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• Drosophila model to clarify the pathological significance of OPA1 in autosomal dominant optic atrophy

  Yohei Nitta , Jiro Osaka , Ryuto Maki , Satoko Hakeda-Suzuki , Emiko Suzuki , Satoshi Ueki , … 全著者表示

  eLife   2023年6月  [査読有り]

  DOI

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  記述言語：英語   掲載種別：研究論文（学術雑誌）   共著  

• Direct evaluation of neuroaxonal degeneration with the causative genes of neurodegenerative diseases in <i>Drosophila</i> using the automated axon quantification system, MeDUsA

  Yohei Nitta, Hiroki Kawai, Ryuto Maki, Jiro Osaka, Satoko Hakeda-Suzuki, Yoshitaka Nagai, Karolína … 全著者表示

  Human Molecular Genetics   32 ( 9 )   1524 - 1538   2023年1月

  DOI CiNii Research

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  記述言語：その他外国語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Oxford University Press (OUP)   共著  

  <jats:title>Abstract</jats:title>
  <jats:p>Drosophila is an excellent model organism for studying human neurodegenerative diseases (NDs). However, there is still almost no experimental system that could directly observe the degeneration of neurons and automatically quantify axonal degeneration. In this study, we created MeDUsA (a ‘method for the quantification of degeneration using fly axons’), a standalone executable computer program based on Python that combines a pre-trained deep-learning masking tool with an axon terminal counting tool. This software automatically quantifies the number of retinal R7 axons in Drosophila from a confocal z-stack image series. Using this software, we were able to directly demonstrate that axons were degenerated by the representative causative genes of NDs for the first time in Drosophila. The fly retinal axon is an excellent experimental system that is capable of mimicking the pathology of axonal degeneration in human NDs. MeDUsA rapidly and accurately quantifies axons in Drosophila photoreceptor neurons. It enables large-scale research into axonal degeneration, including screening to identify genes or drugs that mediate axonal toxicity caused by ND proteins and diagnose the pathological significance of novel variants of human genes in axons.</jats:p>

• Glial insulin regulates cooperative or antagonistic Golden goal/Flamingo interactions during photoreceptor axon guidance

  Takechi, H; Hakeda-Suzuki, S; Nitta, Y; Ishiwata, Y; Iwanaga, R; Sato, M; Sugie, A; Suzuki, T

  ELIFE   10   2021年3月

  DOI Web of Science PubMed CiNii Research

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  記述言語：その他外国語   掲載種別：研究論文（学術雑誌）   出版者・発行元：eLife Sciences Publications, Ltd   共著  

  <jats:p>Transmembrane protein Golden goal (Gogo) interacts with atypical cadherin Flamingo (Fmi) to direct R8 photoreceptor axons in the<jats:italic>Drosophila</jats:italic>visual system. However, the precise mechanisms underlying Gogo regulation during columnar- and layer-specific R8 axon targeting are unknown. Our studies demonstrated that the insulin secreted from surface and cortex glia switches the phosphorylation status of Gogo, thereby regulating its two distinct functions. Non-phosphorylated Gogo mediates the initial recognition of the glial protrusion in the center of the medulla column, whereas phosphorylated Gogo suppresses radial filopodia extension by counteracting Flamingo to maintain a one axon-to-one column ratio. Later, Gogo expression ceases during the midpupal stage, thus allowing R8 filopodia to extend vertically into the M3 layer. These results demonstrate that the long- and short-range signaling between the glia and R8 axon growth cones regulates growth cone dynamics in a stepwise manner, and thus shapes the entire organization of the visual system.</jats:p>

• Activity-dependent endocytosis of Wingless regulates synaptic plasticity in the Drosophila visual system

  Kawamura, H; Hakeda-Suzuki, S; Suzuki, T

  GENES & GENETIC SYSTEMS   95 ( 5 )   235 - 247   2020年10月  [査読有り]

  DOI Web of Science PubMed

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  記述言語：英語   掲載種別：研究論文（学術雑誌）   共著  

• Systematic identification of genes regulating synaptic remodeling in the <i>Drosophila</i> visual system

  Araki, T; Osaka, J; Kato, Y; Shimozono, M; Kawamura, H; Iwanaga, R; Hakeda-Suzuki, S; Suzuki, T

  GENES & GENETIC SYSTEMS   95 ( 3 )   101 - 110   2020年6月  [査読有り]

  DOI Web of Science PubMed

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  記述言語：英語   掲載種別：研究論文（学術雑誌）   共著  

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