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開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

ショウジョウバエにおける自閉症関連遺伝子Centaurin gamma 1Aのドメイン機能解析
Analysis of Functional domains in Centaurin gamma 1A at Drosophila larval Neuromuscular Junctions

  • P2-036
  • 小杉 紗紀子 / Sakiko Kosugi:1 清水 彰 / Akira Shimizu:1 本間 瑞穂 / Mizuho Homma:1 鈴木(羽毛田) 聡子 / Satoko Hakeda-Suzuki:2 鈴木 崇之 / Takashi Suzuki:2 宮川 博義 / Hiroyoshi Miyakawa:1 森本 高子 / Takako Morimoto:1 
  • 1:東京薬科大院生命科学脳神経機能 / Lab of Cellular Neurobiology, Sch of Life Sci, Tokyo Univ of Pharm and Life Sci, Tokyo, Japan 2:東京工業大学情報生命博士教育院生命理工学研究科 / Core division of Advanced Science, Grad. Schl. of Bioscience & Biotechnology, Tokyo Institute of Technology, Yokohama, Japan 

Synaptic dysfunction has been considered to cause psychiatric disorders like autism spectrum disorder and schizophrenia. Although a number of molecules involved in synaptic transmission have been identified, the precise molecular mechanisms have not been fully understood. Synaptic transmissions contain several processes including vesicle recycling. In order to elucidate the molecular mechanisms of synaptic transmissions, we have focused on centaurin, which potentially involves vesicle recycling. Centaurin family members commonly have functional domains, such as GTPase, PH, ArfGAP and ANK domains. In addition, it has been reported that one of centaurin family members is included in the chromosomal deletion region found in autistic patients. Our previous study examined the function of Centaurin gamma 1A (CenG1A), one of Centaurin family members, at Drosophila larval neuromuscular junctions (NMJs). Changes of muscle membrane potentials evoked by nerve stimulation (excitatory junctional potentials; EJPs) and spontaneous changes of postsynaptic membrane potentials (miniature EJPs) were recorded by intracellular recording from muscle cells. When CenG1A function was suppressed, EJPs were found to be increased, suggesting that CenG1A probably functions as a negative regulator of neurotransmitter release (34th annual meeting of the Japan neuroscience society). To clarify the functional domain of CenG1A which is responsible for this negative regulation for neurotransmitter release, we recorded EJPs from mutants in which each domain of CenG1A was deleted, or null mutants in which all domains of CenG1A were deleted. We found mutants which showed increased EJPs as shown in the previous study and further examined genetic interactions of functional domains. We will discuss the functional domain which contributes to increase EJPs and the mechanisms of CenG1A functions.

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