キムラ　トシヤ   KIMURA TOSHIYA   木村　俊哉    所属   関西医科大学  iPS・幹細胞応用医学講座    職種   助教
論文種別	原著(症例報告除く)
言語種別	英語
査読の有無	査読あり
表題	Evidence that dendritic mitochondria negatively regulate dendritic branching in pyramidal neurons in the neocortex.
掲載誌名	正式名：Journal of Neuroscience ISSNコード：15292401
巻・号・頁	34(20),pp.6938-6951
著者・共著者	Toshiya Kimura, Fujio Murakami
担当区分	筆頭著者,責任著者
発行年月	2014/05
概要	The precise branching patterns of dendritic arbors have a profound impact on information processing in individual neurons and the brain. These patterns are established by positive and negative regulation of the dendritic branching. Although the mechanisms for positive regulation have been extensively investigated, little is known about those for negative regulation. Here, we present evidence that mitochondria located in developing dendrites are involved in the negative regulation of dendritic branching. We visualized mitochondria in pyramidal neurons of the mouse neocortex during dendritic morphogenesis using in utero electroporation of a mitochondria-targeted fluorescent construct. We altered the mitochondrial distribution in vivo by overexpressing Mfn1, a mitochondrial shaping protein, or the Miro-binding domain of TRAK2 (TRAK2-MBD), a truncated form of a motor-adaptor protein. We found that dendritic mitochondria were preferentially targeted to the proximal portion of dendrites only during dendritic morphogenesis. Overexpression of Mfn1 or TRAK2-MBD depleted mitochondria from the dendrites, an effect that was accompanied by increased branching of the proximal portion of the dendrites. This dendritic abnormality cannot be accounted for by changes in the distribution of membrane trafficking organelles since the overexpression of Mfn1 did not alter the distributions of the endoplasmic reticulum, Golgi, or endosomes. Additionally, neither did these constructs impair neuronal viability or mitochondrial function. Therefore, our results suggest that dendritic mitochondria play a critical role in the establishment of the precise branching pattern of dendritic arbors by negatively affecting dendritic branching.
DOI	10.1523/JNEUROSCI.5095-13.2014
PMID	24828647