Hopscotch was involved in the control of the viral load in infected flies and was required but not sufficient for the induction of some virus-regulated genes [25].
  • Finally, overexpression of either hop or hopTum-l in Drosophila cell culture results in tyrosine phosphorylation of Hop protein [4].


  1. White spot syndrome virus annexes a shrimp STAT to enhance expression of the immediate-early gene ie1. Liu, W.J., Chang, Y.S., Wang, A.H., Kou, G.H., Lo, C.F. J. Virol. (2007) [Pubmed]
  2. The Drosophila Tumorous-lethal hematopoietic oncogene is a dominant mutation in the hopscotch locus. Hanratty, W.P., Dearolf, C.R. Mol. Gen. Genet. (1993) [Pubmed]
  3. A host parasite interaction rescues Drosophila oogenesis defects. Starr, D.J., Cline, T.W. Nature (2002) [Pubmed]
  4. Activation of a Drosophila Janus kinase (JAK) causes hematopoietic neoplasia and developmental defects. Harrison, D.A., Binari, R., Nahreini, T.S., Gilman, M., Perrimon, N. EMBO J. (1995) [Pubmed]
  5. Drosophila differentiation genes instrumental in tumor suppression. Gateff, E., Kurzik-Dumke, U., Wismar, J., Löffler, T., Habtemichael, N., Konrad, L., Dreschers, S., Kaiser, S., Protin, U. Int. J. Dev. Biol. (1996) [Pubmed]
  6. JAK signaling globally counteracts heterochromatic gene silencing. Shi, S., Calhoun, H.C., Xia, F., Li, J., Le, L., Li, W.X. Nat. Genet. (2006) [Pubmed]
  7. Marelle acts downstream of the Drosophila HOP/JAK kinase and encodes a protein similar to the mammalian STATs. Hou, X.S., Melnick, M.B., Perrimon, N. Cell (1996) [Pubmed]
  8. Drosophila awdK-pn, a homologue of the metastasis suppressor gene nm23, suppresses the Tum-1 haematopoietic oncogene. Zinyk, D.L., McGonnigal, B.G., Dearolf, C.R. Nat. Genet. (1993) [Pubmed]
  9. Control of stem cell self-renewal in Drosophila spermatogenesis by JAK-STAT signaling. Tulina, N., Matunis, E. Science (2001) [Pubmed]
  10. mom identifies a receptor for the Drosophila JAK/STAT signal transduction pathway and encodes a protein distantly related to the mammalian cytokine receptor family. Chen, H.W., Chen, X., Oh, S.W., Marinissen, M.J., Gutkind, J.S., Hou, S.X. Genes Dev. (2002) [Pubmed]
  11. JAK/STAT signaling promotes regional specification by negatively regulating wingless expression in Drosophila. Ekas, L.A., Baeg, G.H., Flaherty, M.S., Ayala-Camargo, A., Bach, E.A. Development (2006) [Pubmed]
  12. The Drosophila homolog of the human tumor suppressor gene BHD interacts with the JAK-STAT and Dpp signaling pathways in regulating male germline stem cell maintenance. Singh, S.R., Zhen, W., Zheng, Z., Wang, H., Oh, S.W., Liu, W., Zbar, B., Schmidt, L.S., Hou, S.X. Oncogene (2006) [Pubmed]
  13. The JAK-STAT pathway in Drosophila. Hou, X.S., Perrimon, N. Trends Genet. (1997) [Pubmed]
  14. Localized JAK/STAT signaling is required for oriented cell rearrangement in a tubular epithelium. Johansen, K.A., Iwaki, D.D., Lengyel, J.A. Development (2003) [Pubmed]
  15. GFP reporters detect the activation of the Drosophila JAK/STAT pathway in vivo. Bach, E.A., Ekas, L.A., Ayala-Camargo, A., Flaherty, M.S., Lee, H., Perrimon, N., Baeg, G.H. Gene Expr. Patterns (2007) [Pubmed]
  16. Drosophila unpaired encodes a secreted protein that activates the JAK signaling pathway. Harrison, D.A., McCoon, P.E., Binari, R., Gilman, M., Perrimon, N. Genes Dev. (1998) [Pubmed]
  17. A directed screen for genes involved in Drosophila blood cell activation. Zettervall, C.J., Anderl, I., Williams, M.J., Palmer, R., Kurucz, E., Ando, I., Hultmark, D. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  18. The Drosophila cytokine receptor Domeless controls border cell migration and epithelial polarization during oogenesis. Ghiglione, C., Devergne, O., Georgenthum, E., Carballès, F., Médioni, C., Cerezo, D., Noselli, S. Development (2002) [Pubmed]
  19. Stripe-specific regulation of pair-rule genes by hopscotch, a putative Jak family tyrosine kinase in Drosophila. Binari, R., Perrimon, N. Genes Dev. (1994) [Pubmed]
  20. Identification of the first invertebrate interleukin JAK/STAT receptor, the Drosophila gene domeless. Brown, S., Hu, N., Hombría, J.C. Curr. Biol. (2001) [Pubmed]
  21. The Dorothy enhancer has Tinman binding sites and drives hopscotch-induced tumor formation. Kimbrell, D.A., Hice, C., Bolduc, C., Kleinhesselink, K., Beckingham, K. Genesis (2002) [Pubmed]
  22. The maternal JAK/STAT pathway of Drosophila regulates embryonic dorsal-ventral patterning. Lopes, E.S., Araujo, H.M. Braz. J. Med. Biol. Res. (2004) [Pubmed]
  23. The Hopscotch Jak kinase requires the Raf pathway to promote blood cell activation and differentiation in Drosophila. Luo, H., Rose, P.E., Roberts, T.M., Dearolf, C.R. Mol. Genet. Genomics (2002) [Pubmed]
  24. JAK signaling is somatically required for follicle cell differentiation in Drosophila. McGregor, J.R., Xi, R., Harrison, D.A. Development (2002) [Pubmed]
  25. The Jak-STAT signaling pathway is required but not sufficient for the antiviral response of drosophila. Dostert, C., Jouanguy, E., Irving, P., Troxler, L., Galiana-Arnoux, D., Hetru, C., Hoffmann, J.A., Imler, J.L. Nat. Immunol. (2005) [Pubmed]
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