Cellular and molecular basis of injury induced-vacuoles in Drosophila central nervous system

• Project/Area Number: 15K06718
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurophysiology / General neuroscience
• Research Institution: Kyorin University
• Principal Investigator: Kato Kentaro 杏林大学, 医学部, 講師 (30733068)
• Project Period (FY): 2015-04-01 – 2020-03-31
• Project Status: Completed (Fiscal Year 2019)
• Budget Amount: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000); Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000); Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000); Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000); Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
• Keywords: グリア細胞 / 損傷応答 / ショウジョウバエ / 中枢神経 / 中枢神経系 / 変性空胞 / 神経損傷

Outline of Final Research Achievements

In some animals, including humans, the central nervous system undergoes vacuolization upon injury. In this study, using Drosophila melanogaster as a model system, a dynamic process of formation and repair of such vacuoles in neuropils was studied. Time-lapse microscopy revealed that vacuoles developed upon injury in neuropils are formed by glial cells. A gene was identified as a regulator of the vacuole formation. This gene in glial cells is also likely to be required for supporting certain neural fibers in damaged neuropil, implying that a glial-neuron interaction contributes to the integrity of the neural tissue upon injury. In addition, a list of candidate genes that have a role in the glial-neuron interaction in response to injury was obtained by gene expression analyses.

Academic Significance and Societal Importance of the Research Achievements

中枢神経系が損傷を受けた時に形成される空胞は神経機能阻害の一因であると考えられている。一般的には、血管系の損傷に、もしくは直接的な損傷に起因する神経終末の脱落、膨張、細胞死が関与すると言われる。しかし、空胞の形成、修復とその影響に関しては十分に明らかになっているとは言えない。本研究は、より単純なショウジョウバエをモデルとして、空胞形成、修復の細胞基盤を整理、形成に関わる遺伝子の一部を同定した。また、損傷時におけるグリア細胞－神経細胞の相互作用に関与しうる候補遺伝子リストを得た。