|Citation||Penney, J., Tsurudome, K., Liao, E.H., Elazzouzi, F., Livingstone, M., Gonzalez, M., Sonenberg, N., Haghighi, A.P. (2012). TOR Is Required for the Retrograde Regulation of Synaptic Homeostasis at the Drosophila Neuromuscular Junction. Neuron 74(1): 166--178. (Export to RIS)|
|Publication Type||Research paper|
|PubMed 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.|
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|Language of Publication||English|
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