A high-resoluton map of SBP1 interactomes in Plasmodium falciparum-infected erythrocytes.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26870021
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cell biology; Veterinary medical science
• Research Institution: Obihiro University of Agriculture and Veterinary Medicine
• Principal Investigator: Takano Ryo 帯広畜産大学, 原虫病研究センター, 研究員 (90722588)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 熱帯熱マラリア / 病原性 / インタラクトーム / マウレル裂 / 輸送タンパク質 / 分泌タンパク質 / 重症マラリア / 免疫沈降

Outline of Final Research Achievements

Plasmodium falciparum parasites, a causative agent of human malaria, export numerous proteins to the host erythrocyte membrane and cytosol. These exported proteins, sometimes referred to as the exportome, facilitate host cell remodeling and are directly associated with the pathology and pathogenesis of severe malaria. Therefore, to understand the molecular basis of severe malaria, it is essential to clarify the exportome. Here, I conducted FLAG-tag-based immunoprecipitation with cell lysates of erythrocytes infected with parasites that expressed FLAG-tagged SBP1, a known Maurer's cleft component, and analyzed the precipitated proteins by using high-sensitive mass spectrometry. The precipitated proteins were predominantly host cytoskeleton and Maurer's cleft components. I further identified novel host and parasite proteins that were recruited to and localized in Maurer's clefts, suggesting the involvement of these proteins in the severe malaria caused by Plasmodium falciparum.

Free Research Field

分子細胞生物学