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Mol. Cells 2013; 36(2): 163-168

Published online June 27, 2013

https://doi.org/10.1007/s10059-013-0147-1

© The Korean Society for Molecular and Cellular Biology

Tbc1d15-17 Regulates Synaptic Development at the Drosophila Neuromuscular Junction

Min-Jung Lee, Sooyeon Jang, Minyeop Nahm, Jin-Ho Yoon, and Seungbok Lee

Department of Cell and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, Seoul 110-749, Korea, 1School of Biological Sciences and Chemistry, Sungshin Women’s University, Seoul 136-742, Korea

Received: May 13, 2013; Accepted: May 23, 2013

Abstract

Members of the Tre-2/Bub2/Cdc16 (TBC) family of proteins are believed to function as GTPase-activating proteins (GAPs) for Rab GTPases, which play pivotal roles in intracellular membrane trafficking. Although membrane trafficking is fundamental to neuronal morphogenesis and function, the roles of TBC-family Rab GAPs have been poorly characterized in the nervous system. In this paper, we provide genetic evidence that Tbc1d15-17, the Drosophila homolog of mammalian Rab7-GAP TBC1d15, is required for normal presynaptic growth and postsynaptic organization at the neuromuscular junction (NMJ). A lossof-function mutation in tbc1d15-17 or its presynaptic knockdown
leads to an increase in synaptic bouton number and NMJ length. tbc1d15-17 mutants are also defective in the distribution of the postsynaptic scaffold Discs-large (Dlg) and in the level of the postsynaptic glutamate subunit GluRIIA. These postsynaptic phenotypes are recapitulated by postsynaptic knockdown of Tbc1d15-17. We also show that presynaptic overexpression of a constitutively active Rab7 mutant in a wild-type background causes a synaptic overgrowth phenotype resembling that of tbc1d15-17 mutants, while a dominant-negative form of Rab7 has the opposite effect. Together, our findings establish a novel role for Tbc1d15-17 and its potential substrate Rab7 in regulating synaptic development.

Keywords Drosophila NMJ, postsynaptic organization, synaptic growth, Tbc1d15-17

Article

Research Article

Mol. Cells 2013; 36(2): 163-168

Published online August 31, 2013 https://doi.org/10.1007/s10059-013-0147-1

Copyright © The Korean Society for Molecular and Cellular Biology.

Tbc1d15-17 Regulates Synaptic Development at the Drosophila Neuromuscular Junction

Min-Jung Lee, Sooyeon Jang, Minyeop Nahm, Jin-Ho Yoon, and Seungbok Lee

Department of Cell and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, Seoul 110-749, Korea, 1School of Biological Sciences and Chemistry, Sungshin Women’s University, Seoul 136-742, Korea

Received: May 13, 2013; Accepted: May 23, 2013

Abstract

Members of the Tre-2/Bub2/Cdc16 (TBC) family of proteins are believed to function as GTPase-activating proteins (GAPs) for Rab GTPases, which play pivotal roles in intracellular membrane trafficking. Although membrane trafficking is fundamental to neuronal morphogenesis and function, the roles of TBC-family Rab GAPs have been poorly characterized in the nervous system. In this paper, we provide genetic evidence that Tbc1d15-17, the Drosophila homolog of mammalian Rab7-GAP TBC1d15, is required for normal presynaptic growth and postsynaptic organization at the neuromuscular junction (NMJ). A lossof-function mutation in tbc1d15-17 or its presynaptic knockdown
leads to an increase in synaptic bouton number and NMJ length. tbc1d15-17 mutants are also defective in the distribution of the postsynaptic scaffold Discs-large (Dlg) and in the level of the postsynaptic glutamate subunit GluRIIA. These postsynaptic phenotypes are recapitulated by postsynaptic knockdown of Tbc1d15-17. We also show that presynaptic overexpression of a constitutively active Rab7 mutant in a wild-type background causes a synaptic overgrowth phenotype resembling that of tbc1d15-17 mutants, while a dominant-negative form of Rab7 has the opposite effect. Together, our findings establish a novel role for Tbc1d15-17 and its potential substrate Rab7 in regulating synaptic development.

Keywords: Drosophila NMJ, postsynaptic organization, synaptic growth, Tbc1d15-17

Mol. Cells
Jun 30, 2023 Vol.46 No.6, pp. 329~398
COVER PICTURE
The cellular proteostasis network is adaptively modulated upon cellular stress, thereby protecting cells from proteostasis collapse. Heat shock induces the translocation of misfolded proteins and the chaperone protein HSP70 into nucleolus, where nuclear protein quality control primarily occurs. Nuclear RNA export factor 1 (green), nucleolar protein fibrillarin (red), and nuclei (blue) were visualized in NIH3T3 cells under basal (left) and heat shock (right) conditions (Park et al., pp. 374-386).

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