Fig. 6: Model for Neuroligin2-RACK1-Cofilin signaling in WT and dnlg2 mutants. | Communications Biology

Fig. 6: Model for Neuroligin2-RACK1-Cofilin signaling in WT and dnlg2 mutants.

From: Neuroligin 2 governs synaptic morphology and function through RACK1-cofilin signaling in Drosophila

Fig. 6

In WT Drosophila NMJs, postsynaptic DNlg2 interacts with RACK1 which can form a complex with downstream Rac1-Cofilin or RhoA-Cofilin signaling components to activate Cofilin phosphorylation. Only if phosphorylated and non-phosphorylated Cofilin kept in a right balance, can actin polymerization/depolymerization be maintained in a good balance. Otherwise, disruption of DNlg2 will destabilize the big DNlg2-RACK1-Rac1 (or RhoA)-Cofilin-signaling complex. This disruption will affect Rac1 and RhoA activation and therefore inhibit downstream Cofilin phosphorylation. The downregulated p-Cofilin will break F-actin polymerization/depolymerization balance to accelerate its depolymerization.

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