Presynaptic CK2α is essential for synapse stability. (A) A stable wild-type NMJ on muscle 4. (B and C) Mutations in CK2α resulted in synaptic retractions ranging between loss of few terminal boutons (B, arrow) and complete eliminations of the NMJ (C, arrow). (D–E) Neuronal but not muscle-specific expression of wild-type CK2α rescued the synaptic retraction phenotype in CK2α mutant animals. Large synaptic retractions were still evident after postsynaptic expression (E, arrow). (F) Neuronal expression of a kinase-dead version of CK2α was not sufficient to restore synapse stability (arrow). Bars: (main panels) 10 µm; (panels below) 5 µm. (G) Quantification of synaptic retraction frequencies of different allelic combinations and tissue-specific rescues on muscles 1/9 and 2/10 (***, P ≤ 0.001; n = 9–22 animals). n.s., not significant. (H) Western blot analysis of larval brain extracts demonstrated a strong reduction in CK2α protein levels in CK2α^P1/P1, CK2α^P1/P2, and CK2α^P1/TikR but not in CK2α^P1/Tik mutant animals (the lower band corresponds to CK2α protein). A corresponding decrease in CK2β protein levels was observed. CK2α and CK2β proteins levels were efficiently restored by neuronal or ubiquitous expression of either wild-type or kinase-dead CK2α. Error bars represent SEM.