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Gene Review

Jag1  -  jagged 1

Mus musculus

Synonyms: ABE2, Gsfabe2, Headturner, Htu, Jagged1, ...
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Disease relevance of Jag1

  • Jag1 encodes a ligand in the Notch pathway and has been identified as the disease-causing gene for the developmental disorder Alagille syndrome [1].
  • Our results show that Notch1 and Jagged1 are first expressed in the otic vesicle, likely involved in differentiation of the VIIIth nerve ganglion neurons, and subsequently within the inner ear sensory epithelia, temporally coincident with initial hair cell differentiation [2].
  • Jagged signalling via Notch receptors on oligodendrocyte precursor cells (OPCs) inhibits their differentiation during development and the finding that both notch and jagged are expressed in multiple sclerosis lesions has fostered the view that this signalling pathway may explain remyelination failure [3].
  • Mutations in the DSL (Delta, Serrate, Lag2) Notch (N) ligand Delta-like (Dll) 3 cause skeletal abnormalities in spondylocostal dysostosis, which is consistent with a critical role for N signaling during somitogenesis [4].

High impact information on Jag1

  • We demonstrate that Jagged constitutes an instructive signal for Th2 differentiation, which is independent of IL4/STAT6 [5].
  • Here we use positional cloning to show that the gene mutated in sm mice encodes the putative Notch ligand Serrate [6].
  • Phosphorylation of histone H4 Ser1 regulates sporulation in yeast and is conserved in fly and mouse spermatogenesis [7].
  • In this study we show that histone H4 Ser1 is phosphorylated (H4 S1ph) during sporulation, starting from mid-sporulation and persisting to germination, and is temporally distinct from earlier meiosis-linked H3 S10ph involved in chromosome condensation [7].
  • Similar vascular defects are observed in Jagged1 and Notch1 knockout mice [8].

Biological context of Jag1


Anatomical context of Jag1

  • In the absence of Jag1, by contrast, the total number of these cells is strongly reduced, with complete loss of cochlear outer hair cells and some groups of vestibular hair cells, indicating that Jag1 is required for the prosensory inductive function of Notch [12].
  • Here, using conditional gene targeting, we show that the Jag1 gene is required for the normal development of all six sensory organs within the inner ear [13].
  • Our findings suggest that in addition to its role in microfibrils, MAGP-2 may also affect cellular differentiation through modulating the Notch signaling pathway either by binding to cell surface DSL ligands or by facilitating release and/or stabilization of a soluble extracellular form of Jagged1 [14].
  • Expression of Jagged1 gene in macrophages and its regulation by hematopoietic growth factors [10].
  • The primary bone marrow fibroblastic stromal cells, and murine stromal cell lines, such as PA6 and ST2, also expressed Jagged1 transcript, at levels comparable to the steady-state level in macrophages [10].

Associations of Jag1 with chemical compounds


Regulatory relationships of Jag1

  • Our findings indicate that the Jagged/Notch signaling pathway might actively participate in the regulation of myelination during central nervous system development and suggest that certain neuronal populations might regulate whether their axons are myelinated by the expression of inhibitory signals such as Jagged1 [19].
  • The Notch ligand encoded by the Jag1 gene was expressed in developing glomeruli in cells adjacent to Notch2-expressing cells [20].
  • Coculture with Balb3T3 cells stably overexpressing Jagged1 induced transactivation of the Hes1 promoter and increased expression of biliary lineage markers, such as cytokeratin-19 and gamma-glutamyl transpeptidase, in WB-F344 cells [21].
  • We show that Jagged1 is required by mitotic cells in the subventricular zone (SVZ) and stimulates self-renewal of multipotent epidermal growth factor-dependent NSCs [22].

Other interactions of Jag1

  • Notch ligands with contrasting functions: Jagged1 and Delta1 in the mouse inner ear [12].
  • Among the Notch ligands, Delta 1 and Jagged 1 were localized exclusively in spermatogonia and Sertoli cells, respectively [11].
  • The related microfibrillar protein MAGP-1 was also found to interact with DSL ligands but, unlike MAGP-2, was unable to facilitate the shedding of Jagged1 [14].
  • Expression of the Jagged1 gene was markedly up-regulated by growth factors for the cells, i.e., M-CSF, granulocyte-macrophage colony-stimulating factor, and interleukin-3 [10].
  • In S-shaped bodies, Hes1 expression was detected in the middle part which gives rise to the proximal tubule, but also extended into the lower and upper parts which give rise to the glomerulus and distal tubule, respectively, and was similar to the proximal-distal expression patterns for Notch1 and Jagged1 in these nephrogenic structures [23].

