Immunohistochemical evaluation of mitochondrial quality control in vivo

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460276
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General anatomy (including histology/embryology)
• Research Institution: Juntendo University
• Principal Investigator: Koike Masato 順天堂大学, 医学(系)研究科(研究院), 教授 (80347210)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: ミトコンドリア / マイトファジー / リソソーム / parkin / オメガソーム / DFCP1

Outline of Final Research Achievements

1. Lysosomal accumulation of mitochondrial subunit c in cathepsin D (CD) deficient neurons were completely inhibited in neurons doubly deficient in CD and Atg7 and only partially reduced in neurons doubly deficient in CD and parkin, indicating the limited contribution of mitophagy mediated by parkin in the mitochondrial quality control in neurons. 2. Intercrossing of the transgenic (Tg) mice expressing iron regulatory protein 2 (IRP2) to Parkin knockout mice perturbed the integrity of neurons specifically in the substantia nigra and provoked motor symptoms. 3. Therefore, we produced antibodies specific to mouse DFCP1, a marker for omegasomes. In HeLa cells under normal conditions, dotted or tubular immunoreactivity for DFCP1 was found along Tom20-positive mitochondria. Moreover, under starved conditions, DFCP1-positive structures were co-localized in one part of the LC3-positive autophagosomes.

Free Research Field

解剖学