title: In Vivo Expression of the PTB-deleted Odin Mutant Results in Hydrocephalus.
abstract: Odin has been implicated in the downstream signaling pathway of receptor tyrosine kinases, such as the epidermal growth factor and Eph receptors. However, the physiologically relevant function of Odin needs to be further determined. In this study, we used Odin heterozygous mice to analyze the Odin expression pattern; the targeted allele contained a β-geo gene trap vector inserted into the 14th intron of the Odin gene. Interestingly, we found that Odin was exclusively expressed in ependymal cells along the brain ventricles. In particular, Odin was highly expressed in the subcommissural organ, a small ependymal glandular tissue. However, we did not observe any morphological abnormalities in the brain ventricles or ependymal cells of Odin null-mutant mice. We also generated BAC transgenic mice that expressed the PTB-deleted Odin (dPTB) after a floxed GFP-STOP cassette was excised by tissue-specific Cre expression. Strikingly, Odin-dPTB expression played a causative role in the development of the hydrocephalic phenotype, primarily in the midbrain. In addition, Odin-dPTB expression disrupted proper development of the subcommissural organ and interfered with ependymal cell maturation in the cerebral aqueduct. Taken together, our findings strongly suggest that Odin plays a role in the differentiation of ependymal cells during early postnatal brain development.
authors.affiliation: Department of Biological Science, Sookmyung Women's University, Seoul 140-742, Korea.
authors.forename: Sunjung
authors.initials: S
authors.lastname: Park
authors.affiliation: Department of Biological Science, Sookmyung Women's University, Seoul 140-742, Korea.
authors.forename: Haeryung
authors.initials: H
authors.lastname: Lee
authors.affiliation: Department of Biological Science, Sookmyung Women's University, Seoul 140-742, Korea.
authors.forename: Soochul
authors.initials: S
authors.lastname: Park
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000818:Animals; D002352:Carrier Proteins / Q000737:chemistry / Q000235:genetics* / Q000378:metabolism*; D002454:Cell Differentiation; D004805:Ependyma / Q000378:metabolism / Q000502:physiology; D055786:Gene Knockout Techniques; D006849:Hydrocephalus / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D008636:Mesencephalon / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008822:Mice, Transgenic; D017384:Sequence Deletion; D013351:Subcommissural Organ / Q000254:growth & development / Q000378:metabolism / Q000473:pathology
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D002352:Carrier Proteins; C498028:Odin protein, mouse
keywords: Odin; ependymal cells; hydrocephalus; subcommissural organ