The mechanism of functional sub-compartment formation in the endoplasmic reticulum by membrane structure

2016 Fiscal Year Final Research Report

• Project/Area Number: 26440110
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cell biology
• Research Institution: Institute of Physical and Chemical Research
• Principal Investigator: Kurokawa Kazuo 国立研究開発法人理化学研究所, 光量子工学研究領域, 専任研究員 (40333504)
• Research Collaborator: ISHII Midori
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 小胞体サブコンパートメント / ERES / COPII小胞 / Sar1

Outline of Final Research Achievements

One third of the proteins are synthesized in the endoplasmic reticulum (ER) and transported as cargo by transported vesicles (COPII vesicles) from the ER exit sites (ERES) to the Golgi apparatus. This mechanism is conserved in all eukaryotic cells. In this research, we aimed to elucidate the molecular mechanism of ERES formation.
By using the high-speed and high-resolution microscope SCLIM exceeding conventional fluorescent microscopy, we examined the localization of Sar1, which is a key regulator for COPII vesicle formation and has a function of membrane bending.
Sar1 showed some accumulation in ERES. High-resolution 3D observation indicated that Sar1 localized at the rims of the COPII vesicle membranes which were connected to the ER, but was excluded from the rest of the COPII vesicle membranes. Additionally, we showed that the reversible membrane association of Sar1 GTPase leads to its localization being restricted to the rims of COPII-coated membranes in vivo.

Free Research Field

細胞生物学