Roles and modes of action of nectins in heterotypic cell-cell adhesions

2016 Fiscal Year Final Research Report

• Project/Area Number: 26251013
• Research Category: Grant-in-Aid for Scientific Research (A)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Functional biochemistry
• Research Institution: Kobe University
• Principal Investigator: Takai Yoshimi 神戸大学, 医学研究科, 特命教授 (60093514)
• Co-Investigator(Kenkyū-buntansha): 下野 洋平 神戸大学, 医学(系)研究科(研究院), 准教授 (90594630) ; 水谷 清人 神戸大学, 医学(系)研究科(研究院), 講師 (50559177) ; 宮田 宗明 神戸大学, 医学(系)研究科(研究院), 助教 (90582007) ; 溝口 明 三重大学, 医学(系)研究科(研究院), 教授 (90181916)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 細胞接着・運動 / 細胞シグナル伝達機構 / 異種細胞間接着 / 細胞膜受容体 / ネクチン / アファディン

Outline of Final Research Achievements

The roles and modes of action of nectins in heterotypic cell-cell adhesions were investigated. We identified a novel cell adhesion apparatus formed by the heterophilic trans-interaction between nectin-4 and nectin-1, which were expressed in the luminal and basal cells in the mammary gland, respectively. Nectin-4 in this apparatus enhanced the prolactin receptor signaling. Moreover, we showed that nectin-2 and nectin-3 expressed in olfactory and supporting cells, respectively, interacted in trans and recruited cadherin to the heterotypic cell junctions, resulting in the formation of the mosaic pattern in the olfactory epithelium. Further, we showed that nectin-2δ was localized on the plasma membranes of astrocytic perivascular endfoot processes facing the basement membrane of blood vessels in the brain. Genetic ablation of nectin-2 caused degeneration of the astrocytic perivascular endfoot processes and neurons, indicating that nectin- 2 is required to maintain the brain structures.

Free Research Field

生化学