Analytical, diagnostic and therapeutic context of Jag1


  1. Bile duct proliferation in liver-specific Jag1 conditional knockout mice: effects of gene dosage. Loomes, K.M., Russo, P., Ryan, M., Nelson, A., Underkoffler, L., Glover, C., Fu, H., Gridley, T., Kaestner, K.H., Oakey, R.J. Hepatology (2007) [Pubmed]
  2. Distinct expression patterns of notch family receptors and ligands during development of the mammalian inner ear. Lewis, A.K., Frantz, G.D., Carpenter, D.A., de Sauvage, F.J., Gao, W.Q. Mech. Dev. (1998) [Pubmed]
  3. Notch1 and Jagged1 are expressed after CNS demyelination, but are not a major rate-determining factor during remyelination. Stidworthy, M.F., Genoud, S., Li, W.W., Leone, D.P., Mantei, N., Suter, U., Franklin, R.J. Brain (2004) [Pubmed]
  4. The divergent DSL ligand Dll3 does not activate Notch signaling but cell autonomously attenuates signaling induced by other DSL ligands. Ladi, E., Nichols, J.T., Ge, W., Miyamoto, A., Yao, C., Yang, L.T., Boulter, J., Sun, Y.E., Kintner, C., Weinmaster, G. J. Cell Biol. (2005) [Pubmed]
  5. Instruction of distinct CD4 T helper cell fates by different notch ligands on antigen-presenting cells. Amsen, D., Blander, J.M., Lee, G.R., Tanigaki, K., Honjo, T., Flavell, R.A. Cell (2004) [Pubmed]
  6. Serrate2 is disrupted in the mouse limb-development mutant syndactylism. Sidow, A., Bulotsky, M.S., Kerrebrock, A.W., Bronson, R.T., Daly, M.J., Reeve, M.P., Hawkins, T.L., Birren, B.W., Jaenisch, R., Lander, E.S. Nature (1997) [Pubmed]
  7. Phosphorylation of histone H4 Ser1 regulates sporulation in yeast and is conserved in fly and mouse spermatogenesis. Krishnamoorthy, T., Chen, X., Govin, J., Cheung, W.L., Dorsey, J., Schindler, K., Winter, E., Allis, C.D., Guacci, V., Khochbin, S., Fuller, M.T., Berger, S.L. Genes Dev. (2006) [Pubmed]
  8. The Notch target genes Hey1 and Hey2 are required for embryonic vascular development. Fischer, A., Schumacher, N., Maier, M., Sendtner, M., Gessler, M. Genes Dev. (2004) [Pubmed]
  9. Expression of notch receptors, notch ligands, and fringe genes in hematopoiesis. Singh, N., Phillips, R.A., Iscove, N.N., Egan, S.E. Exp. Hematol. (2000) [Pubmed]
  10. Expression of Jagged1 gene in macrophages and its regulation by hematopoietic growth factors. Nomaguchi, K., Suzu, S., Yamada, M., Hayasawa, H., Motoyoshi, K. Exp. Hematol. (2001) [Pubmed]
  11. Expression of Notch pathway components in spermatogonia and Sertoli cells of neonatal mice. Dirami, G., Ravindranath, N., Achi, M.V., Dym, M. J. Androl. (2001) [Pubmed]
  12. Notch ligands with contrasting functions: Jagged1 and Delta1 in the mouse inner ear. Brooker, R., Hozumi, K., Lewis, J. Development (2006) [Pubmed]
  13. The Notch ligand JAG1 is required for sensory progenitor development in the mammalian inner ear. Kiernan, A.E., Xu, J., Gridley, T. PLoS Genet. (2006) [Pubmed]
  14. The extracellular matrix protein MAGP-2 interacts with Jagged1 and induces its shedding from the cell surface. Nehring, L.C., Miyamoto, A., Hein, P.W., Weinmaster, G., Shipley, J.M. J. Biol. Chem. (2005) [Pubmed]
  15. Cortisol regulates the expression of Notch in osteoblasts. Pereira, R.M., Delany, A.M., Durant, D., Canalis, E. J. Cell. Biochem. (2002) [Pubmed]
  16. Testosterone influenced the expression of Notch1, Notch2 and Jagged1 induced by lipopolysaccharide in macrophages. Guo, D., Zhang, H., Liu, L., Wang, L., Cheng, Y., Qiao, Z. Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie. (2004) [Pubmed]
  17. Unique patterns of Notch1, Notch4 and Jagged1 expression in ovarian vessels during folliculogenesis and corpus luteum formation. Vorontchikhina, M.A., Zimmermann, R.C., Shawber, C.J., Tang, H., Kitajewski, J. Gene Expr. Patterns (2005) [Pubmed]
  18. Phosphorylation of F-actin-associating G protein gamma12 subunit enhances fibroblast motility. Ueda, H., Yamauchi, J., Itoh, H., Morishita, R., Kaziro, Y., Kato, K., Asano, T. J. Biol. Chem. (1999) [Pubmed]
  19. Central nervous system myelination in mice with deficient expression of Notch1 receptor. Givogri, M.I., Costa, R.M., Schonmann, V., Silva, A.J., Campagnoni, A.T., Bongarzone, E.R. J. Neurosci. Res. (2002) [Pubmed]
  20. Defects in development of the kidney, heart and eye vasculature in mice homozygous for a hypomorphic Notch2 mutation. McCright, B., Gao, X., Shen, L., Lozier, J., Lan, Y., Maguire, M., Herzlinger, D., Weinmaster, G., Jiang, R., Gridley, T. Development (2001) [Pubmed]
  21. The role of notch signaling in the development of intrahepatic bile ducts. Kodama, Y., Hijikata, M., Kageyama, R., Shimotohno, K., Chiba, T. Gastroenterology (2004) [Pubmed]
  22. Jagged1 signals in the postnatal subventricular zone are required for neural stem cell self-renewal. Nyfeler, Y., Kirch, R.D., Mantei, N., Leone, D.P., Radtke, F., Suter, U., Taylor, V. EMBO J. (2005) [Pubmed]
  23. Expression of Hairy/Enhancer of Split genes, Hes1 and Hes5, during murine nephron morphogenesis. Piscione, T.D., Wu, M.Y., Quaggin, S.E. Gene Expr. Patterns (2004) [Pubmed]
  24. Stromal expression of Jagged 1 promotes colony formation by fetal hematopoietic progenitor cells. Jones, P., May, G., Healy, L., Brown, J., Hoyne, G., Delassus, S., Enver, T. Blood (1998) [Pubmed]
  25. Notch1 and Jagged1 expression by the developing pulmonary vasculature. Taichman, D.B., Loomes, K.M., Schachtner, S.K., Guttentag, S., Vu, C., Williams, P., Oakey, R.J., Baldwin, H.S. Dev. Dyn. (2002) [Pubmed]
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