Analyses for the unique machinery of cell division in Helicobacter pylori and pathogenesis of its associated disorders

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08618
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Laboratory medicine
• Research Institution: Kochi University
• Principal Investigator: TAKEUCHI Hiroaki 高知大学, 教育研究部医療学系臨床医学部門, 講師 (90346560)
• Co-Investigator(Kenkyū-buntansha): 松村 敬久 高知大学, 教育研究部医療学系臨床医学部門, 教授 (10274391) ; 杉浦 哲朗 高知大学, 医学部附属病院, 特任教授 (50171145) ; 森本 徳仁 高知大学, 医学部附属病院, 臨床検査技師 (60398055)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ヘリコバクター・ピロリ / H. pylori flora / 細胞分裂制御機構 / 形態形成 / minCDE / ftsZ / 生物学的多様性 / ファージ

Outline of Final Research Achievements

The machinery of cell division in H. pylori is little known. We investigated the function of Min proteins and FtsZ, and provided new insights as follows; 1. All Min proteins (C, D and E) regulated the cell elongation, 2. MinC and D regulated the division site in cells, 3. MinC regulated the Z-ring polymerization and contributed to the FtsZ stability, 4.MinD involved in nucleic occlusion system, and 5. MinE involved in the coccoid conversion at the stationary phase.
We obtained prophage-cured derivative strains from NY43 strain infected with prophage KHP30. The comparative analyses with NY43 and its prophage-cured strains provided new insights as follows; 1. Prophage induced the genetic mutations in cagA, leading to CagA disruption, 2. Prophage influenced the morphology and motility, 3. The prophage-cured derivatives could re-infect with phage, indicating that the repeated/patterned phenomena would be involved in the development of H. pylori evolution with biological polymorphisms.

Free Research Field

臨床検査医学（感染症・微生物学）