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Neuron. 2012 Apr 12;74(1):166-78. doi: 10.1016/j.neuron.2012.01.030.

TOR is required for the retrograde regulation of synaptic homeostasis at the Drosophila neuromuscular junction.

Author information

1
Department of Physiology, McGill University, Montréal, QC H3G 1Y6, Canada.

Abstract

Homeostatic mechanisms operate to stabilize synaptic function; however, we know little about how they are regulated. Exploiting Drosophila genetics, we have uncovered a critical role for the target of rapamycin (TOR) in the regulation of synaptic homeostasis at the Drosophila larval neuromuscular junction. Loss of postsynaptic TOR disrupts a retrograde compensatory enhancement in neurotransmitter release that is normally triggered by a reduction in postsynaptic glutamate receptor activity. Moreover, postsynaptic overexpression of TOR or a phosphomimetic form of S6 ribosomal protein kinase, a common target of TOR, can trigger a strong retrograde increase in neurotransmitter release. Interestingly, heterozygosity for eIF4E, a critical component of the cap-binding protein complex, blocks the retrograde signal in all these cases. Our findings suggest that cap-dependent translation under the control of TOR plays a critical role in establishing the activity dependent homeostatic response at the NMJ.

PMID:
22500638
DOI:
10.1016/j.neuron.2012.01.030
[Indexed for MEDLINE]
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