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First published online October 23, 2009
doi: 10.1242/10.1242/dev.042135

Development 136, 3757-3766 (2009)
Published by The Company of Biologists 2009
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Mitochondrial protein Preli-like is required for development of dendritic arbors and prevents their regression in the Drosophila sensory nervous system

Asako Tsubouchi1, Taiichi Tsuyama1, Makio Fujioka2, Haruyasu Kohda2, Keiko Okamoto-Furuta2, Toshiro Aigaki3 and Tadashi Uemura1,*,{dagger}

1 Graduate School of Biostudies, Kyoto University, Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8507, Japan.
2 Graduate School of Medicine, Kyoto University, Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8507, Japan.
3 Department of Biological Sciences, Tokyo Metropolitan University, 1-1 Minami-osawa, Hachioji-shi, Tokyo, 192-0397, Japan.

{dagger} Author for correspondence (tauemura{at}lif.kyoto-u.ac.jp)

Accepted 8 September 2009

Dynamic morphological changes in mitochondria depend on the balance of fusion and fission in various eukaryotes, and are crucial for mitochondrial activity. Mitochondrial dysfunction has emerged as a common theme that underlies numerous neurological disorders, including neurodegeneration. However, how this abnormal mitochondrial activity leads to neurodegenerative disorders is still largely unknown. Here, we show that the Drosophila mitochondrial protein Preli-like (Prel), a member of the conserved PRELI/MSF1 family, contributes to the integrity of mitochondrial structures, the activity of respiratory chain complex IV and the cellular ATP level. When Prel function was impaired in neurons in vivo, the cellular ATP level decreased and mitochondria became fragmented and sparsely distributed in dendrites and axons. Notably, the dendritic arbors were simplified and downsized, probably as a result of breakage of proximal dendrites and progressive retraction of terminal branches. By contrast, abrogation of the mitochondria transport machinery per se had a much less profound effect on the arbor morphogenesis. Interestingly, overexpression of Drob-1 (Debcl), a Drosophila Bax-like Bcl-2 family protein, in the wild-type background produced dendrite phenotypes that were reminiscent of the prel phenotype. Moreover, expression of the Drob-1 antagonist Buffy in prel mutant neurons substantially restored the dendritic phenotype. Our observations suggest that Prel-dependent regulation of mitochondrial activity is important for both growth and prevention of breakage of dendritic branches.

Key words: Drosophila, Preli, Dendrite, Mitochondria, Neurodegeneration


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Mitochondrial Prel-ude to neurodegeneration

Development 2009 136: e2204. [Full Text]  





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