USP5/Leon deubiquitinase confines postsynaptic growth by maintaining ubiquitin homeostasis through Ubiquilin
- Academia Sinica, Taiwan, Republic of China
- Chang Gung University, Taiwan, Republic of China
Abstract
Synapse formation and growth are tightly controlled processes. How synaptic growth is terminated after reaching proper size remains unclear. Here, we show that Leon, the Drosophila USP5 deubiquitinase, controls postsynaptic growth. In leon mutants, postsynaptic specializations of neuromuscular junctions are dramatically expanded, including the subsynaptic reticulum, the postsynaptic density, and the glutamate receptor cluster. Expansion of these postsynaptic features is caused by a disruption of ubiquitin homeostasis with accumulation of free ubiquitin chains and ubiquitinated substrates in the leon mutant. Accumulation of Ubiquilin (Ubqn), the ubiquitin receptor whose human homolog ubiquilin 2 is associated with familial amyotrophic lateral sclerosis, also contributes to defects in postsynaptic growth and ubiquitin homeostasis. Importantly, accumulations of postsynaptic proteins cause different aspects of postsynaptic overgrowth in leon mutants. Thus, the deubiquitinase Leon maintains ubiquitin homeostasis and proper Ubqn levels, preventing postsynaptic proteins from accumulation to confine postsynaptic growth.
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Academia Sinica
- Chien-Hsiang Wang
- Yi-Chun Huang
- Pei-Yi Chen
- Ying-Ju Cheng
- Cheng-Ting Chien
Ministry of Science and Technology, Taiwan
- Chien-Hsiang Wang
- Yi-Chun Huang
- Pei-Yi Chen
- Ying-Ju Cheng
- Cheng-Ting Chien
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
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© 2017, Wang et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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USP5/Leon deubiquitinase confines postsynaptic growth by maintaining ubiquitin homeostasis through Ubiquilin
eLife 6:e26886.
https://doi.org/10.7554/eLife.26886
