2016 Fiscal Year Final Research Report
Fucosylation regulates reproduction system development.
Project/Area Number |
26460269
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General anatomy (including histology/embryology)
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Research Institution | Chiba University |
Principal Investigator |
BABA Atsushi 千葉大学, 大学院医学研究院, 助教 (70405215)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | 器官形成 / 糖鎖修飾 / フコシル化 / 発生・分化 / 細胞・組織 / 管腔様構造 |
Outline of Final Research Achievements |
Developmental defect in the formation of tubular-like structure, is the relatively common desease in human, but its cause remains unknown. Celsr1 inactivation leads to anatomic block of tublar-like structure in reproductive system, and those phenotypes are mimicked in mice with inactivation of Lunatic fringe, which encodes an O-fucose-Nacetylglucosaminyltransferase. Two EGF-like motifs in Celsr1 are O-fucosylated and subject to Fringe modification. Mutation of O-fucosylation sites hampers decreases cell surface expression of the full length protein. Thus, post-transcriptional glycosylation regulates subcellular localization of Celsr1 protein, and participates in the formation of tubular-like structure.
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Free Research Field |
発生生物学
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