A retrograde GCN2/eIF2α, but ATF4 independent, mechanism maintains synaptic strength under acute amino acid scarcity at the NMJ
Grant Kauwe, Megumi Mori, Edward H. Liao, Gary K. Scott, Ali Pejmun Haghighi
The paper investigates how GCN2/eIF2α signaling maintains synaptic strength during acute amino acid scarcity at the Drosophila NMJ, showing ATF4 is dispensable and the pathway acts retrogradely from muscle to motoneuron.
bioRxiv · Nov 3, 2022 · PreprintNeuroscience