Morphological and functional relationship among HAP1, pericentriolar materials and causative factors for neurodegeneration.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293045
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: General anatomy (including histology/embryology)
• Research Institution: Yamaguchi University
• Principal Investigator: SHINODA Koh 山口大学, 医学(系)研究科(研究院), 教授 (40192108)
• Co-Investigator(Kenkyū-buntansha): YANAI Akie 山口大学, 大学院医学系研究科, 講師 (20284854) ; FUJINAGA Ryutaro 山口大学, 大学院医学系研究科, 講師 (30335723) ; KOKUBU Keiji 山口大学, 大学院医学系研究科, 助教 (00432740) ; HAYASAKA Naoto 山口大学, 大学院医学系研究科, 特任准教授 (80368290)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: stigmoid body / androgen receptor / huntingtin / pericentriolar materials / brain / neurodegeneration / apoptosis / cell cycle

Outline of Final Research Achievements

Androgen receptor (AR) is diffusely distributed in cytoplasm of steroid-free cultured cells without the stigmoid body (STB) and sequestered by the STB formed after HAP1 transfection. Administration of DHT can promote further translocation of AR from the STBs to nucleus. In the brain, AR is frequently expressed in the nucleus of neuron with STB, but not localized to the STB. PCM1 is distributed surrounding the centrosome in cultured cells without the STB, while in HAP1-transfected cultured cells, PCM is translocated to the HAP1-induced STBs. Huntingtin (Htt) is also distributed near the centrosome like PCM1 in cultured cells without STB, whereas Htt is diffusely distributed in cytoplasm. In addition, comparing HAP1-trasfected cultured cells and control, the current study suggests that intracellular induction of STB/HAP1 appears to increase S-phase in cell cycle and that it also specifically suppress apoptosis induced by proteasome inhibition.

Free Research Field

神経解剖学