title: Cartilage acidic protein-1B (LOTUS), an endogenous Nogo receptor antagonist for axon tract formation.
abstract: Neural circuitry formation depends on the molecular control of axonal projection during development. By screening with fluorophore-assisted light inactivation in the developing mouse brain, we identified cartilage acidic protein-1B as a key molecule for lateral olfactory tract (LOT) formation and named it LOT usher substance (LOTUS). We further identified Nogo receptor-1 (NgR1) as a LOTUS-binding protein. NgR1 is a receptor of myelin-derived axon growth inhibitors, such as Nogo, which prevent neural regeneration in the adult. LOTUS suppressed Nogo-NgR1 binding and Nogo-induced growth cone collapse. A defasciculated LOT was present in lotus-deficient mice but not in mice lacking both lotus- and ngr1. These findings suggest that endogenous antagonism of NgR1 by LOTUS is crucial for normal LOT formation.
authors.affiliation: Department of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine, Yokohama 236-0004, Japan.
authors.forename: Yasufumi
authors.initials: Y
authors.lastname: Sato
authors.forename: Masumi
authors.initials: M
authors.lastname: Iketani
authors.forename: Yuji
authors.initials: Y
authors.lastname: Kurihara
authors.forename: Megumi
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: Naoya
authors.initials: N
authors.lastname: Yamashita
authors.forename: Fumio
authors.initials: F
authors.lastname: Nakamura
authors.forename: Yuko
authors.initials: Y
authors.lastname: Arie
authors.forename: Takahiko
authors.initials: T
authors.lastname: Kawasaki
authors.forename: Tatsumi
authors.initials: T
authors.lastname: Hirata
authors.forename: Takaya
authors.initials: T
authors.lastname: Abe
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kiyonari
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Strittmatter
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Goshima
authors.forename: Kohtaro
authors.initials: K
authors.lastname: Takei
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology*; D001665:Binding Sites; D002135:Calcium-Binding Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D002460:Cell Line; D002478:Cells, Cultured; D058851:GPI-Linked Proteins / Q000235:genetics / Q000378:metabolism; D020439:Growth Cones / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008024:Ligands; D051379:Mice; D008813:Mice, Inbred ICR; D009185:Myelin Proteins / Q000235:genetics / Q000378:metabolism*; D000070798:Nogo Proteins; D000070816:Nogo Receptor 1; D009833:Olfactory Pathways / Q000166:cytology* / Q000254:growth & development* / Q000378:metabolism; D016548:Prosencephalon / Q000196:embryology / Q000378:metabolism; D011485:Protein Binding; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D002135:Calcium-Binding Proteins; C560339:Crtac1 protein, mouse; D058851:GPI-Linked Proteins; D008024:Ligands; D009185:Myelin Proteins; D000070798:Nogo Proteins; D000070816:Nogo Receptor 1; C000603199:RTN4 protein, human; D011956:Receptors, Cell Surface; C000603201:Rtn4 protein, mouse; C419790:Rtn4r protein, mouse